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Until Ayushman Bharat, India’s biggest get amoxil prescription online experiment with public health insurance was the Rashtriya Swasthya Bima Yojana (RSBY), literally translated from Hindi as ‘National Health Insurance Program’. Until its launch in 2008, nothing of this magnitude had been attempted. Ayushman Bharat is get amoxil prescription online widely considered a large-scale upgrade of RSBY. The Government of India, on its official website, india.gov.in, the National Portal of India, has had the humility to publicly admit to the failure of past efforts at public health insurance. It goes on to position the RSBY as an get amoxil prescription online attempt at succour.

The target beneficiaries of RSBY were families below poverty line (BPL). Depending on which estimate one looks at, the proportion of the population that is BPL varies get amoxil prescription online from 20% to 30%. Even taking into account the lower end of the estimate, that is, 20%, the approximate population in 2017 that would fall in the BPL category, out of a total population of approximately 1340 million, would be 270 million. The number of families, assuming 4.9 persons get amoxil prescription online per family, would be 55.1 million. Contrast this with the 35.8 million families enrolled under RSBY until 30 September 2017, the last date for which official government data are available, which is more than 9 years after its launch, there is a shortfall of 35%.

If we took the higher end of the estimate, that get amoxil prescription online is, 30%, the approximate population in 2017 that would fall in the BPL category, out of a total population of approximately 1340 million, would be 400 million. The number of families, assuming 4.9 persons per family, would be 81.6 million. The shortfall would get amoxil prescription online then be as high as 56%. One reason for this is that as of 30 September 2017, nine states/union territories of India (Chandigarh, Haryana, Jharkhand, Madhya Pradesh, Pondicherry, Punjab, Rajasthan, Uttar Pradesh and Uttarakhand) were not part of the RSBY, as they ….

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Date published get amoxil prescription more info here. August 26, 2020On this page BackgroundCOVID-19 is an infectious disease caused by the SARS-CoV-2 coronavirus. The World Health Organization declared a global pandemic in March 2020, and the Minister of Health signed the Interim Order Respecting the Importation and Sale of Medical Devices for Use in Relation to COVID-19 on March get amoxil prescription 18, 2020. The Interim Order (IO) allows us to quickly address large-scale public health emergencies.This IO allows for faster authorization of Class I-IV medical devices for COVID-19.This document presents the criteria for safety and effectiveness that apply to test swabs used for COVID-19 sampling. It also provides guidance on how to meet these criteria in an application under the IO pathway.

Diagnostic testing is a key element in both get amoxil prescription. identifying cases of infection preventing the spread of the coronavirus A test swab may be used to collect a sample for either Polymerase Chain Reaction (PCR) laboratory testing or point-of-care testing. Point-of-care testing can be done directly in a hospital or doctor’s office. Once the sample has been taken, the swab is either get amoxil prescription placed in a preserving liquid and sent to a laboratory for testing, or placed directly in a testing device (point-of-care).Swabs may be packaged in a variety of virus transport media (VTM). Specifications for individual VTMs are beyond the scope of this document.

Swabs play a role in the accuracy of COVID-19 diagnostic testing. For example, false negatives can occur in PCR tests if get amoxil prescription. the swab material inhibits the test reaction or the swab design doesn’t provide enough surface area to obtain a sufficient sample Test swabs that are not safe and effective may cause or lead to harm. For example. A swab that breaks during sample collection can cause physical injury a non-sterile swab that produces an incorrect test get amoxil prescription result can lead to harmHealth Canada has published a guidance document to support the preparation of applications submitted under the IO.

It should be read in conjunction with this document. We are processing applications as quickly as possible. To avoid delays, please ensure you have completed your application properly.Medical Devices Regulations (MDR) classification In the Canadian regulatory framework, Class I get amoxil prescription devices present the lowest potential risk and Class IV the highest. Swabs are classified according to their labelling and intended use. For example, if a swab is labelled for nasopharyngeal (NP) or oropharyngeal (OP) use only, it will be classified as a Class I medical device according to Classification Rule 2(2) of the MDR.

If a swab is not exclusively for use in oral or nasal cavities, or its use is not explicitly stated, it will be classified as get amoxil prescription a Class II device by Rule 2(1). These swabs belong to a higher risk class because their use in other body orifices for the collection of tissue samples (for example, to test for chlamydia or ureaplasma) is associated with greater risk. Rule 2 Subject to subrules (2) get amoxil prescription to (4), all invasive devices that penetrate the body through a body orifice or that come into contact with the surface of the eye are classified as Class II. A device described in subrule (1) that is intended to be placed in the oral or nasal cavities as far as the pharynx or in the ear canal up to the ear drum is classified as Class I.Regulatory pathways for COVID-19 devicesManufacturers of Class I swabs may seek authorization to import and sell their products under either. A Medical Device Establishment Licence (MDEL) MDEL is an establishment oversight framework that is not product-specific and not designed to assess safety and effectiveness an IO authorization information on safety and effectiveness are required as part of the application Health Canada is encouraging a sub-group of swab manufacturers to use the IO authorization pathway for Class I swabs, especially if they are.

New to the manufacturing of swabs and manufacturing in Canada (such as a company that has re-tooled to manufacture), or using a new manufacturing process or design for swabs (such as 3D printing or honeycomb design)IO applications for swabs should include the following information.Device description get amoxil prescription The device description should include. A picture and/or engineering drawing identification of all materials used in the production of the swab the intended use(s) (for example, NP swabs)Quality manufacturingManufacturers must either. demonstrate compliance with Quality Manufacturing Systems (for example, ISO 13485 certificate) applicable to the swab, or provide a clear description of the planned quality manufacturing systems that are consistent with similar existing manufacturing systemsDesign verificationProvide swab design verification (bench testing) data in a summary report. It should show that get amoxil prescription the essential minimum design characteristics are met. These data should be based on test samples representative of finished swabs that have undergone sterilization prior to bench testing.Dimensions Swabs should have minimum length specifications and minimum and maximum head diameter specifications in order to be safe and effective.

Minimum length specification for example, adult NP swabs require ≥14 cm to reach the posterior nasopharynx minimum and maximum head diameter specification for example, adult NP swabs require 1–4 mm to pass into the mid-inferior portion of the inferior turbinate and maneuver well FlexibilitySwab flexibility is assessed through. Durability for example, tolerate 20 rough repeated insertions into a 4 mm inner diameter clear plastic tube get amoxil prescription curved back on itself with a curve radius of 3 cm bendability for example, bend tip and neck 90º without breaking ability to maintain initial form for example, restore to initial form following 45º bending Manufacturers may describe the test performed, the number of samples, and a summary of the results.Strength/Breakpoint (failure) To limit the potential for patient harm, the minimum breakpoint distance should be approximately 8 to 9 cm from the nasopharynx. However, no breaks or fractures should occur following reasonable manipulation. Applicants should submit a rationale for the design of the breakpoint distance from the swab tip. It should demonstrate that the breakpoint length can be accommodated by commercially available swab/media tubes.Surface propertiesThe swab get amoxil prescription surface should be free of.

processing aids (such as disinfectants) foreign materials degreasers mold release agents For injection molded swabs, no burrs, flashing, or sharp edges should be present. Design validationProvide swab validation (performance) data in a summary report that demonstrates that the swab. can acquire samples comparable to a commercially available swab control, and will not inhibit the PCR reactionThese get amoxil prescription data should be based on test samples representative of finished swabs that have undergone sterilization prior to testing.Comparable sample acquisition to a control, and PCR compatibilityThe manufacturer should demonstrate test swab cycle threshold (Ct) recovery values (RT-PCR) that are statistically comparable to those obtained from a commercially available swab control using SARS-CoV-2 (or a scientifically justified surrogate).Pass/Fail criteria. Values ≥ 2Cts indicate significantly less efficient ribonucleic acid collection and/or elution.Clinical feasibility/suitability simulationManufacturers should submit either. A clinical test get amoxil prescription report or previous clinical data Clinical test reportThe clinical test report should describe the use of the proposed finished swab (sterilized) in a sufficient number of individuals by trained healthcare professionals in a minimum of 30 patients that have tested positive for SARS-CoV-2, or a scientifically justified surrogate virus.

Include comparisons of the proposed swab against a flocked swab commercially available in Canada with respect to. flexibility fit ability to navigate to the nasopharynx (or other areas specified in the indications) ability to collect a specimen/respiratory epithelial cells for example, using the RNase P housekeeping gene test results agreement for example, ≥ 90% positive % agreement using a composite control (positive % agreement calculation that includes all positive findings from control and test swabs) Clinical testing considerations A scientifically justified surrogate virus may be used if COVID-positive patients are not available. Positive % agreement get amoxil prescription should not be determined using high Ct samples. One-half (1/2) to two-thirds (2/3) of COVID-positive samples should have a high viral loads (Cts <. 30).

Report agreement between control and test swabs in terms of quantitative (Ct) and qualitative (+/- get amoxil prescription test) values with appropriate descriptive statistics. Include patient symptomatology for samples. For example, days from symptom onset, known vs. Suspected COVID status get amoxil prescription. Use of different VTM/universal transport media (V/UTM) across COVID-positive samples may contribute to Ct variability.

Ensure consistency by using the same media/tubes for each specimen within a clinical evaluation. Validate the chosen get amoxil prescription V/UTM media/tubes to show they will not interfere with the PCR test results. For example, allowing 7 days of swab positive specimen incubation with the chosen media/vial is considered a worst-case transportation scenario to evaluate maximal leaching/interaction potential). Use a single PCR test platform throughout each clinical evaluation. The platform should have been previously authorized by HC or another jurisdiction get amoxil prescription.

Location (for example, left vs right nostril) and order of sampling (for example, control vs. Test swab) can affect specimen quality and results variability. Location and swab sampling order should be randomized.For additional information on collecting, handling, and testing COVID-19 specimens, please refer to the Centers for Disease Control and Prevention (CDC) Interim Guidelines get amoxil prescription for Collecting, Handling, and Testing Clinical Specimens for COVID-19.Previous clinical dataPreviously obtained clinical data may be submitted in lieu of clinical testing. Those data should demonstrate the safe and effective use of a swab of identical design and materials in human subjects. The proposed swab should be compared against a flocked swab commercially get amoxil prescription available in Canada with respect to.

flexibility fit ability to navigate to the nasopharynx (or other areas specified in the indications) ability to collect a specimen/respiratory epithelial cells for example, using the RNase P housekeeping gene test results agreement for example, ≥ 90% positive % agreement) using a composite control (positive % agreement calculation that includes all positive findings from control and test swabs) Sterility Provide sterilization validation data in a summary report. It should demonstrate that the chosen sterilization method will achieve a minimum Sterility Assurance Level (SAL) of 10-6 for the proposed swab, using an appropriate biological indicator (BI) organism (see below). If the swab will be sterilized using an get amoxil prescription ethylene oxide (EtO) method, you should demonstrate that EtO and ethylene chlorohydrin (ECH) residuals meet the tolerable contact limits (TCL) specified in ISO 10993-7. Commonly used swab materials, compatible sterilization methods, and appropriate biological indicators are described below. Sterilization Method Swab Materials EtO(for example, ISO 11135) Gamma Irradiation(ISO 11137) Polystyrene handle, polyester bicomponent fiber tipFootnote * X(for example, Puritan 25-3316-H/U) Not applicable Polystyrene handle, nylon flocked fiber tipFootnote * X(for example, Copan 503CS01) X(for example, BD 220252) Footnote * The CDC provides guidance on the types of swabs that should be used for optimal specimen collection for PCR testing.

They include swabs that are made of polyester (for example, Dacron), get amoxil prescription rayon, or nylon-flocked. Cotton-tipped or calcium alginate swabs are not acceptable because residues present in those materials inhibit the PCR reaction. Return to footnote * referrer Appropriate BIIf ionizing radiation will be used to sterilize the swab. Bacillus pumilus spores are recommended for doses of 25 get amoxil prescription kGy Bacillus cereus or Bacillus sphaericus spores are recommended for doses of >. 25 kGy (World Health Organization, The International Pharmacopoeia, 9th Ed., 2019) Sterilization Process Spore (Indicator Organism) Steam Geobacillus stearothermophilus(formerly Bacillus stearothermophilus) Dry Heat Bacillus atrophaeus (formerly Bacillus subtilis var.

Niger) Ethlylene Oxide Bacillus atrophaeus (formerly Bacillus subtilis var. Niger) Hydrogen Peroxide Geobacillus stearothermophilus(formerly Bacillus get amoxil prescription stearothermophilus) Source. US Food and Drug Administration, "Biological Indicator (BI) Premarket Notification [510(k)] Submissions," October 2007. [Online].Packaging validation Provide packaging validation data in a summary report. It should demonstrate that the swab packaging system will maintain a sterile environment across get amoxil prescription the labelled shelf life (for example, ASTM F1980).

without leakage (for example, ASTM D3078-02) with adequate seal strength (for example, ASTM F88/EN 868-5)Test packaging samples should be representative of finished swab packages that have undergone sterilization prior to testing.Biocompatibility Provide biocompatibility data in a summary report. It should demonstrate compliance with biocompatibility tests recommended for devices in limited contact (≤24 hrs) with mucosal membranes, as per ISO 10993-1. These include get amoxil prescription. cytotoxicity sensitization irritation/intracutaneous reactivityThese data should be based on test samples representative of finished swabs that have undergone sterilization prior to testing.LabellingSwabs should be individually packaged and labelled. The application get amoxil prescription must include the swab label, which must include.

The name and model number of the device the term ‘sterile’, along with the sterilization method (EtO = ethylene oxide. R = gamma irradiation), if the swab is intended to be sold in a sterile condition the name and address of the manufacturer manufacturing and expiry datesIf swabs are not sterile but must be sterilized at the user facility, then the sterilization parameters and method should be clearly described in accompanying instructions for use documentation.Post-market requirementsAs stated in Section 12 of the IO, within 10 days of becoming aware of an incident in Canada, all IO authorization holders must. report the get amoxil prescription incident specify the nature of the incident specify the circumstances surrounding the incidentOn this page About face shields Personal protective equipment (PPE) can help prevent potential exposure to infectious disease. They are considered medical devices in Canada and therefore must follow the requirements outlined in the Medical Devices Regulations. Medical devices are classified into 4 groups (Class I, II, III and IV) based on their risk to health and safety.

Class I devices, such as gauze bandages, pose the lowest potential risk, while Class IV devices, such as pacemakers, pose the greatest potential get amoxil prescription risk. In Canada, face shields are Class I medical devices. A face shield has a transparent window or visor that shields the face and associated mucous membranes (eyes, nose and mouth). It protects the wearer against exposure from splashes and sprays of get amoxil prescription body fluids. Face shields are made of shatterproof plastic, fit over the face and are held in place by head straps or caps.

They may be made of polycarbonate, propionate, acetate, polyvinyl chloride, or polyethylene terephthalate. They are usually get amoxil prescription worn with other PPE, such as a medical mask, respirator or eyewear. Health Canada strongly advises against the use of plastic bags as an alternative to face shields. Standards and requirements for face shields Organizations that are manufacturing face shields are advised to consult some or all of the following standards throughout the design and testing stages. ANSI/ISEA Z.87.1 (2015), American National Standard for Occupational and Educational Personal Eye and Face Protection Devices CSA Z94.3 (2020), Eye and get amoxil prescription Face Protectors CSA Z94.3.1 (2016), Guideline for Selection, Use, and Care of Eye and Face Protectors BS EN 166 (2002), Personal Eye Protection.

Specifications. Minimum specifications must be incorporated into the design and verification stages to ensure safe and effective face shields. Provide adequate get amoxil prescription coverage (CSA Z94.3 Sections 0.2.1/10.2.2/10.3/10.4). The size of the face shield is important because it must protect the face and front part of the head. This includes the eyes, forehead, cheeks, nose, mouth, and chin.

Protection may also need to get amoxil prescription extend to the front of the neck in situations with flying particles and sprays of hazardous liquids. Fit snugly to afford a good seal to the forehead area and to prevent slippage of the device Footnote 1. Be made of optically clear, distortion-free, lightweight materials (CSA Z94.3.1-16 and Footnote get amoxil prescription 1). Be free of visible defects or flaws that would impede vision (ANSI Z87.1 Section 9.4). Be comfortable and easy to assemble, use and remove by health care professionals.

Provide adequate space between the wearer’s face and the inner surface of the visor to allow for the use of ancillary equipment (for example, medical get amoxil prescription mask, respirator, eyewear) Footnote 1. The characteristics and performance requirements of face shields must not be altered when attaching shields to other protective equipment, such as hats or caps. Display anti-fog characteristics on inside and outside of shield (CSA Z94.3.1-16). For face shields that are not fog get amoxil prescription resistant, anti-fog spray must be provided. Provide user-contacting materials that have adequate material biocompatibility (skin sensitivity and cytotoxic testing) (ISO 10993-5, 10).

Other items to take note of include. Face shields used for protection in hospital settings do not get amoxil prescription have to be impact- or flame- resistant. If the device is specifically designed to withstand impact from sharp or fast projectiles, it must comply with set-out standards (ANSI Z87.1, sections 9.2 and 9.3, CSA Z94.3, section 10.1). For reuse, manufacturers must provide validated cleaning instructions. Sterilization procedures must not compromise the shield in get amoxil prescription any way, such as deformation or cracking.

Regulatory authorization Most PPE, including face shields, are Class I medical devices if they are manufactured, sold or represented for use for reducing the risk of or preventing the user from infection. This includes COVID-19. Face shields may be authorized for sale or import into get amoxil prescription Canada through the following regulatory pathways. Pathway 1. Interim order authorization to import and sell medical devices related to COVID-19.

Pathway 2 get amoxil prescription. Expedited review and issuance of Medical Device Establishment Licences (MDEL) related to COVID-19. MDEL holders that import and sell face shields should take measures to ensure they are safe and get amoxil prescription effective. Pathway 3. Exceptional importation and sale of certain non-compliant medical devices related to COVID-19.

Note that a sale generally requires the transfer of ownership of a device from one party to another and does not necessitate any transfer of money get amoxil prescription. Applicants should carefully review the pathways and select the most appropriate authorization route for their product. For more information, see Personal protective equipment (COVID-19). How to get amoxil prescription get authorization. If you intend to manufacture 3D print face shields in response to the COVID-19 crisis, see.

3D printing and other manufacturing of personal protective equipment in response to COVID-19 Feedback If you have any questions or comments about this notice, contact the Medical Devices Directorate at hc.meddevices-instrumentsmed.sc@canada.ca R. J. Roberge, "Face shields for infection control. A review," Journal of Occupational and Environmental Hygiene, pp. 235-242, 2016.

Related links FootnotesFootnote 1 R. J. Roberge, "Face shields for infection control. A review," Journal of Occupational and Environmental Hygiene, pp. 235-242, 2016.Return to footnote 1 referrer.

Date published get amoxil prescription online order amoxil. August 26, 2020On this page BackgroundCOVID-19 is an infectious disease caused by the SARS-CoV-2 coronavirus. The World Health Organization declared a global pandemic get amoxil prescription online in March 2020, and the Minister of Health signed the Interim Order Respecting the Importation and Sale of Medical Devices for Use in Relation to COVID-19 on March 18, 2020. The Interim Order (IO) allows us to quickly address large-scale public health emergencies.This IO allows for faster authorization of Class I-IV medical devices for COVID-19.This document presents the criteria for safety and effectiveness that apply to test swabs used for COVID-19 sampling. It also provides guidance on how to meet these criteria in an application under the IO pathway.

Diagnostic testing get amoxil prescription online is a key element in both. identifying cases of infection preventing the spread of the coronavirus A test swab may be used to collect a sample for either Polymerase Chain Reaction (PCR) laboratory testing or point-of-care testing. Point-of-care testing can be done directly in a hospital or doctor’s office. Once the get amoxil prescription online sample has been taken, the swab is either placed in a preserving liquid and sent to a laboratory for testing, or placed directly in a testing device (point-of-care).Swabs may be packaged in a variety of virus transport media (VTM). Specifications for individual VTMs are beyond the scope of this document.

Swabs play a role in the accuracy of COVID-19 diagnostic testing. For example, false negatives can occur get amoxil prescription online in PCR tests if. the swab material inhibits the test reaction or the swab design doesn’t provide enough surface area to obtain a sufficient sample Test swabs that are not safe and effective may cause or lead to harm. For example. A swab that breaks during sample collection can cause get amoxil prescription online physical injury a non-sterile swab that produces an incorrect test result can lead to harmHealth Canada has published a guidance document to support the preparation of applications submitted under the IO.

It should be read in conjunction with this document. We are processing applications as quickly as possible. To avoid get amoxil prescription online delays, please ensure you have completed your application properly.Medical Devices Regulations (MDR) classification In the Canadian regulatory framework, Class I devices present the lowest potential risk and Class IV the highest. Swabs are classified according to their labelling and intended use. For example, if a swab is labelled for nasopharyngeal (NP) or oropharyngeal (OP) use only, it will be classified as a Class I medical device according to Classification Rule 2(2) of the MDR.

If a swab is not exclusively get amoxil prescription online for use in oral or nasal cavities, or its use is not explicitly stated, it will be classified as a Class II device by Rule 2(1). These swabs belong to a higher risk class because their use in other body orifices for the collection of tissue samples (for example, to test for chlamydia or ureaplasma) is associated with greater risk. Rule 2 Subject to subrules (2) to (4), all invasive devices that penetrate get amoxil prescription online the body through a body orifice or that come into contact with the surface of the eye are classified as Class II. A device described in subrule (1) that is intended to be placed in the oral or nasal cavities as far as the pharynx or in the ear canal up to the ear drum is classified as Class I.Regulatory pathways for COVID-19 devicesManufacturers of Class I swabs may seek authorization to import and sell their products under either. A Medical Device Establishment Licence (MDEL) MDEL is an establishment oversight framework that is not product-specific and not designed to assess safety and effectiveness an IO authorization information on safety and effectiveness are required as part of the application Health Canada is encouraging a sub-group of swab manufacturers to use the IO authorization pathway for Class I swabs, especially if they are.

New to the manufacturing of swabs and manufacturing in Canada (such as a company that has re-tooled to manufacture), or using a new manufacturing process or design for swabs (such as 3D printing or honeycomb design)IO applications for swabs get amoxil prescription online should include the following information.Device description The device description should include. A picture and/or engineering drawing identification of all materials used in the production of the swab the intended use(s) (for example, NP swabs)Quality manufacturingManufacturers must either. demonstrate compliance with Quality Manufacturing Systems (for example, ISO 13485 certificate) applicable to the swab, or provide a clear description of the planned quality manufacturing systems that are consistent with similar existing manufacturing systemsDesign verificationProvide swab design verification (bench testing) data in a summary report. It should show that the get amoxil prescription online essential minimum design characteristics are met. These data should be based on test samples representative of finished swabs that have undergone sterilization prior to bench testing.Dimensions Swabs should have minimum length specifications and minimum and maximum head diameter specifications in order to be safe and effective.

Minimum length specification for example, adult NP swabs require ≥14 cm to reach the posterior nasopharynx minimum and maximum head diameter specification for example, adult NP swabs require 1–4 mm to pass into the mid-inferior portion of the inferior turbinate and maneuver well FlexibilitySwab flexibility is assessed through. Durability for example, tolerate 20 rough repeated insertions into a 4 mm inner diameter clear plastic tube curved back on itself with a curve radius of 3 cm bendability for example, bend tip and neck 90º without breaking ability to maintain get amoxil prescription online initial form for example, restore to initial form following 45º bending Manufacturers may describe the test performed, the number of samples, and a summary of the results.Strength/Breakpoint (failure) To limit the potential for patient harm, the minimum breakpoint distance should be approximately 8 to 9 cm from the nasopharynx. However, no breaks or fractures should occur following reasonable manipulation. Applicants should submit a rationale for the design of the breakpoint distance from the swab tip. It should demonstrate that the breakpoint length can be accommodated by commercially available swab/media tubes.Surface propertiesThe get amoxil prescription online swab surface should be free of.

processing aids (such as disinfectants) foreign materials degreasers mold release agents For injection molded swabs, no burrs, flashing, or sharp edges should be present. Design validationProvide swab validation (performance) data in a summary report that demonstrates that the swab. can acquire samples comparable get amoxil prescription online to a commercially available swab control, and will not inhibit the PCR reactionThese data should be based on test samples representative of finished swabs that have undergone sterilization prior to testing.Comparable sample acquisition to a control, and PCR compatibilityThe manufacturer should demonstrate test swab cycle threshold (Ct) recovery values (RT-PCR) that are statistically comparable to those obtained from a commercially available swab control using SARS-CoV-2 (or a scientifically justified surrogate).Pass/Fail criteria. Values ≥ 2Cts indicate significantly less efficient ribonucleic acid collection and/or elution.Clinical feasibility/suitability simulationManufacturers should submit either. A clinical test report or previous clinical data Clinical test reportThe clinical test report should describe the use get amoxil prescription online of the proposed finished swab (sterilized) in a sufficient number of individuals by trained healthcare professionals in a minimum of 30 patients that have tested positive for SARS-CoV-2, or a scientifically justified surrogate virus.

Include comparisons of the proposed swab against a flocked swab commercially available in Canada with respect to. flexibility fit ability to navigate to the nasopharynx (or other areas specified in the indications) ability to collect a specimen/respiratory epithelial cells for example, using the RNase P housekeeping gene test results agreement for example, ≥ 90% positive % agreement using a composite control (positive % agreement calculation that includes all positive findings from control and test swabs) Clinical testing considerations A scientifically justified surrogate virus may be used if COVID-positive patients are not available. Positive % agreement should not be determined using high Ct get amoxil prescription online samples. One-half (1/2) to two-thirds (2/3) of COVID-positive samples should have a high viral loads (Cts <. 30).

Report agreement between control and test swabs in terms of quantitative (Ct) and qualitative (+/- test) values get amoxil prescription online with appropriate descriptive statistics. Include patient symptomatology for samples. For example, days from symptom onset, known vs. Suspected COVID status get amoxil prescription online. Use of different VTM/universal transport media (V/UTM) across COVID-positive samples may contribute to Ct variability.

Ensure consistency by using the same media/tubes for each specimen within a clinical evaluation. Validate the chosen V/UTM media/tubes to show they will not interfere with get amoxil prescription online the PCR test results. For example, allowing 7 days of swab positive specimen incubation with the chosen media/vial is considered a worst-case transportation scenario to evaluate maximal leaching/interaction potential). Use a single PCR test platform throughout each clinical evaluation. The platform should have been get amoxil prescription online previously authorized by HC or another jurisdiction.

Location (for example, left vs right nostril) and order of sampling (for example, control vs. Test swab) can affect specimen quality and results variability. Location and swab sampling order should be randomized.For additional information on collecting, handling, and testing COVID-19 specimens, please refer to the Centers for Disease Control and Prevention (CDC) Interim Guidelines for Collecting, Handling, and Testing Clinical Specimens for COVID-19.Previous clinical dataPreviously obtained clinical data may be get amoxil prescription online submitted in lieu of clinical testing. Those data should demonstrate the safe and effective use of a swab of identical design and materials in human subjects. The proposed swab should be compared against a flocked swab commercially available in Canada with respect to get amoxil prescription online.

flexibility fit ability to navigate to the nasopharynx (or other areas specified in the indications) ability to collect a specimen/respiratory epithelial cells for example, using the RNase P housekeeping gene test results agreement for example, ≥ 90% positive % agreement) using a composite control (positive % agreement calculation that includes all positive findings from control and test swabs) Sterility Provide sterilization validation data in a summary report. It should demonstrate that the chosen sterilization method will achieve a minimum Sterility Assurance Level (SAL) of 10-6 for the proposed swab, using an appropriate biological indicator (BI) organism (see below). If the swab will be sterilized using an ethylene oxide (EtO) method, you get amoxil prescription online should demonstrate that EtO and ethylene chlorohydrin (ECH) residuals meet the tolerable contact limits (TCL) specified in ISO 10993-7. Commonly used swab materials, compatible sterilization methods, and appropriate biological indicators are described below. Sterilization Method Swab Materials EtO(for example, ISO 11135) Gamma Irradiation(ISO 11137) Polystyrene handle, polyester bicomponent fiber tipFootnote * X(for example, Puritan 25-3316-H/U) Not applicable Polystyrene handle, nylon flocked fiber tipFootnote * X(for example, Copan 503CS01) X(for example, BD 220252) Footnote * The CDC provides guidance on the types of swabs that should be used for optimal specimen collection for PCR testing.

They include get amoxil prescription online swabs that are made of polyester (for example, Dacron), rayon, or nylon-flocked. Cotton-tipped or calcium alginate swabs are not acceptable because residues present in those materials inhibit the PCR reaction. Return to footnote * referrer Appropriate BIIf ionizing radiation will be used to sterilize the swab. Bacillus pumilus spores are recommended for doses of 25 kGy Bacillus cereus or Bacillus sphaericus spores are recommended for doses of > get amoxil prescription online. 25 kGy (World Health Organization, The International Pharmacopoeia, 9th Ed., 2019) Sterilization Process Spore (Indicator Organism) Steam Geobacillus stearothermophilus(formerly Bacillus stearothermophilus) Dry Heat Bacillus atrophaeus (formerly Bacillus subtilis var.

Niger) Ethlylene Oxide Bacillus atrophaeus (formerly Bacillus subtilis var. Niger) Hydrogen Peroxide Geobacillus stearothermophilus(formerly get amoxil prescription online Bacillus stearothermophilus) Source. US Food and Drug Administration, "Biological Indicator (BI) Premarket Notification [510(k)] Submissions," October 2007. [Online].Packaging validation Provide packaging validation data in a summary report. It should demonstrate that the swab packaging system will maintain a sterile environment across the labelled shelf get amoxil prescription online life (for example, ASTM F1980).

without leakage (for example, ASTM D3078-02) with adequate seal strength (for example, ASTM F88/EN 868-5)Test packaging samples should be representative of finished swab packages that have undergone sterilization prior to testing.Biocompatibility Provide biocompatibility data in a summary report. It should demonstrate compliance with biocompatibility tests recommended for devices in limited contact (≤24 hrs) with mucosal membranes, as per ISO 10993-1. These include get amoxil prescription online. cytotoxicity sensitization irritation/intracutaneous reactivityThese data should be based on test samples representative of finished swabs that have undergone sterilization prior to testing.LabellingSwabs should be individually packaged and labelled. The application must include the swab label, which get amoxil prescription online must include.

The name and model number of the device the term ‘sterile’, along with the sterilization method (EtO = ethylene oxide. R = gamma irradiation), if the swab is intended to be sold in a sterile condition the name and address of the manufacturer manufacturing and expiry datesIf swabs are not sterile but must be sterilized at the user facility, then the sterilization parameters and method should be clearly described in accompanying instructions for use documentation.Post-market requirementsAs stated in Section 12 of the IO, within 10 days of becoming aware of an incident in Canada, all IO authorization holders must. report the incident specify the nature of the incident specify the circumstances surrounding the incidentOn this page About face shields Personal protective equipment (PPE) get amoxil prescription online can help prevent potential exposure to infectious disease. They are considered medical devices in Canada and therefore must follow the requirements outlined in the Medical Devices Regulations. Medical devices are classified into 4 groups (Class I, II, III and IV) based on their risk to health and safety.

Class I devices, such as gauze bandages, pose the lowest potential risk, while get amoxil prescription online Class IV devices, such as pacemakers, pose the greatest potential risk. In Canada, face shields are Class I medical devices. A face shield has a transparent window or visor that shields the face and associated mucous membranes (eyes, nose and mouth). It protects the wearer against exposure from splashes and sprays of get amoxil prescription online body fluids. Face shields are made of shatterproof plastic, fit over the face and are held in place by head straps or caps.

They may be made of polycarbonate, propionate, acetate, polyvinyl chloride, or polyethylene terephthalate. They are usually worn with other PPE, such as a medical mask, respirator or get amoxil prescription online eyewear. Health Canada strongly advises against the use of plastic bags as an alternative to face shields. Standards and requirements for face shields Organizations that are manufacturing face shields are advised to consult some or all of the following standards throughout the design and testing stages. ANSI/ISEA Z.87.1 (2015), American National Standard for Occupational and Educational Personal Eye and Face Protection Devices CSA Z94.3 (2020), Eye and Face Protectors CSA Z94.3.1 (2016), Guideline for Selection, Use, and Care of Eye and get amoxil prescription online Face Protectors BS EN 166 (2002), Personal Eye Protection.

Specifications. Minimum specifications must be incorporated into the design and verification stages to ensure safe and effective face shields. Provide adequate coverage get amoxil prescription online (CSA Z94.3 Sections 0.2.1/10.2.2/10.3/10.4). The size of the face shield is important because it must protect the face and front part of the head. This includes the eyes, forehead, cheeks, nose, mouth, and chin.

Protection may also need to extend to get amoxil prescription online the front of the neck in situations with flying particles and sprays of hazardous liquids. Fit snugly to afford a good seal to the forehead area and to prevent slippage of the device Footnote 1. Be made of optically clear, distortion-free, lightweight materials get amoxil prescription online (CSA Z94.3.1-16 and Footnote 1). Be free of visible defects or flaws that would impede vision (ANSI Z87.1 Section 9.4). Be comfortable and easy to assemble, use and remove by health care professionals.

Provide adequate space between the wearer’s face and the inner surface of the visor to allow for the use of ancillary equipment (for example, medical mask, get amoxil prescription online respirator, eyewear) Footnote 1. The characteristics and performance requirements of face shields must not be altered when attaching shields to other protective equipment, such as hats or caps. Display anti-fog characteristics on inside and outside of shield (CSA Z94.3.1-16). For face shields that are not fog resistant, get amoxil prescription online anti-fog spray must be provided. Provide user-contacting materials that have adequate material biocompatibility (skin sensitivity and cytotoxic testing) (ISO 10993-5, 10).

Other items to take note of include. Face shields used for protection in hospital settings do not have to be impact- or flame- resistant get amoxil prescription online. If the device is specifically designed to withstand impact from sharp or fast projectiles, it must comply with set-out standards (ANSI Z87.1, sections 9.2 and 9.3, CSA Z94.3, section 10.1). For reuse, manufacturers must provide validated cleaning instructions. Sterilization procedures must not compromise get amoxil prescription online the shield in any way, such as deformation or cracking.

Regulatory authorization Most PPE, including face shields, are Class I medical devices if they are manufactured, sold or represented for use for reducing the risk of or preventing the user from infection. This includes COVID-19. Face shields may get amoxil prescription online be authorized for sale or import into Canada through the following regulatory pathways. Pathway 1. Interim order authorization to import and sell medical devices related to COVID-19.

Pathway 2 get amoxil prescription online. Expedited review and issuance of Medical Device Establishment Licences (MDEL) related to COVID-19. MDEL holders get amoxil prescription online that import and sell face shields should take measures to ensure they are safe and effective. Pathway 3. Exceptional importation and sale of certain non-compliant medical devices related to COVID-19.

Note that a sale generally requires the get amoxil prescription online transfer of ownership of a device from one party to another and does not necessitate any transfer of money. Applicants should carefully review the pathways and select the most appropriate authorization route for their product. For more information, see Personal protective equipment (COVID-19). How to get amoxil prescription online get authorization. If you intend to manufacture 3D print face shields in response to the COVID-19 crisis, see.

3D printing and other manufacturing of personal protective equipment in response to COVID-19 Feedback If you have any questions or comments about this notice, contact the Medical Devices Directorate at hc.meddevices-instrumentsmed.sc@canada.ca R. J. Roberge, "Face shields for infection control. A review," Journal of Occupational and Environmental Hygiene, pp. 235-242, 2016.

Related links FootnotesFootnote 1 R. J. Roberge, "Face shields for infection control. A review," Journal of Occupational and Environmental Hygiene, pp. 235-242, 2016.Return to footnote 1 referrer.

What should I watch for while using Amoxil?

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Over 12,000 home health agencies served 5 amoxil amoxicillin 250mg million buy amoxil pill disabled and older Americans in 2018. Home health aides help their clients with the tasks of daily living, like eating and showering, as well as with clinical tasks, like taking blood pressure and leading physical therapy exercises. Medicare relies on home health care services because they help patients discharged from the hospital and skilled nursing facilities recover but at a much lower cost buy amoxil pill. Together, Medicare and Medicaid make up 76% of all home health spending.Home health care workers serve a particularly important role in rural areas.

As rural areas lose physicians and hospitals, home health agencies often buy amoxil pill replace primary care providers. The average age of residents living in rural counties is seven years older than in urban counties, and this gap is growing. The need for home health agencies serving the elderly in rural areas will continue to grow over the coming decades.Rural home health agencies face unique challenges. Low concentrations of people are dispersed over large geographic areas leading to long travel times for buy amoxil pill workers to drive to clients’ homes.

Agencies in rural areas also have difficulties recruiting and maintaining a workforce. Due to these difficulties, agencies may not be able to serve all rural beneficiaries, initiate care on time, or deliver all covered services.Congress has supported measures to encourage home health agencies to work in rural areas since the buy amoxil pill 1980s by using rural add-on payments. A rural add-on is a percentage increase on top of per visit and episode-of-care payments. When a home health aide works in a rural county, Medicare pays buy amoxil pill their home health agency a standard fee plus a rural add-on.

With a 5% add-on, Medicare would pay $67.78 for an aide home visit in a city and $71.17 for the same care in a rural area.Home health care workers serve a particularly important role in rural areas. As rural areas lose physicians and hospitals, home health agencies often replace primary care providers.Rural add-on payments have fluctuated based on Congressional budgets and political priorities. From 2003 to 2019, the amount Medicare paid agencies buy amoxil pill changed eight times. For instance, the add-on dropped from 10% to nothing in April 2003.

Then, in April 2004, buy amoxil pill Congress set the rural add-on to 5%.The variation in payments created a natural experiment for researchers. Tracy Mroz and colleagues assessed how rural add-ons affected the supply of home health agencies in rural areas. They asked if the number of agencies in urban and rural counties varied depending on the presence and dollar amount of rural add-ons between 2002 and 2018. Though rural add-ons have been in place for over 30 years, researchers had not previously investigated their effect on the availability of home healthcare.The researchers found that rural areas adjacent buy amoxil pill to urban areas were not affected by rural add-ons.

They had similar supply to urban areas whether or not add-ons were in place. In contrast, isolated rural areas were affected buy amoxil pill substantially by add-ons. Without add-ons, the number of agencies in isolated rural areas lagged behind those in urban areas. When the add-ons were at least 5%, the availability of home health in isolated rural areas was buy amoxil pill comparable to urban areas.In 2020, Congress implemented a system of payment reform that reimburses home health agencies in rural counties by population density and home health use.

Under the new system, counties with low population densities and low home health use will receive the greatest rural add-on payments. These payments aim to increase and maintain the availability of care in the most vulnerable rural home health markets. Time will tell if this approach gives sufficient incentive to ensure access to buy amoxil pill quality care in the nation’s most isolated areas.Photo via Getty ImagesStart Preamble Correction In proposed rule document 2020-13792 beginning on page 39408 in the issue of Tuesday, June 30, 2020, make the following correction. On page 39408, in the first column, in the DATES section, “August 31, 2020” should read “August 24, 2020”.

End Preamble buy amoxil pill [FR Doc. C1-2020-13792 Filed 7-17-20. 8:45 am]BILLING CODE 1301-00-D.

Over 12,000 home health agencies served 5 million disabled and older Americans in get amoxil prescription online 2018. Home health aides help their clients with the tasks of daily living, like eating and showering, as well as with clinical tasks, like taking blood pressure and leading physical therapy exercises. Medicare relies on home health care services because they help patients discharged from the hospital and skilled nursing facilities recover but at a get amoxil prescription online much lower cost. Together, Medicare and Medicaid make up 76% of all home health spending.Home health care workers serve a particularly important role in rural areas. As rural get amoxil prescription online areas lose physicians and hospitals, home health agencies often replace primary care providers.

The average age of residents living in rural counties is seven years older than in urban counties, and this gap is growing. The need for home health agencies serving the elderly in rural areas will continue to grow over the coming decades.Rural home health agencies face unique challenges. Low concentrations of get amoxil prescription online people are dispersed over large geographic areas leading to long travel times for workers to drive to clients’ homes. Agencies in rural areas also have difficulties recruiting and maintaining a workforce. Due to these difficulties, agencies may not be able to serve all rural beneficiaries, initiate care on time, or deliver all covered services.Congress has supported measures to encourage home health agencies to work in rural areas since the 1980s by using rural add-on payments get amoxil prescription online.

A rural add-on is a percentage increase on top of per visit and episode-of-care payments. When a get amoxil prescription online home health aide works in a rural county, Medicare pays their home health agency a standard fee plus a rural add-on. With a 5% add-on, Medicare would pay $67.78 for an aide home visit in a city and $71.17 for the same care in a rural area.Home health care workers serve a particularly important role in rural areas. As rural areas lose physicians and hospitals, home health agencies often replace primary care providers.Rural add-on payments have fluctuated based on Congressional budgets and political priorities. From 2003 to 2019, the amount get amoxil prescription online Medicare paid agencies changed eight times.

For instance, the add-on dropped from 10% to nothing in April 2003. Then, in get amoxil prescription online April 2004, Congress set the rural add-on to 5%.The variation in payments created a natural experiment for researchers. Tracy Mroz and colleagues assessed how rural add-ons affected the supply of home health agencies in rural areas. They asked if the number of agencies in urban and rural counties varied depending on the presence and dollar amount of rural add-ons between 2002 and 2018. Though rural add-ons have been in get amoxil prescription online place for over 30 years, researchers had not previously investigated their effect on the availability of home healthcare.The researchers found that rural areas adjacent to urban areas were not affected by rural add-ons.

They had similar supply to urban areas whether or not add-ons were in place. In contrast, isolated rural areas get amoxil prescription online were affected substantially by add-ons. Without add-ons, the number of agencies in isolated rural areas lagged behind those in urban areas. When the add-ons were at least 5%, the availability of home health in isolated rural areas was comparable to urban areas.In 2020, Congress implemented a system of payment reform that reimburses get amoxil prescription online home health agencies in rural counties by population density and home health use. Under the new system, counties with low population densities and low home health use will receive the greatest rural add-on payments.

These payments aim to increase and maintain the availability of care in the most vulnerable rural home health markets. Time will tell if this approach gives sufficient incentive to ensure access to quality care in the nation’s most isolated areas.Photo via Getty ImagesStart Preamble Correction get amoxil prescription online In proposed rule document 2020-13792 beginning on page 39408 in the issue of Tuesday, June 30, 2020, make the following correction. On page 39408, in the first column, in the DATES section, “August 31, 2020” should read “August 24, 2020”. End Preamble [FR Doc get amoxil prescription online. C1-2020-13792 Filed 7-17-20.

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The role amoxil dosage for dogs of personality in health has been under speculation for decades. The rise of coherent theories of personality and amoxil dosage for dogs the inclusion of modern personality trait measures in large-scale epidemiological studies has only rather recently enabled to examine this question profoundly. Numerous studies have shown that from the five major personality traits, conscientiousness—describing individual differences, for example, in self-regulation, orderliness and carefulness—has emerged as maybe the most important personality factor in lifespan health with low consciousness being associated with a wide range of measures of health and well-being,1 including reduced life expectancy.2 This has sparked several calls highlighting the policy relevance of personality traits.3 4 However, personality traits are typically not included in health guidelines, and the potential causality between personality traits and health outcomes has remained inconclusive.The study by Singh-Manoux et al5 makes an important contribution ….

The role of personality get amoxil prescription online in health has been under speculation for decades. The rise of coherent theories of personality get amoxil prescription online and the inclusion of modern personality trait measures in large-scale epidemiological studies has only rather recently enabled to examine this question profoundly. Numerous studies have shown that from the five major personality traits, conscientiousness—describing individual differences, for example, in self-regulation, orderliness and carefulness—has emerged as maybe the most important personality factor in lifespan health with low consciousness being associated with a wide range of measures of health and well-being,1 including reduced life expectancy.2 This has sparked several calls highlighting the policy relevance of personality traits.3 4 However, personality traits are typically not included in health guidelines, and the potential causality between personality traits and health outcomes has remained inconclusive.The study by Singh-Manoux et al5 makes an important contribution ….

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€‚For the podcast associated with this article, please visit amoxil street price https://academic.oup.com/eurheartj/pages/Podcasts. First scienceThe COVID-19 pandemic has changed the world and has refocused science, including cardiovascular (CV) research.1 This virus not only affects the throat and lungs, but also profoundly impacts the CV system. First of all, male sex, obesity, hypertension,2 diabetes and cardiac conditions at amoxil street price large increased the risk of infection, possibly related to angiotensin-converting enzyme (ACE) expression,3,4 and of an unfavourable disease course. Secondly, COVID-19 affects the heart, leading to myocarditis,5,6 myocardial injury,7 scar formation and arrhythmias, and heart block,8 as well as affecting the blood vessels, leading to vascular occlusion due to local thrombus formation or embolism and eventually cardiac death.9 The mechanisms involved are the usual suspects, as outlined in the Viewpoint ‘COVID-19 is, in the end, an endothelial disease’, by Peter Libby from the Brigham and Women’s Hospital in Boston, USA and myself.

It is well known that the vascular endothelium provides the crucial interface between the circulating blood and tissues, and displays remarkable amoxil street price properties that normally maintain homeostasis.10 This tightly regulated array of functions includes control of haemostasis, fibrinolysis, inflammation, oxidative stress, vascular permeability, and eventually vasomotion and vascular structure. While these functions participate in the moment to moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions overreach and turn against the host, as is the case with SARS-CoV-2, the virus causing the current pandemic (Figure 1). Figure 1Cytokine storm amoxil street price. Proinflammatory cytokines such as IL-1 and TNF-α induce each other’s gene expression, unleashing an amplification loop that sustains the cytokine storm.

The endothelial cell is a key target of cytokines, as they induce action of a central proinflammatory transcriptional hub, nuclear factor-κB. IL-1 also cause substantial increases in production by endothelial and other amoxil street price cells of IL-6, the instigator of the hepatocyte acute phase response. The acute phase reactants include fibrinogen, the precursor of clot, and PAI-1, the major inhibitor of our endogenous fibrinolytic system. C-reactive protein, amoxil street price commonly elevated in COVID-19, provides a readily measured biomarker of inflammatory status.

The alterations in the thrombotic/fibrinolytic balance due to the acute phase response predisposes towards thrombosis in arteries, in the microvasculature including that of organs such as the myocardium and kidney, and in veins, causing deep vein thrombosis and predisposing towards pulmonary embolism. Thus, the very same cytokines that elicit abnormal endothelial functions can unleash the acute phase response which together with local endothelial dysfunction amoxil street price can conspire to cause the clinical complications of COVID-19. The right side of this diagram aligns therapeutic agents that attack these mechanisms of the cytokine storm and may thus limit its devastating consequences (from Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease.

See pages amoxil street price 3038–3044).Figure 1Cytokine storm. Proinflammatory cytokines such as IL-1 and TNF-α induce each other’s gene expression, unleashing an amplification loop that sustains the cytokine storm. The endothelial cell is a key target of cytokines, as they induce action of a central proinflammatory transcriptional hub, nuclear amoxil street price factor-κB. IL-1 also cause substantial increases in production by endothelial and other cells of IL-6, the instigator of the hepatocyte acute phase response.

The acute phase reactants include fibrinogen, the precursor of clot, and PAI-1, amoxil street price the major inhibitor of our endogenous fibrinolytic system. C-reactive protein, commonly elevated in COVID-19, provides a readily measured biomarker of inflammatory status. The alterations in the thrombotic/fibrinolytic balance due to the acute phase response predisposes towards thrombosis in arteries, in the microvasculature including that of organs such as the myocardium and kidney, and in veins, causing deep vein thrombosis and predisposing towards pulmonary embolism. Thus, the very same cytokines that elicit abnormal endothelial functions can unleash the amoxil street price acute phase response which together with local endothelial dysfunction can conspire to cause the clinical complications of COVID-19.

The right side of this diagram aligns therapeutic agents that attack these mechanisms of the cytokine storm and may thus limit its devastating consequences (from Libby P, Lüscher T. COVID-19 is, in amoxil street price the end, an endothelial disease. See pages 3038–3044).It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and the vasculature. This Viewpoint presents amoxil street price the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease.

Cytokines, protein proinflammatory mediators, are key signals that shift endothelial function from the homeostatic into the defensive mode. The endgame of COVID-19 involves a cytokine storm with positive feedback loops amoxil street price governing cytokine production that overwhelm counter-regulatory mechanisms. This concept provides a unifying concept of this raging infection and a framework for rational treatment strategies at a time when we possess an only modest evidence base to guide our therapeutic attempts to confront this novel pandemic.11Surprisingly, emergency unit visits for acute cardiac conditions have declined markedly.12 Several reasons have been suggested. First, patients may have been wary of visiting hospitals during the pandemic.12,13 Secondly, with life on standstill, plaque ruptures and aortic dissections may have become less likely, and, thirdly, the marked reduction in pollution may also have had an influence.14 The first hypothesis is supported by the Fast Track manuscript ‘COVID-19 kills at home.

The close relationship between the epidemic and the increase of out-of-hospital cardiac amoxil street price arrests’ by Simone Savastano and colleagues from the Fondazione IRCCS Policlinico San Matteo in Italy.15 They included all consecutive out-of-hospital cardiac arrests (OHCAs) occurring in the Provinces of Lodi, Cremona, Pavia, and Mantova in the 2 months following the first documented case of COVID-19 in Lombardia compared with those that occurred in the same time window in 2019. The cumulative incidence of COVID-19 from 21 February to 20 April 2020 was 956/100 000 inhabitants and the cumulative incidence of OHCA was 21/100 000 inhabitants, with a 52% increase as compared with 2019 (Figure 2). A significant amoxil street price correlation was found between the difference in cumulative incidence of OHCA and the cumulative incidence of COVID-19. Thus, the OHCA excess in 2020 is closely correlated to the COVID-19 pandemic.

These findings are important for furthering the understanding of the reduced emergency unit visits and for planning of future pandemics, as outlined in an Editorial by Hanno Tan from the Academic Medical Center in Amsterdam, the Netherlands.16 Figure 2(A) Over a period of 60 days from 20 February, the cumulative incidence of COVID-19 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (upper part), amoxil street price and the trend of the difference of OHCA between 2020 and 2019 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (bottom part). (B) The cumulative incidence of the difference in OHCA between 2020 and 2019 per 100 000 inhabitants as a function of the cumulative incidence of COVID-19 per 100 000 inhabitants, since 20 February 2020. Dots are the observed values. The red line is the amoxil street price function fitted using fractional polynomials.

The shaded area is the 95% CI for the estimates (from Baldi E, Maria Sechi G, Mare C, Canevari F, Brancaglione A, Primi R, Klersy C, Palo A, Contri E, Ronchi V, Beretta G, Reali F, Parogni P, Facchin F, Rizzi U, Bussi D, Ruggeri S, Visconti LO, Savastano S, on behalf of the Lombardia CARe researchers. COVID-19 kills amoxil street price at home. The close relationship between the epidemic and the increase of out-of-hospital cardiac arrests. See pages 3045–3054).Figure 2(A) Over a period of 60 amoxil street price days from 20 February, the cumulative incidence of COVID-19 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (upper part), and the trend of the difference of OHCA between 2020 and 2019 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (bottom part).

(B) The cumulative incidence of the difference in OHCA between 2020 and 2019 per 100 000 inhabitants as a function of the cumulative incidence of COVID-19 per 100 000 inhabitants, since 20 February 2020. Dots are the observed values. The red line is the function fitted amoxil street price using fractional polynomials. The shaded area is the 95% CI for the estimates (from Baldi E, Maria Sechi G, Mare C, Canevari F, Brancaglione A, Primi R, Klersy C, Palo A, Contri E, Ronchi V, Beretta G, Reali F, Parogni P, Facchin F, Rizzi U, Bussi D, Ruggeri S, Visconti LO, Savastano S, on behalf of the Lombardia CARe researchers.

COVID-19 kills amoxil street price at home. The close relationship between the epidemic and the increase of out-of-hospital cardiac arrests. See pages 3045–3054).With amoxil street price a prothrombotic state of the endothelium, thrombo-embolism should increase during the COVID-19 pandemic.17 This hypothesis is pursued in a Fast Track entitled ‘Pulmonary embolism in COVID-19 patients. A French multicentre cohort study’ by Ariel Cohen from the Hopital Saint-Antoine in Paris, France.18 In a retrospective multicentric observational study, the authors included consecutive patients hospitalized for COVID-19.

Among 1527 patients, 6.7% patients had pulmonary embolism confirmed by computed tomographty pulmonary angiography (CTPA). Intensive care unit amoxil street price (ICU) transfer and mechanical ventilation were significantly higher in the pulmonary embolism group. In a univariable analysis, traditional venous thrombo-embolic risk factors and pulmonary lesion extension in chest CT were not associated with pulmonary embolism, while patients under anticoagulation prior to hospitalization or in whom it was introduced during hospitalization had a lower risk of pulmonary embolism, with an odds ratio of 0.37. Male gender, prophylactic or therapeutic anticoagulation, C-reactive protein, and time from symptom onset to hospitalization were associated with pulmonary amoxil street price embolism.

Thus, risk factors for pulmonary embolism in COVID-19 do not include traditional thrombo-embolic risk factors, but rather independent clinical and biological findings at admission. In line with the concept outlined above, inflammation is a major driver of pulmonary embolism in COVID-19, as further discussed in a thought-provoking Editorial by Adam Torbicki from the Centre of Postgraduate Medical Education in Otwock, Poland.19Inflammation is also a trigger for atrial fibrillation as it changes the electrical properties of the atrial myocardium and eventually favours tissue fibrosis.20 Furthermore, inflammation may trigger tissue factor expression in the atrial endothelium and favour thrombus formation.21 On the other hand, life on standstill may reduce sympathetic drive and hence reduce the likelihood of new-onset atrial fibrillation.22 In their amoxil street price article entitled ‘New-onset atrial fibrillation. Incidence, characteristics, and related events following a national COVID-19 lockdown of 5.6 million people’, Anders Holt and colleagues from the Copenhagen University Hospital, Herlev and Gentofte in Hellerup, Denmark resolved this conundrum.23 During 3 weeks of lockdown, weekly incidence rates of new-onset AF were 2.3, 1.8, and 1.5 per 1000 person-years, while during the corresponding weeks in 2019, incidence rates were 3.5, 3.4, and 3.6 per 1000 person-years. Incidence rate ratios amoxil street price comparing the same weeks were 0.66, 0.53, and 0.41.

Patients diagnosed during lockdown were younger and had lower CHA2DS2-VASc-scores. During the first 3 weeks of lockdown, 7.8% of patients experienced an ischaemic stroke or death within 7 days of new-onset atrial fibrillation compared with 5.6% during the equivalent weeks in 2019, corresponding to an odds ratio of 1.41. Thus, following a national lockdown in Denmark, new-onset atrial fibrillation amoxil street price declined by 47%, while ischaemic stroke or death within 7 days increased. These complex findings are put into context in an excellent Editorial by Carina Blomstrom-Lundqvist from the Department of Medical Science in Uppsala, Sweden.24Myocardial injury after non-cardiac surgery or MINS is caused by myocardial ischaemia due to a supply–demand mismatch or thrombus and is associated with an increased risk of mortality and major adverse CV events or MACE.25 In their review ‘Myocardial injury after non-cardiac surgery.

Diagnosis and management’ Philip Devereaux and colleagues from McMaster University in Hamilton, Canada note amoxil street price that the diagnostic criteria for MINS include elevated post-operative troponin levels with no evidence of a non-ischaemic aetiology during or within 30 days after non-cardiac surgery, and without ischaemic features such as chest pain or ECG changes.26 Patients with MINS should receive aspirin and a statin, unless contraindicated, and an NOAC (non-vitamin K antagonist oral anticoagulant) if not at high bleeding risk. Cardiac catheterization is only recommended for those with recurrent ischaemia, heart failure, or high risk based on non-invasive imaging. Troponin should be measured for the first few days after surgery in patients ≥65 years or with atherosclerotic disease to avoid missing MINS and the opportunity for secondary prophylactic measures and follow-up.Finally, the issue is complemented by various Discussion Forum contributions on this amoxil street price very timely topic. In a contribution entitled ‘Should atrial fibrillation be considered a cardiovascular risk factor for a worse prognosis in COVID-19 patients?.

€™, Fabian Sanchis-Gomar from the Faculty of Medicine at the University of Valencia, Spain discuss the recent publication ‘Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy’ by Marco Metra and colleagues from Brescia, Italy.9,27 Metra et al. Respond in turn amoxil street price. In a comment entitled ‘ACE2 is on the X chromosome. Could this explain COVID-19 gender differences? amoxil street price.

€™ Felix Hernandez from the Universidad Autonoma de Madrid Centro de Biologia Molecular Severo Ochoa in Madrid, and his colleague Esther Culebras discuss the recent publication entitled ‘Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women with heart failure and effects of renin–angiotensin–aldosterone inhibitors’ by Adriaan Voors and colleagues from the University Medical Center Groningen in the Netherlands.3,28 Voors et al. Respond in a separate comment.29In a contribution entitled ‘Circulating plasma angiotensin-converting enzyme 2 concentrations in patients with kidney disease’, Insa amoxil street price Marie Schmidt and colleagues from the Boston University in Massachusetts, USA also comment on the article by Voors et al.3,30 Voors and colleagues respond in a separate message to this piece.31 Time for the last wordsThis is my last Issue@aGlance in the European Heart Journal in my role of Editor-in-Chief. It has been a pleasure and honour to serve both authors and readers of this fine journal and the European Society of Cardiology over more than a decade. My goal has always been to make it more attractive and informative for clinicians and important and stimulating for scientists worldwide.

I hope you have amoxil street price enjoyed it. Needless to say, that was only possible thanks to an amazing team of editors, reviewers, authors, and editorial staff. I hope that you enjoy amoxil street price this very last issue under my leadership. The time has come to hand the European Heart Journal over to the new Editor-in-Chief, Filippo Crea from Rome.

I am certain Professor Crea will do an excellent job with his new team, retaining amoxil street price some of the experienced editorial staff from Zurich. Thank you for submitting to, reviewing for, and reading the European Heart Journal, and goodbye—I am sure we will stay in touch.With thanks to Amelia Meier-Batschelet for help with compilation of this article. References1Anker SD, Butler J, Khan MS, Abraham WT, Bauersachs J, Bocchi E, Bozkurt B, Braunwald E, Chopra VK, Cleland JG, Ezekowitz J, Filippatos G, Friede T, Hernandez AF, Lam CSP, Lindenfeld J, McMurray JJV, Mehra M, Metra M, Packer M, Pieske B, Pocock SJ, Ponikowski P, Rosano GMC, Teerlink JR, Tsutsui H, Van Veldhuisen DJ, Verma S, Voors AA, Wittes J, Zannad F, Zhang J, Seferovic P, Coats AJS. Conducting clinical trials amoxil street price in heart failure during (and after) the COVID-19 pandemic.

An Expert Consensus Position Paper from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur Heart J 2020;41:2109–2117.2Gao C, Cai Y, Zhang K, Zhou L, Zhang Y, Zhang X, Li Q, Li W, Yang S, Zhao X, Zhao Y, Wang H, Liu Y, Yin Z, Zhang R, Wang R, Yang M, Hui C, Wijns W, McEvoy JW, amoxil street price Soliman O, Onuma Y, Serruys PW, Tao L, Li F. Association of hypertension and antihypertensive treatment with COVID-19 mortality. A retrospective observational amoxil street price study.

Eur Heart J 2020;41:2058–2066.3Sama IE, Ravera A, Santema BT, van Goor H, Ter Maaten JM, Cleland JGF, Rienstra M, Friedrich AW, Samani NJ, Ng LL, Dickstein K, Lang CC, Filippatos G, Anker SD, Ponikowski P, Metra M, van Veldhuisen DJ, Voors AA. Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women with amoxil street price heart failure and effects of renin–angiotensin–aldosterone inhibitors. Eur Heart J 2020;41:1810–1817.4Nicin L, Abplanalp WT, Mellentin H, Kattih B, Tombor L, John D, Schmitto JD, Heineke J, Emrich F, Arsalan M, Holubec T, Walther T, Zeiher AM, Dimmeler S. Cell type-specific expression of the putative SARS-CoV-2 receptor ACE2 in human hearts.

Eur Heart amoxil street price J 2020;41:1804–1806.5Kim IC, Kim JY, Kim HA, Han S. COVID-19-related myocarditis in a 21-year-old female patient. Eur Heart J 2020;41:1859.6Zhou amoxil street price R. Does SARS-CoV-2 cause viral myocarditis in COVID-19 patients?.

Eur Heart J 2020;41:2123.7Shi S, Qin M, Cai Y, Liu T, Shen B, Yang F, Cao S, Liu X, Xiang Y, Zhao amoxil street price Q, Huang H, Yang B, Huang C. Characteristics and clinical significance of myocardial injury in patients with severe coronavirus disease 2019. Eur Heart J 2020;41:2070–2079.8Azarkish M, Laleh Far V, Eslami M, Mollazadeh R. Transient complete heart block amoxil street price in a patient with critical COVID-19.

Eur Heart J 2020;41:2131.9Inciardi RM, Adamo M, Lupi L, Cani DS, Di Pasquale M, Tomasoni D, Italia L, Zaccone G, Tedino C, Fabbricatore D, Curnis A, Faggiano P, Gorga E, Lombardi CM, Milesi G, Vizzardi E, Volpini M, Nodari S, Specchia C, Maroldi R, Bezzi M, Metra M. Characteristics and outcomes of patients amoxil street price hospitalized for COVID-19 and cardiac disease in Northern Italy. Eur Heart J 2020;41:1821–1829.10Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease amoxil street price.

Eur Heart J 2020;41:3038–3044.11Pericàs JM, Hernandez-Meneses M, Sheahan TP, Quintana E, Ambrosioni J, Sandoval E, Falces C, Marcos MA, Tuset M, Vilella A, Moreno A, Miro JM. COVID-19. From epidemiology amoxil street price to treatment. Eur Heart J 2020;41:2092–2112.12De Rosa S, Spaccarotella C, Basso C, Calabrò MP, Curcio A, Filardi PP, Mancone M, Mercuro G, Muscoli S, Nodari S, Pedrinelli R, Sinagra G, Indolfi C.

Reduction of hospitalizations for myocardial infarction in Italy in the COVID-19 era amoxil street price. Eur Heart J 2020;41:2083–2088.13Mafham MM, Spata E, Goldacre R, Gair D, Curnow P, Bray M, Hollings S, Roebuck C, Gale CP, Mamas MA, Deanfield JE, de Belder MA, Luescher TF, Denwood T, Landray MJ, Emberson JR, Collins R, Morris EJA, Casadei B, Baigent C. COVID-19 pandemic and admission rates for amoxil street price and management of acute coronary syndromes in England. Lancet 2020;396:381–389.14Lelieveld J, Münzel T.

Air pollution, the underestimated cardiovascular risk amoxil street price factor. Eur Heart J 2020;41:904–905.15Baldi E, Sechi GM, Mare C, Canevari F, Brancaglione A, Primi R, Klersy C, Palo A, Contri E, Ronchi V, Beretta G, Reali F, Parogni P, Facchin F, Rizzi U, Bussi D, Ruggeri S, Oltrona Visconti L, Savastano S. COVID-19 kills at home. The close amoxil street price relationship between the epidemic and the increase of out-of-hospital cardiac arrests.

Eur Heart J 2020;41:3045–3054.16Tan HL. How does amoxil street price COVID-19 kill at home. And what should we do about it?. Eur Heart J 2020;41:3055–3057.17Gue YX, Gorog amoxil street price DA.

Reduction in ACE2 may mediate the prothrombotic phenotype in COVID-19. Eur Heart J 2020;doi:10.1093/eurheartj/ehaa534.18Fauvel C, Weizman O, Trimaille A, Mika D, Pommier T, Pace N, Douair A, Barbin E, Fraix A, Bouchot O, Benmansour O, Godeau G, Mecheri Y, Lebourdon R, Yvorel C, Massin M, Leblon T, Chabbi C, Cugney E, Benabou L, Aubry M, Chan C, Boufoula I, Barnaud C, Bothorel L, Duceau B, Sutter W, Waldmann V, Bonnet G, Cohen A, Pezel T. Pulmonary embolism amoxil street price in COVID-19 patients. A French multicentre cohort study.

Eur Heart amoxil street price J 2020;41:3058–3068.19Torbicki A. COVID-19 and pulmonary embolism. An unwanted alliance amoxil street price. Eur Heart J 2020;41:3069–3071.20Lazzerini PE, Laghi-Pasini F, Acampa M, Srivastava U, Bertolozzi I, Giabbani B, Finizola F, Vanni F, Dokollari A, Natale M, Cevenini G, Selvi E, Migliacci N, Maccherini M, Boutjdir M, Capecchi PL.

Systemic inflammation rapidly induces reversible atrial electrical remodeling. The role amoxil street price of interleukin-6-mediated changes in connexin expression. J Am Heart Assoc 2019;8:e011006.21Steffel J, Lüscher TF, Tanner FC. Tissue factor in amoxil street price cardiovascular diseases.

Molecular mechanisms and clinical implications. Circulation 2006;113:722–731.22Chen amoxil street price PS, Chen LS, Fishbein MC, Lin SF, Nattel S. Role of the autonomic nervous system in atrial fibrillation. Pathophysiology and therapy.

Circ Res 2014;114:1500–1515.23Holt A, Gislason GH, Schou M, Zareini B, Biering-Sørensen amoxil street price T, Phelps M, Kragholm K, Andersson C, Fosbøl EL, Hansen ML, Gerds TA, Køber L, Torp-Pedersen C, Lamberts M. New-onset atrial fibrillation. Incidence, characteristics, and related events following amoxil street price a national COVID-19 lockdown of 5.6 million people. Eur Heart J 2020;41:3072–3079.24Blomström-Lundqvist C.

Effects of COVID-19 lockdown strategies on management of atrial amoxil street price fibrillation. Eur Heart J 2020;41:3080–3082.25Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galiè N, Gibbs JSR, Huisman MV, Humbert M, Kucher N, Lang I, Lankeit M, Lekakis J, Maack C, Mayer E, Meneveau N, Perrier A, Pruszczyk P, Rasmussen LH, Schindler TH, Svitil P, Vonk Noordegraaf A, Zamorano JL, Zompatori M, Zamorano JL, Achenbach S, Baumgartner H, Bax JJ, Bueno H, Dean V, Deaton C, Erol Ç, Fagard R, Ferrari R, Hasdai D, Hoes A, Kirchhof P, Knuuti J, Kolh P, Lancellotti P, Linhart A, Nihoyannopoulos P, Piepoli MF, Ponikowski P, Sirnes PA, Tamargo JL, Tendera M, Torbicki A, Wijns W, Windecker S, Erol Ç, Jimenez D, Ageno W, Agewall S, Asteggiano R, Bauersachs R, Becattini C, Bounameaux H, Büller HR, Davos CH, Deaton C, Geersing G-J, Sanchez MAG, Hendriks J, Hoes A, Kilickap M, Mareev V, Monreal M, Morais J, Nihoyannopoulos P, Popescu BA, Sanchez O, Spyropoulos AC. 2014 ESC Guidelines amoxil street price on the diagnosis and management of acute pulmonary embolism. The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).

Endorsed by the European Respiratory Society (ERS). Eur Heart J 2014;35:3033–3080.26Devereaux PJ, amoxil street price Szczeklik W. Myocardial injury after non-cardiac surgery. Diagnosis and amoxil street price management.

Eur Heart J 2020;41:3083–3091.27Sanchis-Gomar F, Perez-Quilis C, Lavie CJ. Should atrial fibrillation be considered a cardiovascular risk factor for amoxil street price a worse prognosis in COVID-19 patients?. Eur Heart J 2020;41:3092–3093.28Culebras E, Hernández F. ACE2 is on the X chromosome.

Could this amoxil street price explain COVID-19 gender differences?. Eur Heart J 2020;41:3095.29Sama IE, Voors AA. Men more vulnerable to amoxil street price COVID-19. Explained by ACE2 on the X chromosome?.

Eur Heart J amoxil street price 2020;41:3096.30Schmidt IM, Verma A, Waikar SS. Circulating plasma angiotensin-converting enzyme 2 concentrations in patients with kidney disease. Eur Heart J 2020;41:3097–3098.31Sama IE, Voors AA. Circulating plasma angiotensin-converting enzyme 2 concentration is elevated in patients with kidney disease and diabetes amoxil street price.

Eur Heart J 2020;41:3099. Published on amoxil street price behalf of the European Society of Cardiology. All rights reserved. © The Author(s) amoxil street price 2020.

For permissions, please email. Journals.permissions@oup.com..

€‚For the podcast get amoxil prescription online associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts. First scienceThe COVID-19 pandemic has changed the world and has refocused science, including cardiovascular (CV) research.1 This virus not only affects the throat and lungs, but also profoundly impacts the CV system. First of all, male sex, obesity, hypertension,2 diabetes and cardiac conditions at large increased the risk of infection, possibly related to angiotensin-converting enzyme get amoxil prescription online (ACE) expression,3,4 and of an unfavourable disease course.

Secondly, COVID-19 affects the heart, leading to myocarditis,5,6 myocardial injury,7 scar formation and arrhythmias, and heart block,8 as well as affecting the blood vessels, leading to vascular occlusion due to local thrombus formation or embolism and eventually cardiac death.9 The mechanisms involved are the usual suspects, as outlined in the Viewpoint ‘COVID-19 is, in the end, an endothelial disease’, by Peter Libby from the Brigham and Women’s Hospital in Boston, USA and myself. It is well known that the vascular endothelium provides the crucial interface between the circulating blood and tissues, and displays remarkable properties that normally maintain homeostasis.10 This tightly regulated array of functions includes control of haemostasis, fibrinolysis, inflammation, oxidative stress, vascular permeability, and eventually vasomotion and vascular structure get amoxil prescription online. While these functions participate in the moment to moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions overreach and turn against the host, as is the case with SARS-CoV-2, the virus causing the current pandemic (Figure 1).

Figure get amoxil prescription online 1Cytokine storm. Proinflammatory cytokines such as IL-1 and TNF-α induce each other’s gene expression, unleashing an amplification loop that sustains the cytokine storm. The endothelial cell is a key target of cytokines, as they induce action of a central proinflammatory transcriptional hub, nuclear factor-κB.

IL-1 also cause substantial increases in production by endothelial get amoxil prescription online and other cells of IL-6, the instigator of the hepatocyte acute phase response. The acute phase reactants include fibrinogen, the precursor of clot, and PAI-1, the major inhibitor of our endogenous fibrinolytic system. C-reactive protein, commonly elevated in COVID-19, provides a readily measured biomarker of inflammatory get amoxil prescription online status.

The alterations in the thrombotic/fibrinolytic balance due to the acute phase response predisposes towards thrombosis in arteries, in the microvasculature including that of organs such as the myocardium and kidney, and in veins, causing deep vein thrombosis and predisposing towards pulmonary embolism. Thus, the very same cytokines that elicit abnormal endothelial functions can unleash the get amoxil prescription online acute phase response which together with local endothelial dysfunction can conspire to cause the clinical complications of COVID-19. The right side of this diagram aligns therapeutic agents that attack these mechanisms of the cytokine storm and may thus limit its devastating consequences (from Libby P, Lüscher T.

COVID-19 is, in the end, an endothelial disease. See pages 3038–3044).Figure 1Cytokine get amoxil prescription online storm. Proinflammatory cytokines such as IL-1 and TNF-α induce each other’s gene expression, unleashing an amplification loop that sustains the cytokine storm.

The endothelial cell is a key target of cytokines, as they induce action of a central proinflammatory transcriptional get amoxil prescription online hub, nuclear factor-κB. IL-1 also cause substantial increases in production by endothelial and other cells of IL-6, the instigator of the hepatocyte acute phase response. The acute phase reactants include fibrinogen, the precursor get amoxil prescription online of clot, and PAI-1, the major inhibitor of our endogenous fibrinolytic system.

C-reactive protein, commonly elevated in COVID-19, provides a readily measured biomarker of inflammatory status. The alterations in the thrombotic/fibrinolytic balance due to the acute phase response predisposes towards thrombosis in arteries, in the microvasculature including that of organs such as the myocardium and kidney, and in veins, causing deep vein thrombosis and predisposing towards pulmonary embolism. Thus, the very same cytokines that elicit abnormal endothelial functions can unleash the acute phase response which together with local endothelial dysfunction can conspire to cause the clinical complications of get amoxil prescription online COVID-19.

The right side of this diagram aligns therapeutic agents that attack these mechanisms of the cytokine storm and may thus limit its devastating consequences (from Libby P, Lüscher T. COVID-19 is, in the end, an endothelial get amoxil prescription online disease. See pages 3038–3044).It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and the vasculature.

This Viewpoint presents the hypothesis that COVID-19, particularly get amoxil prescription online in the later complicated stages, represents an endothelial disease. Cytokines, protein proinflammatory mediators, are key signals that shift endothelial function from the homeostatic into the defensive mode. The endgame of COVID-19 involves a get amoxil prescription online cytokine storm with positive feedback loops governing cytokine production that overwhelm counter-regulatory mechanisms.

This concept provides a unifying concept of this raging infection and a framework for rational treatment strategies at a time when we possess an only modest evidence base to guide our therapeutic attempts to confront this novel pandemic.11Surprisingly, emergency unit visits for acute cardiac conditions have declined markedly.12 Several reasons have been suggested. First, patients may have been wary of visiting hospitals during the pandemic.12,13 Secondly, with life on standstill, plaque ruptures and aortic dissections may have become less likely, and, thirdly, the marked reduction in pollution may also have had an influence.14 The first hypothesis is supported by the Fast Track manuscript ‘COVID-19 kills at home. The close relationship between the epidemic and the increase of out-of-hospital cardiac arrests’ by Simone Savastano and colleagues from the Fondazione IRCCS Policlinico San Matteo in Italy.15 They included all consecutive out-of-hospital cardiac arrests (OHCAs) occurring in the Provinces get amoxil prescription online of Lodi, Cremona, Pavia, and Mantova in the 2 months following the first documented case of COVID-19 in Lombardia compared with those that occurred in the same time window in 2019.

The cumulative incidence of COVID-19 from 21 February to 20 April 2020 was 956/100 000 inhabitants and the cumulative incidence of OHCA was 21/100 000 inhabitants, with a 52% increase as compared with 2019 (Figure 2). A significant correlation was found between the difference in cumulative incidence get amoxil prescription online of OHCA and the cumulative incidence of COVID-19. Thus, the OHCA excess in 2020 is closely correlated to the COVID-19 pandemic.

These findings are important for get amoxil prescription online furthering the understanding of the reduced emergency unit visits and for planning of future pandemics, as outlined in an Editorial by Hanno Tan from the Academic Medical Center in Amsterdam, the Netherlands.16 Figure 2(A) Over a period of 60 days from 20 February, the cumulative incidence of COVID-19 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (upper part), and the trend of the difference of OHCA between 2020 and 2019 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (bottom part). (B) The cumulative incidence of the difference in OHCA between 2020 and 2019 per 100 000 inhabitants as a function of the cumulative incidence of COVID-19 per 100 000 inhabitants, since 20 February 2020. Dots are the observed values.

The red line is get amoxil prescription online the function fitted using fractional polynomials. The shaded area is the 95% CI for the estimates (from Baldi E, Maria Sechi G, Mare C, Canevari F, Brancaglione A, Primi R, Klersy C, Palo A, Contri E, Ronchi V, Beretta G, Reali F, Parogni P, Facchin F, Rizzi U, Bussi D, Ruggeri S, Visconti LO, Savastano S, on behalf of the Lombardia CARe researchers. COVID-19 kills at home get amoxil prescription online.

The close relationship between the epidemic and the increase of out-of-hospital cardiac arrests. See pages get amoxil prescription online 3045–3054).Figure 2(A) Over a period of 60 days from 20 February, the cumulative incidence of COVID-19 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (upper part), and the trend of the difference of OHCA between 2020 and 2019 per 100 000 inhabitants in the four provinces and in the overall territory (dotted line) (bottom part). (B) The cumulative incidence of the difference in OHCA between 2020 and 2019 per 100 000 inhabitants as a function of the cumulative incidence of COVID-19 per 100 000 inhabitants, since 20 February 2020.

Dots are the observed values. The red line is the function fitted using fractional polynomials get amoxil prescription online. The shaded area is the 95% CI for the estimates (from Baldi E, Maria Sechi G, Mare C, Canevari F, Brancaglione A, Primi R, Klersy C, Palo A, Contri E, Ronchi V, Beretta G, Reali F, Parogni P, Facchin F, Rizzi U, Bussi D, Ruggeri S, Visconti LO, Savastano S, on behalf of the Lombardia CARe researchers.

COVID-19 kills at home get amoxil prescription online. The close relationship between the epidemic and the increase of out-of-hospital cardiac arrests. See pages 3045–3054).With a prothrombotic state of the endothelium, thrombo-embolism should get amoxil prescription online increase during the COVID-19 pandemic.17 This hypothesis is pursued in a Fast Track entitled ‘Pulmonary embolism in COVID-19 patients.

A French multicentre cohort study’ by Ariel Cohen from the Hopital Saint-Antoine in Paris, France.18 In a retrospective multicentric observational study, the authors included consecutive patients hospitalized for COVID-19. Among 1527 patients, 6.7% patients had pulmonary embolism confirmed by computed tomographty pulmonary angiography (CTPA). Intensive care unit (ICU) transfer get amoxil prescription online and mechanical ventilation were significantly higher in the pulmonary embolism group.

In a univariable analysis, traditional venous thrombo-embolic risk factors and pulmonary lesion extension in chest CT were not associated with pulmonary embolism, while patients under anticoagulation prior to hospitalization or in whom it was introduced during hospitalization had a lower risk of pulmonary embolism, with an odds ratio of 0.37. Male gender, prophylactic or therapeutic anticoagulation, C-reactive protein, and time from symptom get amoxil prescription online onset to hospitalization were associated with pulmonary embolism. Thus, risk factors for pulmonary embolism in COVID-19 do not include traditional thrombo-embolic risk factors, but rather independent clinical and biological findings at admission.

In line with the concept outlined above, inflammation is a major driver of pulmonary embolism in COVID-19, as further discussed in a thought-provoking Editorial by Adam Torbicki from the Centre of Postgraduate Medical Education in Otwock, Poland.19Inflammation is also a trigger for atrial fibrillation as it changes the electrical properties of the atrial myocardium and eventually favours tissue fibrosis.20 Furthermore, inflammation may trigger tissue factor expression in the atrial endothelium and favour thrombus formation.21 On the other hand, life on standstill may reduce sympathetic drive and hence reduce the likelihood of new-onset atrial fibrillation.22 In their article entitled ‘New-onset atrial get amoxil prescription online fibrillation. Incidence, characteristics, and related events following a national COVID-19 lockdown of 5.6 million people’, Anders Holt and colleagues from the Copenhagen University Hospital, Herlev and Gentofte in Hellerup, Denmark resolved this conundrum.23 During 3 weeks of lockdown, weekly incidence rates of new-onset AF were 2.3, 1.8, and 1.5 per 1000 person-years, while during the corresponding weeks in 2019, incidence rates were 3.5, 3.4, and 3.6 per 1000 person-years. Incidence rate ratios comparing the same weeks were 0.66, 0.53, get amoxil prescription online and 0.41.

Patients diagnosed during lockdown were younger and had lower CHA2DS2-VASc-scores. During the first 3 weeks of lockdown, 7.8% of patients experienced an ischaemic stroke or death within 7 days of new-onset atrial fibrillation compared with 5.6% during the equivalent weeks in 2019, corresponding to an odds ratio of 1.41. Thus, following a national lockdown in Denmark, get amoxil prescription online new-onset atrial fibrillation declined by 47%, while ischaemic stroke or death within 7 days increased.

These complex findings are put into context in an excellent Editorial by Carina Blomstrom-Lundqvist from the Department of Medical Science in Uppsala, Sweden.24Myocardial injury after non-cardiac surgery or MINS is caused by myocardial ischaemia due to a supply–demand mismatch or thrombus and is associated with an increased risk of mortality and major adverse CV events or MACE.25 In their review ‘Myocardial injury after non-cardiac surgery. Diagnosis and management’ Philip Devereaux and colleagues from McMaster University in Hamilton, Canada note that the diagnostic criteria for MINS include elevated post-operative troponin levels with no evidence of a non-ischaemic aetiology during or within 30 days after non-cardiac surgery, and without ischaemic features such as chest pain or get amoxil prescription online ECG changes.26 Patients with MINS should receive aspirin and a statin, unless contraindicated, and an NOAC (non-vitamin K antagonist oral anticoagulant) if not at high bleeding risk. Cardiac catheterization is only recommended for those with recurrent ischaemia, heart failure, or high risk based on non-invasive imaging.

Troponin should be measured for the first few days after surgery in patients ≥65 years or with atherosclerotic disease to avoid missing MINS and the opportunity for secondary prophylactic measures and follow-up.Finally, the issue is complemented by various Discussion Forum contributions get amoxil prescription online on this very timely topic. In a contribution entitled ‘Should atrial fibrillation be considered a cardiovascular risk factor for a worse prognosis in COVID-19 patients?. €™, Fabian Sanchis-Gomar from the Faculty of Medicine at the University of Valencia, Spain discuss the recent publication ‘Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy’ by Marco Metra and colleagues from Brescia, Italy.9,27 Metra et al.

Respond in get amoxil prescription online turn. In a comment entitled ‘ACE2 is on the X chromosome. Could this explain COVID-19 gender get amoxil prescription online differences?.

€™ Felix Hernandez from the Universidad Autonoma de Madrid Centro de Biologia Molecular Severo Ochoa in Madrid, and his colleague Esther Culebras discuss the recent publication entitled ‘Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women with heart failure and effects of renin–angiotensin–aldosterone inhibitors’ by Adriaan Voors and colleagues from the University Medical Center Groningen in the Netherlands.3,28 Voors et al. Respond in a separate comment.29In a contribution get amoxil prescription online entitled ‘Circulating plasma angiotensin-converting enzyme 2 concentrations in patients with kidney disease’, Insa Marie Schmidt and colleagues from the Boston University in Massachusetts, USA also comment on the article by Voors et al.3,30 Voors and colleagues respond in a separate message to this piece.31 Time for the last wordsThis is my last Issue@aGlance in the European Heart Journal in my role of Editor-in-Chief. It has been a pleasure and honour to serve both authors and readers of this fine journal and the European Society of Cardiology over more than a decade.

My goal has always been to make it more attractive and informative for clinicians and important and stimulating for scientists worldwide. I hope get amoxil prescription online you have enjoyed it. Needless to say, that was only possible thanks to an amazing team of editors, reviewers, authors, and editorial staff.

I hope get amoxil prescription online that you enjoy this very last issue under my leadership. The time has come to hand the European Heart Journal over to the new Editor-in-Chief, Filippo Crea from Rome. I am get amoxil prescription online certain Professor Crea will do an excellent job with his new team, retaining some of the experienced editorial staff from Zurich.

Thank you for submitting to, reviewing for, and reading the European Heart Journal, and goodbye—I am sure we will stay in touch.With thanks to Amelia Meier-Batschelet for help with compilation of this article. References1Anker SD, Butler J, Khan MS, Abraham WT, Bauersachs J, Bocchi E, Bozkurt B, Braunwald E, Chopra VK, Cleland JG, Ezekowitz J, Filippatos G, Friede T, Hernandez AF, Lam CSP, Lindenfeld J, McMurray JJV, Mehra M, Metra M, Packer M, Pieske B, Pocock SJ, Ponikowski P, Rosano GMC, Teerlink JR, Tsutsui H, Van Veldhuisen DJ, Verma S, Voors AA, Wittes J, Zannad F, Zhang J, Seferovic P, Coats AJS. Conducting clinical trials in heart failure during (and get amoxil prescription online after) the COVID-19 pandemic.

An Expert Consensus Position Paper from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur Heart J 2020;41:2109–2117.2Gao C, Cai Y, Zhang K, Zhou L, Zhang Y, Zhang X, get amoxil prescription online Li Q, Li W, Yang S, Zhao X, Zhao Y, Wang H, Liu Y, Yin Z, Zhang R, Wang R, Yang M, Hui C, Wijns W, McEvoy JW, Soliman O, Onuma Y, Serruys PW, Tao L, Li F. Association of hypertension and antihypertensive treatment with COVID-19 mortality.

A retrospective get amoxil prescription online observational study. Eur Heart J 2020;41:2058–2066.3Sama IE, Ravera A, Santema BT, van Goor H, Ter Maaten JM, Cleland JGF, Rienstra M, Friedrich AW, Samani NJ, Ng LL, Dickstein K, Lang CC, Filippatos G, Anker SD, Ponikowski P, Metra M, van Veldhuisen DJ, Voors AA. Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women get amoxil prescription online with heart failure and effects of renin–angiotensin–aldosterone inhibitors.

Eur Heart J 2020;41:1810–1817.4Nicin L, Abplanalp WT, Mellentin H, Kattih B, Tombor L, John D, Schmitto JD, Heineke J, Emrich F, Arsalan M, Holubec T, Walther T, Zeiher AM, Dimmeler S. Cell type-specific expression of the putative SARS-CoV-2 receptor ACE2 in human hearts. Eur Heart J 2020;41:1804–1806.5Kim IC, Kim JY, Kim HA, Han S get amoxil prescription online.

COVID-19-related myocarditis in a 21-year-old female patient. Eur Heart J 2020;41:1859.6Zhou R get amoxil prescription online. Does SARS-CoV-2 cause viral myocarditis in COVID-19 patients?.

Eur Heart J 2020;41:2123.7Shi S, Qin M, Cai Y, Liu T, Shen B, Yang get amoxil prescription online F, Cao S, Liu X, Xiang Y, Zhao Q, Huang H, Yang B, Huang C. Characteristics and clinical significance of myocardial injury in patients with severe coronavirus disease 2019. Eur Heart J 2020;41:2070–2079.8Azarkish M, Laleh Far V, Eslami M, Mollazadeh R.

Transient complete heart block in get amoxil prescription online a patient with critical COVID-19. Eur Heart J 2020;41:2131.9Inciardi RM, Adamo M, Lupi L, Cani DS, Di Pasquale M, Tomasoni D, Italia L, Zaccone G, Tedino C, Fabbricatore D, Curnis A, Faggiano P, Gorga E, Lombardi CM, Milesi G, Vizzardi E, Volpini M, Nodari S, Specchia C, Maroldi R, Bezzi M, Metra M. Characteristics and outcomes of patients hospitalized get amoxil prescription online for COVID-19 and cardiac disease in Northern Italy.

Eur Heart J 2020;41:1821–1829.10Libby P, Lüscher T. COVID-19 is, in the end, an endothelial get amoxil prescription online disease. Eur Heart J 2020;41:3038–3044.11Pericàs JM, Hernandez-Meneses M, Sheahan TP, Quintana E, Ambrosioni J, Sandoval E, Falces C, Marcos MA, Tuset M, Vilella A, Moreno A, Miro JM.

COVID-19. From epidemiology to get amoxil prescription online treatment. Eur Heart J 2020;41:2092–2112.12De Rosa S, Spaccarotella C, Basso C, Calabrò MP, Curcio A, Filardi PP, Mancone M, Mercuro G, Muscoli S, Nodari S, Pedrinelli R, Sinagra G, Indolfi C.

Reduction of hospitalizations for myocardial get amoxil prescription online infarction in Italy in the COVID-19 era. Eur Heart J 2020;41:2083–2088.13Mafham MM, Spata E, Goldacre R, Gair D, Curnow P, Bray M, Hollings S, Roebuck C, Gale CP, Mamas MA, Deanfield JE, de Belder MA, Luescher TF, Denwood T, Landray MJ, Emberson JR, Collins R, Morris EJA, Casadei B, Baigent C. COVID-19 pandemic and get amoxil prescription online admission rates for and management of acute coronary syndromes in England.

Lancet 2020;396:381–389.14Lelieveld J, Münzel T. Air pollution, get amoxil prescription online the underestimated cardiovascular risk factor. Eur Heart J 2020;41:904–905.15Baldi E, Sechi GM, Mare C, Canevari F, Brancaglione A, Primi R, Klersy C, Palo A, Contri E, Ronchi V, Beretta G, Reali F, Parogni P, Facchin F, Rizzi U, Bussi D, Ruggeri S, Oltrona Visconti L, Savastano S.

COVID-19 kills at home. The close relationship between the epidemic and get amoxil prescription online the increase of out-of-hospital cardiac arrests. Eur Heart J 2020;41:3045–3054.16Tan HL.

How does get amoxil prescription online COVID-19 kill at home. And what should we do about it?. Eur get amoxil prescription online Heart J 2020;41:3055–3057.17Gue YX, Gorog DA.

Reduction in ACE2 may mediate the prothrombotic phenotype in COVID-19. Eur Heart J 2020;doi:10.1093/eurheartj/ehaa534.18Fauvel C, Weizman O, Trimaille A, Mika D, Pommier T, Pace N, Douair A, Barbin E, Fraix A, Bouchot O, Benmansour O, Godeau G, Mecheri Y, Lebourdon R, Yvorel C, Massin M, Leblon T, Chabbi C, Cugney E, Benabou L, Aubry M, Chan C, Boufoula I, Barnaud C, Bothorel L, Duceau B, Sutter W, Waldmann V, Bonnet G, Cohen A, Pezel T. Pulmonary embolism get amoxil prescription online in COVID-19 patients.

A French multicentre cohort study. Eur Heart J 2020;41:3058–3068.19Torbicki A get amoxil prescription online. COVID-19 and pulmonary embolism.

An unwanted get amoxil prescription online alliance. Eur Heart J 2020;41:3069–3071.20Lazzerini PE, Laghi-Pasini F, Acampa M, Srivastava U, Bertolozzi I, Giabbani B, Finizola F, Vanni F, Dokollari A, Natale M, Cevenini G, Selvi E, Migliacci N, Maccherini M, Boutjdir M, Capecchi PL. Systemic inflammation rapidly induces reversible atrial electrical remodeling.

The role of interleukin-6-mediated changes get amoxil prescription online in connexin expression. J Am Heart Assoc 2019;8:e011006.21Steffel J, Lüscher TF, Tanner FC. Tissue factor get amoxil prescription online in cardiovascular diseases.

Molecular mechanisms and clinical implications. Circulation 2006;113:722–731.22Chen PS, Chen get amoxil prescription online LS, Fishbein MC, Lin SF, Nattel S. Role of the autonomic nervous system in atrial fibrillation.

Pathophysiology and therapy. Circ Res 2014;114:1500–1515.23Holt A, Gislason GH, Schou get amoxil prescription online M, Zareini B, Biering-Sørensen T, Phelps M, Kragholm K, Andersson C, Fosbøl EL, Hansen ML, Gerds TA, Køber L, Torp-Pedersen C, Lamberts M. New-onset atrial fibrillation.

Incidence, characteristics, and related get amoxil prescription online events following a national COVID-19 lockdown of 5.6 million people. Eur Heart J 2020;41:3072–3079.24Blomström-Lundqvist C. Effects of COVID-19 lockdown strategies on management of get amoxil prescription online atrial fibrillation.

Eur Heart J 2020;41:3080–3082.25Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galiè N, Gibbs JSR, Huisman MV, Humbert M, Kucher N, Lang I, Lankeit M, Lekakis J, Maack C, Mayer E, Meneveau N, Perrier A, Pruszczyk P, Rasmussen LH, Schindler TH, Svitil P, Vonk Noordegraaf A, Zamorano JL, Zompatori M, Zamorano JL, Achenbach S, Baumgartner H, Bax JJ, Bueno H, Dean V, Deaton C, Erol Ç, Fagard R, Ferrari R, Hasdai D, Hoes A, Kirchhof P, Knuuti J, Kolh P, Lancellotti P, Linhart A, Nihoyannopoulos P, Piepoli MF, Ponikowski P, Sirnes PA, Tamargo JL, Tendera M, Torbicki A, Wijns W, Windecker S, Erol Ç, Jimenez D, Ageno W, Agewall S, Asteggiano R, Bauersachs R, Becattini C, Bounameaux H, Büller HR, Davos CH, Deaton C, Geersing G-J, Sanchez MAG, Hendriks J, Hoes A, Kilickap M, Mareev V, Monreal M, Morais J, Nihoyannopoulos P, Popescu BA, Sanchez O, Spyropoulos AC. 2014 ESC Guidelines on the diagnosis and management of acute pulmonary get amoxil prescription online embolism. The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).

Endorsed by the European Respiratory Society (ERS). Eur Heart J get amoxil prescription online 2014;35:3033–3080.26Devereaux PJ, Szczeklik W. Myocardial injury after non-cardiac surgery.

Diagnosis and management get amoxil prescription online. Eur Heart J 2020;41:3083–3091.27Sanchis-Gomar F, Perez-Quilis C, Lavie CJ. Should atrial fibrillation be considered a cardiovascular risk factor for a worse prognosis in COVID-19 get amoxil prescription online patients?.

Eur Heart J 2020;41:3092–3093.28Culebras E, Hernández F. ACE2 is on the X chromosome. Could this explain get amoxil prescription online COVID-19 gender differences?.

Eur Heart J 2020;41:3095.29Sama IE, Voors AA. Men more vulnerable to get amoxil prescription online COVID-19. Explained by ACE2 on the X chromosome?.

Eur get amoxil prescription online Heart J 2020;41:3096.30Schmidt IM, Verma A, Waikar SS. Circulating plasma angiotensin-converting enzyme 2 concentrations in patients with kidney disease. Eur Heart J 2020;41:3097–3098.31Sama IE, Voors AA.

Circulating plasma angiotensin-converting enzyme 2 concentration is get amoxil prescription online elevated in patients with kidney disease and diabetes. Eur Heart J 2020;41:3099. Published get amoxil prescription online on behalf of the European Society of Cardiology.

All rights reserved. © The get amoxil prescription online Author(s) 2020. For permissions, please email.

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In 2003, severe acute cheap amoxil respiratory syndrome (SARS) spread through 26 countries, infecting at least 8098 and causing at least click to read more 774 deaths (a case fatality rate of 9.6%). Middle East respiratory syndrome (MERS) by January 2020 caused 2519 cases and 866 deaths (a case fatality rate of 34%). SARS and cheap amoxil MERS are coronaviruses and both are not as easily transmitted as COVID-19 because they require close contact with those infected (or also with camels in the case of MERS), and infected humans tend not to transmit before they have symptoms. Transmission of both mostly occurred within healthcare settings and could be controlled by improving infection control in hospitals.In 2015, Bill Gates in a TED lecture warned that we were more at risk of a global pandemic (he thought it would be influenza) than we were from nuclear war.COVID-19 probably first entered the human population in China in November 2019 in Wuhan and was first identified as such in December 2019.

It spreads easily with a R0 (basic reproduction number) that represents the average number of people the average infected person would infect being between 1.5 and 3.5, depending on the surrounding circumstances. While a large cheap amoxil proportion of infections are asymptomatic, there is a significant mortality rate (about 3.4% worldwide). Survival rates are worse in the elderly, in men and in those with comorbidities. There are no suitable mammal models to study.Because there is a significant proportion of asymptomatic infectious people, monitoring of epidemics necessitates screening to determine (1) the proportion of the population that is actively infected and or (2) the total number of those who have been infected.

Both require cheap amoxil screening. To gain significant data, then whole populations or representative samples have to be tested. In many circumstances, only those with high probability are tested.DNA polymerase techniques on throat swabs (notably real-time reverse transcription PCR) can identify the actively infected, but such tests will need to be repeated, especially in healthcare staff who are both at increased risk of infection and could provide an increased risk of infection to their contacts.Antibody tests in theory can reveal who has been infected. However, such tests may not provide 100% reliable results, including the fact that their sensitivity will cheap amoxil vary according to how common the infection is.

If an infection is common, then a very sensitive test will identify all those infected and also a small number of false positives, but when the infection becomes less common, then the proportion of false positives will rise and a positive test could become less useful. Moreover, for how long would the antibody-person be immune? cheap amoxil. Counting the number of hospital deaths attributed to COVID-19 may be a guide to an epidemic, but deaths may be difficult to count in the community. In any case, changes in death numbers usually lag a few weeks behind the time of infection.Would a lower infecting dose cause the following illness to be less severe?.

Does the virus need several extra cheap amoxil doubling times to exert its effects such that in this gained time host responses will be in a better position to combat the infection in high-risk groups or in groups where medical care is minimal?. Could low-dose vaccination with COVID-19 itself be useful?. Shakespeare’s Hamlet (not an epidemiologist) suggested, ‘Diseases desperate grown, By desperate appliance are relieved, Or not at all’.All the aforementioned are key questions, the answers to many of which are not known at the time of writing and, even if they were, the answers might change with the passage of time.Various countries have made various policy choicesAt the time of writing (April 2020), COVID-19 has probably been in the human population for only about 6 months. In most countries, there are cheap amoxil concerns about how the epidemic was initially handled, and it is possible to predict some damming retrospective judgements.

However, we should concentrate on where we are, not where we might have been. Recriminations should wait.Many important decisions have to be made based on incomplete information. Most COVID-19 decisions have to be made on speculations (guesswork and wishful thinking), on hypotheses (propositions made as a basis for reasoning, without an assumption of its truth) or on theories (suppositions or systems of ideas explaining something based on general cheap amoxil principles). All COVID-19 decisions have to be made at the time ‘We have to start from where we are’ guided by the experiences of other countries that are ahead of us in the epidemic.Pandemics usually reveal inequalities and the poor, or those in unstable employment or in crowded accommodation, or with underlying health issues, or where healthcare is less affordable, or are in the less well educated will suffer the most.

They will also comply less cheap amoxil with restrictions. Ideologies, power blocks, leaders, social cohesion beliefs, the relevance of centralised or regional decision making, the abilities of popularism (political doctrines chosen to appeal to a majority of the electorate), welfare states (usually capitalist nations that recognise that food, shelter, education and medicine are basic rights to be ensured by government actions) and authoritarianism are all being stress tested by COVID-19. In the future, it will be interesting to judge how these societal systems played out when confronting the conflicting requirement to reconcile conflicting priorities of health and economic factors that involve conflicts between responding and planning for deaths (‘How should we cope with these’) and actually planning deaths. €˜We will have to accept amoxil generic name uk that we will cause deaths whatever policy we adopt’.There is only one cheap amoxil initial response to COVID-19 that reduces infection rates and death rates.

Dramatic quarantine ‘total lockdown’ measures. Some countries, including China, South Korea, Hong Kong, Taiwan and Singapore, hit the epidemic hard and early with lockdown quarantine to reduce the epidemic. Such countries perhaps tend towards acceptance of cheap amoxil authoritarianism and their citizens less rebellious than in other countries. New Zealand did similarly.

I could not possibly comment on the US responses. However, on what criteria and at what speed should liberalisation of quarantine cheap amoxil measure occur to avoid re-emergences?. There are in theory three final paths out of the COVID-19 crisis:First, a vaccine. Even a cheap amoxil perfect vaccine would be difficult to evaluate with changing risks in the community.

How protective would a vaccine be and for how long would it be effective?. Second, the identification of a treatment, either preventative or curative, so that the disease becomes a considerably less worrisome prospect even for those with comorbidities.Third, herd immunity, when enough of the population has acquired and survived COVID-19 and thus developed immunity with the infection persisting at a low level. Currently the only, not entirely definitive, way of estimating this is by measuring antibodies such that there would not be enough opportunities for disease transmission for cheap amoxil the virus to continue circulating through populations with an Ro of less than 1, but the risk would not disappear entirely. Moreover, how should immunity be monitored if antibody testing may not reflect herd immunity?.

Allowing herd immunity to develop initially would result in a huge spike in hospitalisations and deaths that could overwhelm most healthcare services, and that is why flattening such spikes by quarantine was indicated. With flattening, there would still be illness and deaths but at a controlled slower rate and hopefully also smaller cheap amoxil numbers, such that healthcare services could cope.There is a lot of opinion and numerous contributions by official and unofficial organisations and individuals who think their “single issue advice” should be followed. No one individual has the expertise required for management of all the complexities. Committees are required, including microbiologists, infectious diseases doctors, public health doctors, epidemiologists, hospital and general practice representatives, epidemic mathematical modellers and economic advisers.

Politicians have the cheap amoxil responsibility to deliver decisions when, especially when, information is imperfect. How many people would be infected if we did nothing?. What would the epidemic curve look cheap amoxil like in various situations?. What proportion of those infected would infect others in various situations?.

How many of which population groups would require what extra healthcare services in various situations?. What would be the effect of various measures at various times? cheap amoxil. What economic impacts might there be when these in themselves affect mortality rates?. I predict that COVID-19 will cause two significant changes in political thought.

First, it cheap amoxil has to be realised that globalisation of such epidemics, and there will be more to come, will demand an integrated globalised response. Second, in 1987, Margaret Thatcher, the UK Prime Minister, said that ‘There is no such thing as society… the quality of our lives will depend on how much each of us is prepared to take responsibility for ourselves and each of us prepared to turn round and help by our own efforts those who are unfortunate’. The current UK Prime Minister in March 2020 presented a new synthesis, ‘There really is such a thing as society’.Finally, it is important to realise that everyone, no matter where they are, for better or worse, has to rely on their existing rulers or governments..

In 2003, severe acute respiratory get amoxil prescription online syndrome (SARS) spread through 26 countries, infecting at least 8098 and causing at least 774 deaths (a case fatality rate of 9.6%). Middle East respiratory syndrome (MERS) by January 2020 caused 2519 cases and 866 deaths (a case fatality rate of 34%). SARS and MERS are coronaviruses and both are not as easily transmitted as COVID-19 because they require close get amoxil prescription online contact with those infected (or also with camels in the case of MERS), and infected humans tend not to transmit before they have symptoms. Transmission of both mostly occurred within healthcare settings and could be controlled by improving infection control in hospitals.In 2015, Bill Gates in a TED lecture warned that we were more at risk of a global pandemic (he thought it would be influenza) than we were from nuclear war.COVID-19 probably first entered the human population in China in November 2019 in Wuhan and was first identified as such in December 2019. It spreads easily with a R0 (basic reproduction number) that represents the average number of people the average infected person would infect being between 1.5 and 3.5, depending on the surrounding circumstances.

While a large proportion get amoxil prescription online of infections are asymptomatic, there is a significant mortality rate (about 3.4% worldwide). Survival rates are worse in the elderly, in men and in those with comorbidities. There are no suitable mammal models to study.Because there is a significant proportion of asymptomatic infectious people, monitoring of epidemics necessitates screening to determine (1) the proportion of the population that is actively infected and or (2) the total number of those who have been infected. Both require get amoxil prescription online screening. To gain significant data, then whole populations or representative samples have to be tested.

In many circumstances, only those with high probability are tested.DNA polymerase techniques on throat swabs (notably real-time reverse transcription PCR) can identify the actively infected, but such tests will need to be repeated, especially in healthcare staff who are both at increased risk of infection and could provide an increased risk of infection to their contacts.Antibody tests in theory can reveal who has been infected. However, such tests may not provide 100% reliable results, including the fact that their sensitivity will vary according to how common the get amoxil prescription online infection is. If an infection is common, then a very sensitive test will identify all those infected and also a small number of false positives, but when the infection becomes less common, then the proportion of false positives will rise and a positive test could become less useful. Moreover, for how long would get amoxil prescription online the antibody-person be immune?. Counting the number of hospital deaths attributed to COVID-19 may be a guide to an epidemic, but deaths may be difficult to count in the community.

In any case, changes in death numbers usually lag a few weeks behind the time of infection.Would a lower infecting dose cause the following illness to be less severe?. Does the virus need get amoxil prescription online several extra doubling times to exert its effects such that in this gained time host responses will be in a better position to combat the infection in high-risk groups or in groups where medical care is minimal?. Could low-dose vaccination with COVID-19 itself be useful?. Shakespeare’s Hamlet (not an epidemiologist) suggested, ‘Diseases desperate grown, By desperate appliance are relieved, Or not at all’.All the aforementioned are key questions, the answers to many of which are not known at the time of writing and, even if they were, the answers might change with the passage of time.Various countries have made various policy choicesAt the time of writing (April 2020), COVID-19 has probably been in the human population for only about 6 months. In most countries, there are concerns about how the epidemic was initially handled, and it is possible to predict some damming retrospective judgements get amoxil prescription online.

However, we should concentrate on where we are, not where we might have been. Recriminations should wait.Many important decisions have to be made based on incomplete information. Most COVID-19 decisions have to be made on speculations (guesswork and wishful thinking), on hypotheses (propositions made as a basis for reasoning, without an assumption of its truth) or on theories (suppositions or systems of ideas explaining something based on general principles) get amoxil prescription online. All COVID-19 decisions have to be made at the time ‘We have to start from where we are’ guided by the experiences of other countries that are ahead of us in the epidemic.Pandemics usually reveal inequalities and the poor, or those in unstable employment or in crowded accommodation, or with underlying health issues, or where healthcare is less affordable, or are in the less well educated will suffer the most. They will get amoxil prescription online also comply less with restrictions.

Ideologies, power blocks, leaders, social cohesion beliefs, the relevance of centralised or regional decision making, the abilities of popularism (political doctrines chosen to appeal to a majority of the electorate), welfare states (usually capitalist nations that recognise that food, shelter, education and medicine are basic rights to be ensured by government actions) and authoritarianism are all being stress tested by COVID-19. In the future, it will be interesting to judge how these societal systems played out when confronting the conflicting requirement to reconcile conflicting priorities of health and economic factors that involve conflicts between responding and planning for deaths (‘How should we cope with these’) and actually planning deaths. €˜We will have to accept get amoxil prescription online that we will cause deaths whatever policy we adopt’.There is only one initial response to COVID-19 that reduces infection rates and death rates. Dramatic quarantine ‘total lockdown’ measures. Some countries, including China, South Korea, Hong Kong, Taiwan and Singapore, hit the epidemic hard and early with lockdown quarantine to reduce the epidemic.

Such countries get amoxil prescription online perhaps tend towards acceptance of authoritarianism and their citizens less rebellious than in other countries. New Zealand did similarly. I could not possibly comment on the US responses. However, on what criteria and at what speed should liberalisation get amoxil prescription online of quarantine measure occur to avoid re-emergences?. There are in theory three final paths out of the COVID-19 crisis:First, a vaccine.

Even a perfect vaccine would be difficult to evaluate with get amoxil prescription online changing risks in the community. How protective would a vaccine be and for how long would it be effective?. Second, the identification of a treatment, either preventative or curative, so that the disease becomes a considerably less worrisome prospect even for those with comorbidities.Third, herd immunity, when enough of the population has acquired and survived COVID-19 and thus developed immunity with the infection persisting at a low level. Currently the only, not entirely definitive, way of estimating this is by measuring antibodies such that get amoxil prescription online there would not be enough opportunities for disease transmission for the virus to continue circulating through populations with an Ro of less than 1, but the risk would not disappear entirely. Moreover, how should immunity be monitored if antibody testing may not reflect herd immunity?.

Allowing herd immunity to develop initially would result in a huge spike in hospitalisations and deaths that could overwhelm most healthcare services, and that is why flattening such spikes by quarantine was indicated. With flattening, there would still be illness and deaths but at a controlled slower rate and hopefully also smaller numbers, such that healthcare services could cope.There is a lot of opinion and numerous contributions by official and unofficial organisations and individuals who think get amoxil prescription online their “single issue advice” should be followed. No one individual has the expertise required for management of all the complexities. Committees are required, including microbiologists, infectious diseases doctors, public health doctors, epidemiologists, hospital and general practice representatives, epidemic mathematical modellers and economic advisers. Politicians have the responsibility to get amoxil prescription online deliver decisions when, especially when, information is imperfect.

How many people would be infected if we did nothing?. What would the get amoxil prescription online epidemic curve look like in various situations?. What proportion of those infected would infect others in various situations?. How many of which population groups would require what extra healthcare services in various situations?. What would be the effect of various measures get amoxil prescription online at various times?.

What economic impacts might there be when these in themselves affect mortality rates?. I predict that COVID-19 will cause two significant changes in political thought. First, it get amoxil prescription online has to be realised that globalisation of such epidemics, and there will be more to come, will demand an integrated globalised response. Second, in 1987, Margaret Thatcher, the UK Prime Minister, said that ‘There is no such thing as society… the quality of our lives will depend on how much each of us is prepared to take responsibility for ourselves and each of us prepared to turn round and help by our own efforts those who are unfortunate’. The current UK Prime Minister in March 2020 presented a new synthesis, ‘There really is such a thing as society’.Finally, it is important to realise that everyone, no matter where they are, for better or worse, has to rely on their existing rulers or governments..

Amoxil 500mg price

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How to amoxil 500mg price cite this article:Singh O P More Bonuses. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is one of the highly publicized events in our amoxil 500mg price country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as newspapers, news channels, and social media were full of stories providing minute details amoxil 500mg price of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, amoxil 500mg price print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly amoxil 500mg price started getting distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has amoxil 500mg price adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were amoxil 500mg price full of speculations about the person's mental condition and illness and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society amoxil 500mg price has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists amoxil 500mg price and mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, amoxil 500mg price myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have amoxil 500mg price witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have amoxil 500mg price guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments amoxil 500mg price are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P SinghAA 304, amoxil 500mg price Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically.

Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods. These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies.

And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies.

The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness.

However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT.

Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past.

In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain.

The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al.

Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies.

In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al. In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala.

In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al.

In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al.

Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al.

In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered. Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT.

In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable.

The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite.

However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis.

Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT.

Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique.

In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al.

In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied.

In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus. This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT.

However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT.

Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests.

Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al.

In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail. And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this.

These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood.

Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J.

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How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21.

44.Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis.

Acta Psychiatr Scand 2018;138:180-95. 45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy.

Biol Psychiatry 2018;84:574-81. 46.Breggin PR. Brain-Disabling Treatments in Psychiatry.

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48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies. Neuroscience 1991;45:37-45.

49.Obergriesser T, Ende G, Braus DF, Henn FA. Long-term follow-up of magnetic resonance-detectable choline signal changes in the hippocampus of patients treated with electroconvulsive therapy. J Clin Psychiatry 2003;64:775-80.

50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis.

Prog Neurobiol 2005;76:99-125. 51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders.

Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al. Serum and plasma BDNF levels in major depression.

A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80.

54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al. Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder. A meta-analysis study.

J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in depressive disorders.

A systematic review and meta-analysis. Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM.

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58.Tulving E, Madigan SA. Memory and verbal learning. Annu Rev Psychol 1970;21:437-84.

59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy. Systematic review.

BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy.

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP.

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62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy. Arch Gen Psychiatry 1975;32:1557-64.

63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy.

Long-term follow-up. Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC.

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66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33.

67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;57:425-34.

68.Abrams R. Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3.

69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia. A pilot study.

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A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al.

Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46. 73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ.

Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ.

Subjective memory complaints prior to and following electroconvulsive therapy. Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A.

A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24. 77.Brodaty H, Hickie I, Mason C, Prenter L.

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Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to cite this article:Singh official source O P get amoxil prescription online. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is get amoxil prescription online one of the highly publicized events in our country.

Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide. As expected, the media went into a frenzy as get amoxil prescription online newspapers, news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor.

All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of get amoxil prescription online many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media. We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident.

Psychiatrists suddenly started getting distress calls from their patients in despair get amoxil prescription online with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill person without his consent.[1] The Press Council of India has adopted the guidelines of World Health get amoxil prescription online Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental condition and illness get amoxil prescription online and also his relationships and finances.

Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him. The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact get amoxil prescription online of negative suicide reporting on the lives of many vulnerable persons, there is even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident.

Many psychiatrists and get amoxil prescription online mental health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so. There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist.

These types of viewpoints perpetuate stigma, myths, and “misleading concepts” get amoxil prescription online about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” get amoxil prescription online by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and get amoxil prescription online resource books for interacting with media, and psychiatrists should familiarize themselves with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion.

It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media. Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental get amoxil prescription online health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr.

O P get amoxil prescription online SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest. NoneDOI.

10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically.

Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods. These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies.

And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords.

Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies.

The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time. Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness.

However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions. These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT.

Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past.

In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT. In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain.

The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes. A single study by Coffey et al.

Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al.

Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al. That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies.

In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al. In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala.

In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al.

In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression. It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus.

The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe. It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al.

Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al.

In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered. Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT.

In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage. Metabolic Neuroimaging Studies.

Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable.

The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT. Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite.

However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations. The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis.

Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT.

Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT. Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique.

In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT. This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al.

In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al.

In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al. In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied.

In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus. This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT.

However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT.

Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder. The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration.

However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests.

Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al.

In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail. And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this.

These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered. However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons.

Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood.

Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question. However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J.

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Correspondence Address:Dr. Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

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Rules and Household Size 3. The Three MSP Programs - What are they and how are they Different?. 4. FOUR Special Benefits of MSP Programs.

Back Door to Extra Help with Part D MSPs Automatically Waive Late Enrollment Penalties for Part B - and allow enrollment in Part B year-round outside of the short Annual Enrollment Period No Medicaid Lien on Estate to Recover Payment of Expenses Paid by MSP Food Stamps/SNAP not reduced by Decreased Medical Expenses when Enroll in MSP - at least temporarily 5. Enrolling in an MSP - Automatic Enrollment &. Applications for People who Have Medicare What is Application Process?. 6.

Enrolling in an MSP for People age 65+ who Do Not Qualify for Free Medicare Part A - the "Part A Buy-In Program" 7. What Happens After MSP Approved - How Part B Premium is Paid 8 Special Rules for QMBs - How Medicare Cost-Sharing Works 1. NO ASSET LIMIT!. Since April 1, 2008, none of the three MSP programs have resource limits in New York -- which means many Medicare beneficiaries who might not qualify for Medicaid because of excess resources can qualify for an MSP.

1.A. SUMMARY CHART OF MSP BENEFITS QMB SLIMB QI-1 Eligibility ASSET LIMIT NO LIMIT IN NEW YORK STATE INCOME LIMIT (2020) Single Couple Single Couple Single Couple $1,064 $1,437 $1,276 $1,724 $1,436 $1,940 Federal Poverty Level 100% FPL 100 – 120% FPL 120 – 135% FPL Benefits Pays Monthly Part B premium?. YES, and also Part A premium if did not have enough work quarters and meets citizenship requirement. See “Part A Buy-In” YES YES Pays Part A &.

B deductibles &. Co-insurance YES - with limitations NO NO Retroactive to Filing of Application?. Yes - Benefits begin the month after the month of the MSP application. 18 NYCRR §360-7.8(b)(5) Yes – Retroactive to 3rd month before month of application, if eligible in prior months Yes – may be retroactive to 3rd month before month of applica-tion, but only within the current calendar year.

(No retro for January application). See GIS 07 MA 027. Can Enroll in MSP and Medicaid at Same Time?. YES YES NO!.

Must choose between QI-1 and Medicaid. Cannot have both, not even Medicaid with a spend-down. 2. INCOME LIMITS and RULES Each of the three MSP programs has different income eligibility requirements and provides different benefits.

The income limits are tied to the Federal Poverty Level (FPL). 2019 FPL levels were released by NYS DOH in GIS 20 MA/02 - 2020 Federal Poverty Levels -- Attachment II and have been posted by Medicaid.gov and the National Council on Aging and are in the chart below. NOTE. There is usually a lag in time of several weeks, or even months, from January 1st of each year until the new FPLs are release, and then before the new MSP income limits are officially implemented.

During this lag period, local Medicaid offices should continue to use the previous year's FPLs AND count the person's Social Security benefit amount from the previous year - do NOT factor in the Social Security COLA (cost of living adjustment). Once the updated guidelines are released, districts will use the new FPLs and go ahead and factor in any COLA. See 2019 Fact Sheet on MSP in NYS by Medicare Rights Center ENGLISH SPANISH Income is determined by the same methodology as is used for determining in eligibility for SSI The rules for counting income for SSI-related (Aged 65+, Blind, or Disabled) Medicaid recipients, borrowed from the SSI program, apply to the MSP program, except for the new rules about counting household size for married couples. N.Y.

Soc. Serv. L. 367-a(3)(c)(2), NYS DOH 2000-ADM-7, 89-ADM-7 p.7.

Gross income is counted, although there are certain types of income that are disregarded. The most common income disregards, also known as deductions, include. (a) The first $20 of your &. Your spouse's monthly income, earned or unearned ($20 per couple max).

(b) SSI EARNED INCOME DISREGARDS. * The first $65 of monthly wages of you and your spouse, * One-half of the remaining monthly wages (after the $65 is deducted). * Other work incentives including PASS plans, impairment related work expenses (IRWEs), blind work expenses, etc. For information on these deductions, see The Medicaid Buy-In for Working People with Disabilities (MBI-WPD) and other guides in this article -- though written for the MBI-WPD, the work incentives apply to all Medicaid programs, including MSP, for people age 65+, disabled or blind.

(c) monthly cost of any health insurance premiums but NOT the Part B premium, since Medicaid will now pay this premium (may deduct Medigap supplemental policies, vision, dental, or long term care insurance premiums, and the Part D premium but only to the extent the premium exceeds the Extra Help benchmark amount) (d) Food stamps not counted. You can get a more comprehensive listing of the SSI-related income disregards on the Medicaid income disregards chart. As for all benefit programs based on financial need, it is usually advantageous to be considered a larger household, because the income limit is higher. The above chart shows that Households of TWO have a higher income limit than households of ONE.

The MSP programs use the same rules as Medicaid does for the Disabled, Aged and Blind (DAB) which are borrowed from the SSI program for Medicaid recipients in the “SSI-related category.” Under these rules, a household can be only ONE or TWO. 18 NYCRR 360-4.2. See DAB Household Size Chart. Married persons can sometimes be ONE or TWO depending on arcane rules, which can force a Medicare beneficiary to be limited to the income limit for ONE person even though his spouse who is under 65 and not disabled has no income, and is supported by the client applying for an MSP.

EXAMPLE. Bob's Social Security is $1300/month. He is age 67 and has Medicare. His wife, Nancy, is age 62 and is not disabled and does not work.

Under the old rule, Bob was not eligible for an MSP because his income was above the Income limit for One, even though it was well under the Couple limit. In 2010, NYS DOH modified its rules so that all married individuals will be considered a household size of TWO. DOH GIS 10 MA 10 Medicare Savings Program Household Size, June 4, 2010. This rule for household size is an exception to the rule applying SSI budgeting rules to the MSP program.

Under these rules, Bob is now eligible for an MSP. When is One Better than Two?. Of course, there may be couples where the non-applying spouse's income is too high, and disqualifies the applying spouse from an MSP. In such cases, "spousal refusal" may be used SSL 366.3(a).

(Link is to NYC HRA form, can be adapted for other counties). 3. The Three Medicare Savings Programs - what are they and how are they different?. 1.

Qualified Medicare Beneficiary (QMB). The QMB program provides the most comprehensive benefits. Available to those with incomes at or below 100% of the Federal Poverty Level (FPL), the QMB program covers virtually all Medicare cost-sharing obligations. Part B premiums, Part A premiums, if there are any, and any and all deductibles and co-insurance.

QMB coverage is not retroactive. The program’s benefits will begin the month after the month in which your client is found eligible. ** See special rules about cost-sharing for QMBs below - updated with new CMS directive issued January 2012 ** See NYC HRA QMB Recertification form ** Even if you do not have Part A automatically, because you did not have enough wages, you may be able to enroll in the Part A Buy-In Program, in which people eligible for QMB who do not otherwise have Medicare Part A may enroll, with Medicaid paying the Part A premium (Materials by the Medicare Rights Center). 2.

Specifiedl Low-Income Medicare Beneficiary (SLMB). For those with incomes between 100% and 120% FPL, the SLMB program will cover Part B premiums only. SLMB is retroactive, however, providing coverage for three months prior to the month of application, as long as your client was eligible during those months. 3.

Qualified Individual (QI-1). For those with incomes between 120% and 135% FPL, and not receiving Medicaid, the QI-1 program will cover Medicare Part B premiums only. QI-1 is also retroactive, providing coverage for three months prior to the month of application, as long as your client was eligible during those months. However, QI-1 retroactive coverage can only be provided within the current calendar year.

(GIS 07 MA 027) So if you apply in January, you get no retroactive coverage. Q-I-1 recipients would be eligible for Medicaid with a spend-down, but if they want the Part B premium paid, they must choose between enrolling in QI-1 or Medicaid. They cannot be in both. It is their choice.

DOH MRG p. 19. In contrast, one may receive Medicaid and either QMB or SLIMB. 4.

Four Special Benefits of MSPs (in addition to NO ASSET have a peek at this web-site TEST). Benefit 1. Back Door to Medicare Part D "Extra Help" or Low Income Subsidy -- All MSP recipients are automatically enrolled in Extra Help, the subsidy that makes Part D affordable. They have no Part D deductible or doughnut hole, the premium is subsidized, and they pay very low copayments.

Once they are enrolled in Extra Help by virtue of enrollment in an MSP, they retain Extra Help for the entire calendar year, even if they lose MSP eligibility during that year. The "Full" Extra Help subsidy has the same income limit as QI-1 - 135% FPL. However, many people may be eligible for QI-1 but not Extra Help because QI-1 and the other MSPs have no asset limit. People applying to the Social Security Administration for Extra Help might be rejected for this reason.

Recent (2009-10) changes to federal law called "MIPPA" requires the Social Security Administration (SSA) to share eligibility data with NYSDOH on all persons who apply for Extra Help/ the Low Income Subsidy. Data sent to NYSDOH from SSA will enable NYSDOH to open MSP cases on many clients. The effective date of the MSP application must be the same date as the Extra Help application. Signatures will not be required from clients.

In cases where the SSA data is incomplete, NYSDOH will forward what is collected to the local district for completion of an MSP application. The State implementing procedures are in DOH 2010 ADM-03. Also see CMS "Dear State Medicaid Director" letter dated Feb. 18, 2010 Benefit 2.

MSPs Automatically Waive Late Enrollment Penalties for Part B Generally one must enroll in Part B within the strict enrollment periods after turning age 65 or after 24 months of Social Security Disability. An exception is if you or your spouse are still working and insured under an employer sponsored group health plan, or if you have End Stage Renal Disease, and other factors, see this from Medicare Rights Center. If you fail to enroll within those short periods, you might have to pay higher Part B premiums for life as a Late Enrollment Penalty (LEP). Also, you may only enroll in Part B during the Annual Enrollment Period from January 1 - March 31st each year, with Part B not effective until the following July.

Enrollment in an MSP automatically eliminates such penalties... For life.. Even if one later ceases to be eligible for the MSP. AND enrolling in an MSP will automatically result in becoming enrolled in Part B if you didn't already have it and only had Part A.

See Medicare Rights Center flyer. Benefit 3. No Medicaid Lien on Estate to Recover MSP Benefits Paid Generally speaking, states may place liens on the Estates of deceased Medicaid recipients to recover the cost of Medicaid services that were provided after the recipient reached the age of 55. Since 2002, states have not been allowed to recover the cost of Medicare premiums paid under MSPs.

In 2010, Congress expanded protection for MSP benefits. Beginning on January 1, 2010, states may not place liens on the Estates of Medicaid recipients who died after January 1, 2010 to recover costs for co-insurance paid under the QMB MSP program for services rendered after January 1, 2010. The federal government made this change in order to eliminate barriers to enrollment in MSPs. See NYS DOH GIS 10-MA-008 - Medicare Savings Program Changes in Estate Recovery The GIS clarifies that a client who receives both QMB and full Medicaid is exempt from estate recovery for these Medicare cost-sharing expenses.

Benefit 4. SNAP (Food Stamp) benefits not reduced despite increased income from MSP - at least temporarily Many people receive both SNAP (Food Stamp) benefits and MSP. Income for purposes of SNAP/Food Stamps is reduced by a deduction for medical expenses, which includes payment of the Part B premium. Since approval for an MSP means that the client no longer pays for the Part B premium, his/her SNAP/Food Stamps income goes up, so their SNAP/Food Stamps go down.

Here are some protections. Do these individuals have to report to their SNAP worker that their out of pocket medical costs have decreased?. And will the household see a reduction in their SNAP benefits, since the decrease in medical expenses will increase their countable income?. The good news is that MSP households do NOT have to report the decrease in their medical expenses to the SNAP/Food Stamp office until their next SNAP/Food Stamp recertification.

Even if they do report the change, or the local district finds out because the same worker is handling both the MSP and SNAP case, there should be no reduction in the household’s benefit until the next recertification. New York’s SNAP policy per administrative directive 02 ADM-07 is to “freeze” the deduction for medical expenses between certification periods. Increases in medical expenses can be budgeted at the household’s request, but NYS never decreases a household’s medical expense deduction until the next recertification. Most elderly and disabled households have 24-month SNAP certification periods.

Eventually, though, the decrease in medical expenses will need to be reported when the household recertifies for SNAP, and the household should expect to see a decrease in their monthly SNAP benefit. It is really important to stress that the loss in SNAP benefits is NOT dollar for dollar. A $100 decrease in out of pocket medical expenses would translate roughly into a $30 drop in SNAP benefits. See more info on SNAP/Food Stamp benefits by the Empire Justice Center, and on the State OTDA website.

Some clients will be automatically enrolled in an MSP by the New York State Department of Health (NYSDOH) shortly after attaining eligibility for Medicare. Others need to apply. The 2010 "MIPPA" law introduced some improvements to increase MSP enrollment. See 3rd bullet below.

Also, some people who had Medicaid through the Affordable Care Act before they became eligible for Medicare have special procedures to have their Part B premium paid before they enroll in an MSP. See below. WHO IS AUTOMATICALLY ENROLLED IN AN MSP. Clients receiving even $1.00 of Supplemental Security Income should be automatically enrolled into a Medicare Savings Program (most often QMB) under New York State’s Medicare Savings Program Buy-in Agreement with the federal government once they become eligible for Medicare.

They should receive Medicare Parts A and B. Clients who are already eligible for Medicare when they apply for Medicaid should be automatically assessed for MSP eligibility when they apply for Medicaid. (NYS DOH 2000-ADM-7 and GIS 05 MA 033). Clients who apply to the Social Security Administration for Extra Help, but are rejected, should be contacted &.

Enrolled into an MSP by the Medicaid program directly under new MIPPA procedures that require data sharing. Strategy TIP. Since the Extra Help filing date will be assigned to the MSP application, it may help the client to apply online for Extra Help with the SSA, even knowing that this application will be rejected because of excess assets or other reason. SSA processes these requests quickly, and it will be routed to the State for MSP processing.

Since MSP applications take a while, at least the filing date will be retroactive. Note. The above strategy does not work as well for QMB, because the effective date of QMB is the month after the month of application. As a result, the retroactive effective date of Extra Help will be the month after the failed Extra Help application for those with QMB rather than SLMB/QI-1.

Applying for MSP Directly with Local Medicaid Program. Those who do not have Medicaid already must apply for an MSP through their local social services district. (See more in Section D. Below re those who already have Medicaid through the Affordable Care Act before they became eligible for Medicare.

If you are applying for MSP only (not also Medicaid), you can use the simplified MSP application form (theDOH-4328(Rev. 8/2017-- English) (2017 Spanish version not yet available). Either application form can be mailed in -- there is no interview requirement anymore for MSP or Medicaid. See 10 ADM-04.

Applicants will need to submit proof of income, a copy of their Medicare card (front &. Back), and proof of residency/address. See the application form for other instructions. One who is only eligible for QI-1 because of higher income may ONLY apply for an MSP, not for Medicaid too.

One may not receive Medicaid and QI-1 at the same time. If someone only eligible for QI-1 wants Medicaid, s/he may enroll in and deposit excess income into a pooled Supplemental Needs Trust, to bring her countable income down to the Medicaid level, which also qualifies him or her for SLIMB or QMB instead of QI-1. Advocates in NYC can sign up for a half-day "Deputization Training" conducted by the Medicare Rights Center, at which you'll be trained and authorized to complete an MSP application and to submit it via the Medicare Rights Center, which submits it to HRA without the client having to apply in person. Enrolling in an MSP if you already have Medicaid, but just become eligible for Medicare Those who, prior to becoming enrolled in Medicare, had Medicaid through Affordable Care Act are eligible to have their Part B premiums paid by Medicaid (or the cost reimbursed) during the time it takes for them to transition to a Medicare Savings Program.

In 2018, DOH clarified that reimbursement of the Part B premium will be made regardless of whether the individual is still in a Medicaid managed care (MMC) plan. GIS 18 MA/001 Medicaid Managed Care Transition for Enrollees Gaining Medicare ( PDF) provides, "Due to efforts to transition individuals who gain Medicare eligibility and who require LTSS, individuals may not be disenrolled from MMC upon receipt of Medicare. To facilitate the transition and not disadvantage the recipient, the Medicaid program is approving reimbursement of Part B premiums for enrollees in MMC." The procedure for getting the Part B premium paid is different for those whose Medicaid was administered by the NYS of Health Exchange (Marketplace), as opposed to their local social services district. The procedure is also different for those who obtain Medicare because they turn 65, as opposed to obtaining Medicare based on disability.

Either way, Medicaid recipients who transition onto Medicare should be automatically evaluated for MSP eligibility at their next Medicaid recertification. NYS DOH 2000-ADM-7 Individuals can also affirmatively ask to be enrolled in MSP in between recertification periods. IF CLIENT HAD MEDICAID ON THE MARKETPLACE (NYS of Health Exchange) before obtaining Medicare. IF they obtain Medicare because they turn age 65, they will receive a letter from their local district asking them to "renew" Medicaid through their local district.

See 2014 LCM-02. Now, their Medicaid income limit will be lower than the MAGI limits ($842/ mo reduced from $1387/month) and they now will have an asset test. For this reason, some individuals may lose full Medicaid eligibility when they begin receiving Medicare. People over age 65 who obtain Medicare do NOT keep "Marketplace Medicaid" for 12 months (continuous eligibility) See GIS 15 MA/022 - Continuous Coverage for MAGI Individuals.

Since MSP has NO ASSET limit. Some individuals may be enrolled in the MSP even if they lose Medicaid, or if they now have a Medicaid spend-down. If a Medicare/Medicaid recipient reports income that exceeds the Medicaid level, districts must evaluate the person’s eligibility for MSP. 08 OHIP/ADM-4 ​If you became eligible for Medicare based on disability and you are UNDER AGE 65, you are entitled to keep MAGI Medicaid for 12 months from the month it was last authorized, even if you now have income normally above the MAGI limit, and even though you now have Medicare.

This is called Continuous Eligibility. EXAMPLE. Sam, age 60, was last authorized for Medicaid on the Marketplace in June 2016. He became enrolled in Medicare based on disability in August 2016, and started receiving Social Security in the same month (he won a hearing approving Social Security disability benefits retroactively, after first being denied disability).

Even though his Social Security is too high, he can keep Medicaid for 12 months beginning June 2016. Sam has to pay for his Part B premium - it is deducted from his Social Security check. He may call the Marketplace and request a refund. This will continue until the end of his 12 months of continues MAGI Medicaid eligibility.

He will be reimbursed regardless of whether he is in a Medicaid managed care plan. See GIS 18 MA/001 Medicaid Managed Care Transition for Enrollees Gaining Medicare (PDF) When that ends, he will renew Medicaid and apply for MSP with his local district. Individuals who are eligible for Medicaid with a spenddown can opt whether or not to receive MSP. (Medicaid Reference Guide (MRG) p.

19). Obtaining MSP may increase their spenddown. MIPPA - Outreach by Social Security Administration -- Under MIPPA, the SSA sends a form letter to people who may be eligible for a Medicare Savings Program or Extra Help (Low Income Subsidy - LIS) that they may apply. The letters are.

· Beneficiary has Extra Help (LIS), but not MSP · Beneficiary has no Extra Help (LIS) or MSP 6. Enrolling in MSP for People Age 65+ who do Not have Free Medicare Part A - the "Part A Buy-In Program" Seniors WITHOUT MEDICARE PART A or B -- They may be able to enroll in the Part A Buy-In program, in which people eligible for QMB who are age 65+ who do not otherwise have Medicare Part A may enroll in Part A, with Medicaid paying the Part A premium. See Step-by-Step Guide by the Medicare Rights Center). This guide explains the various steps in "conditionally enrolling" in Part A at the SSA office, which must be done before applying for QMB at the Medicaid office, which will then pay the Part A premium.

See also GIS 04 MA/013. In June, 2018, the SSA revised the POMS manual procedures for the Part A Buy-In to to address inconsistencies and confusion in SSA field offices and help smooth the path for QMB enrollment. The procedures are in the POMS Section HI 00801.140 "Premium-Free Part A Enrollments for Qualified Medicare BenefiIaries." It includes important clarifications, such as. SSA Field Offices should explain the QMB program and conditional enrollment process if an individual lacks premium-free Part A and appears to meet QMB requirements.

SSA field offices can add notes to the “Remarks” section of the application and provide a screen shot to the individual so the individual can provide proof of conditional Part A enrollment when applying for QMB through the state Medicaid program. Beneficiaries are allowed to complete the conditional application even if they owe Medicare premiums. In Part A Buy-in states like NYS, SSA should process conditional applications on a rolling basis (without regard to enrollment periods), even if the application coincides with the General Enrollment Period. (The General Enrollment Period is from Jan 1 to March 31st every year, in which anyone eligible may enroll in Medicare Part A or Part B to be effective on July 1st).

7. What happens after the MSP approval - How is Part B premium paid For all three MSP programs, the Medicaid program is now responsible for paying the Part B premiums, even though the MSP enrollee is not necessarily a recipient of Medicaid. The local Medicaid office (DSS/HRA) transmits the MSP approval to the NYS Department of Health – that information gets shared w/ SSA and CMS SSA stops deducting the Part B premiums out of the beneficiary’s Social Security check. SSA also refunds any amounts owed to the recipient.

) CMS “deems” the MSP recipient eligible for Part D Extra Help/ Low Income Subsidy (LIS). ​Can the MSP be retroactive like Medicaid, back to 3 months before the application?. ​The answer is different for the 3 MSP programs. QMB -No Retroactive Eligibility – Benefits begin the month after the month of the MSP application.

18 NYCRR § 360-7.8(b)(5) SLIMB - YES - Retroactive Eligibility up to 3 months before the application, if was eligible This means applicant may be reimbursed for the 3 months of Part B benefits prior to the month of application. QI-1 - YES up to 3 months but only in the same calendar year. No retroactive eligibility to the previous year. 7.

QMBs -Special Rules on Cost-Sharing. QMB is the only MSP program which pays not only the Part B premium, but also the Medicare co-insurance. However, there are limitations. First, co-insurance will only be paid if the provide accepts Medicaid.

See Medicare Rights Learn More Center chart on Extra get amoxil prescription online Help Income and Asset Limits - updated annually You can apply for Extra Help and MSP at the same time through SSA. SSA will forward your Extra Help application data to the New York State Department of Health, who will use that data to assess your eligibility for MSP. Individuals who apply for LIS through SSA and those who are deemed into LIS should receive written confirmation of their Extra Help status through SSA.

Of course, individuals who apply for get amoxil prescription online LIS through SSA and are found ineligible are also entitled to a written notice and have appeal rights. Benefits of Extra Help 1) Assistance with Part D cost-sharing The Extra Help program provides a subsidy which covers most (but not all) of beneficiary’s cost sharing obligations. Extra Help beneficiaries do not have to worry about hitting the “donut hole” – the LIS subsidy continues to cover them through the donut hole and into catastrophic coverage.

Full Extra get amoxil prescription online Help. LIS beneficiaries with incomes up to 135% FPL are generally eligible for "full" Extra Help -- meaning they pay no Part D deductible, no charge for monthly premiums up to the benchmark amount, and fixed, relatively low co-pays (between $1.30 and $8.95 for 2020 depending on the person's income level and the tier category of the drug. Medicaid beneficiaries in nursing homes, waiver programs, or managed long term care have $0 co-pays).

Full Extra get amoxil prescription online Help beneficiaries who hit the catastrophic coverage limit have $0 co-pays. See current co-pay levels here. Partial Extra Help.

Beneficiaries between 135%-150% FPL receive "partial" Extra Help, which limits the Part D deductible to $89 get amoxil prescription online (2020 figure - click here for updated chart). Sets sliding scale fees for monthly premiums. And limits co-pays to 15%, until the beneficiary reaches the catastrophic coverage limit, at which point co-pays are limited to a $8.95 maximum (2020 or see current amount here) or 5% of the drug cost, whichever is greater.

2) Facilitated enrollment into a Part D plan Extra Help recipients who aren’t already enrolled in a Part D plan and don’t want get amoxil prescription online to choose one on their own will be automatically enrolled into a benchmark plan by CMS. This facilitated enrollment ensures that Extra Help recipients have Part D coverage. However, the downside to facilitated enrollment is that the plan may not be the best “fit” for the beneficiary, if it doesn’t cover all his/her drugs, assesses a higher tier level for covered drugs than other comparable plans, and/or requires the beneficiary to go through administrative hoops like prior authorization, quantity limits and/or step therapy.

Fortunately, Extra Help recipients can always enroll get amoxil prescription online in a new plan … see #3 below. 3) Continuous special enrollment period Extra Help recipients have a continuous special enrollment period, meaning that they can switch plans at any time. They are not “locked into” the annual open enrollment period (October 15-December 7).

NOTE get amoxil prescription online. This changed in 2019. Starting in 2019, those with Extra Help will no longer have a continuous enrollment period.

Instead, Extra Help recipients will be eligible to get amoxil prescription online enroll no more than once per quarter for each of the first three quarters of the year. 4) No late enrollment penalty Non LIS beneficiaries generally face a premium penalty (higher monthly premium) if they delayed their enrollment into Part D, meaning that they didn’t enroll when they were initially eligible and didn’t have “creditable coverage.” Extra Help recipients do not have to worry about this problem – the late enrollment penalty provision does not apply to LIS beneficiaries. 1) For “deemed” beneficiaries (Medicaid/Medicare Savings Program recipients).

Extra Help status lasts at least until the end of the get amoxil prescription online current calendar year, even if the individual loses their Medicaid or Medicare Savings Program coverage during that year. Individuals who receive Medicaid or a Medicare Savings Program any month between July and December keep their LIS status for the remainder of that calendar year and the following year. Getting Medicaid coverage for even just a short period of time (ie, meeting a spenddown for just one month) can help ensure that the individual obtains Extra Help coverage for at least 6 months, and possibly as long as 18 months.

TIP get amoxil prescription online. People with a high spend-down who want to receive Medicaid for just one month in order to get Extra Help for 6-18 months can use past medical bills to meet their spend-down for that one month. There are different rules for using past paid medical bills verses past unpaid medical bills.

For information get amoxil prescription online see Spend down training materials. Individuals who are losing their deemed status at the end of a calendar year because they are no longer receiving Medicaid or the Medicare Savings Program should be notified in advance by SSA, and given an opportunity to file an Extra Help application through SSA. 2) For “non-deemed” beneficiaries (those who filed their LIS applications through SSA) Non-deemed beneficiaries retain their LIS status until/unless SSA does a redetermination and finds the individual ineligible for Extra Help.

There get amoxil prescription online are no reporting requirements per se in the Extra Help program, but beneficiaries must respond to SSA’s redetermination request. What to do if the Part D plan doesn't know that someone has Extra Help Sometimes there are lengthy delays between the date that someone is approved for Medicaid or a Medicare Savings Program and when that information is formally conveyed to the Part D plan by CMS. As a practical matter, this often results in beneficiaries being charged co-pays, premiums and/or deductibles that they can't afford and shouldn't have to pay.

To protect LIS beneficiaries, CMS get amoxil prescription online has a "Best Available Evidence" policy which requires plans to accept alternative forms of proof of someone's LIS status and adjust the person's cost-sharing obligation accordingly. LIS beneficiaries who are being charged improperly should be sure to contact their plan and provide proof of their LIS status. If the plan still won't recognize their LIS status, the person or their advocate should file a complaint with the CMS regional office.

The federal regulations governing the Low Income Subsidy program can be found at 42 CFR Subpart P (sections 423.771 through get amoxil prescription online 423.800). Also, CMS provides detailed guidance on the LIS provisions in chapter 13 of its Medicare Prescription Drug Benefit Manual. This article was authored by the Empire Justice Center.Medicare Savings Programs (MSPs) pay for the monthly Medicare Part B premium for low-income Medicare beneficiaries and qualify enrollees for the "Extra Help" subsidy for Part D prescription drugs.

There are three separate MSP programs, the Qualified Medicare Beneficiary (QMB) Program, the Specified Low Income Medicare Beneficiary (SLMB) Program and the get amoxil prescription online Qualified Individual (QI) Program, each of which is discussed below. Those in QMB receive additional subsidies for Medicare costs. See 2019 Fact Sheet on MSP in NYS by Medicare Rights Center ENGLISH SPANISH State law.

N.Y get amoxil prescription online. Soc. Serv.

L. § 367-a(3)(a), (b), and (d). 2020 Medicare 101 Basics for New York State - 1.5 hour webinar by Eric Hausman, sponsored by NYS Office of the Aging TOPICS COVERED IN THIS ARTICLE 1.

No Asset Limit 1A. Summary Chart of MSP Programs 2. Income Limits &.

Rules and Household Size 3. The Three MSP Programs - What are they and how are they Different?. 4.

FOUR Special Benefits of MSP Programs. Back Door to Extra Help with Part D MSPs Automatically Waive Late Enrollment Penalties for Part B - and allow enrollment in Part B year-round outside of the short Annual Enrollment Period No Medicaid Lien on Estate to Recover Payment of Expenses Paid by MSP Food Stamps/SNAP not reduced by Decreased Medical Expenses when Enroll in MSP - at least temporarily 5. Enrolling in an MSP - Automatic Enrollment &.

Applications for People who Have Medicare What is Application Process?. 6. Enrolling in an MSP for People age 65+ who Do Not Qualify for Free Medicare Part A - the "Part A Buy-In Program" 7.

What Happens After MSP Approved - How Part B Premium is Paid 8 Special Rules for QMBs - How Medicare Cost-Sharing Works 1. NO ASSET LIMIT!. Since April 1, 2008, none of the three MSP programs have resource limits in New York -- which means many Medicare beneficiaries who might not qualify for Medicaid because of excess resources can qualify for an MSP.

1.A. SUMMARY CHART OF MSP BENEFITS QMB SLIMB QI-1 Eligibility ASSET LIMIT NO LIMIT IN NEW YORK STATE INCOME LIMIT (2020) Single Couple Single Couple Single Couple $1,064 $1,437 $1,276 $1,724 $1,436 $1,940 Federal Poverty Level 100% FPL 100 – 120% FPL 120 – 135% FPL Benefits Pays Monthly Part B premium?. YES, and also Part A premium if did not have enough work quarters and meets citizenship requirement.

See “Part A Buy-In” YES YES Pays Part A &. B deductibles &. Co-insurance YES - with limitations NO NO Retroactive to Filing of Application?.

Yes - Benefits begin the month after the month of the MSP application. 18 NYCRR §360-7.8(b)(5) Yes – Retroactive to 3rd month before month of application, if eligible in prior months Yes – may be retroactive to 3rd month before month of applica-tion, but only within the current calendar year. (No retro for January application).

See GIS 07 MA 027. Can Enroll in MSP and Medicaid at Same Time?. YES YES NO!.

Must choose between QI-1 and Medicaid. Cannot have both, not even Medicaid with a spend-down. 2.

INCOME LIMITS and RULES Each of the three MSP programs has different income eligibility requirements and provides different benefits. The income limits are tied to the Federal Poverty Level (FPL). 2019 FPL levels were released by NYS DOH in GIS 20 MA/02 - 2020 Federal Poverty Levels -- Attachment II and have been posted by Medicaid.gov and the National Council on Aging and are in the chart below.

NOTE. There is usually a lag in time of several weeks, or even months, from January 1st of each year until the new FPLs are release, and then before the new MSP income limits are officially implemented. During this lag period, local Medicaid offices should continue to use the previous year's FPLs AND count the person's Social Security benefit amount from the previous year - do NOT factor in the Social Security COLA (cost of living adjustment).

Once the updated guidelines are released, districts will use the new FPLs and go ahead and factor in any COLA. See 2019 Fact Sheet on MSP in NYS by Medicare Rights Center ENGLISH SPANISH Income is determined by the same methodology as is used for determining in eligibility for SSI The rules for counting income for SSI-related (Aged 65+, Blind, or Disabled) Medicaid recipients, borrowed from the SSI program, apply to the MSP program, except for the new rules about counting household size for married couples. N.Y.

367-a(3)(c)(2), NYS DOH 2000-ADM-7, 89-ADM-7 p.7. Gross income is counted, although there are certain types of income that are disregarded. The most common income disregards, also known as deductions, include.

(a) The first $20 of your &. Your spouse's monthly income, earned or unearned ($20 per couple max). (b) SSI EARNED INCOME DISREGARDS.

* The first $65 of monthly wages of you and your spouse, * One-half of the remaining monthly wages (after the $65 is deducted). * Other work incentives including PASS plans, impairment related work expenses (IRWEs), blind work expenses, etc. For information on these deductions, see The Medicaid Buy-In for Working People with Disabilities (MBI-WPD) and other guides in this article -- though written for the MBI-WPD, the work incentives apply to all Medicaid programs, including MSP, for people age 65+, disabled or blind.

(c) monthly cost of any health insurance premiums but NOT the Part B premium, since Medicaid will now pay this premium (may deduct Medigap supplemental policies, vision, dental, or long term care insurance premiums, and the Part D premium but only to the extent the premium exceeds the Extra Help benchmark amount) (d) Food stamps not counted. You can get a more comprehensive listing of the SSI-related income disregards on the Medicaid income disregards chart. As for all benefit programs based on financial need, it is usually advantageous to be considered a larger household, because the income limit is higher.

The above chart shows that Households of TWO have a higher income limit than households of ONE. The MSP programs use the same rules as Medicaid does for the Disabled, Aged and Blind (DAB) which are borrowed from the SSI program for Medicaid recipients in the “SSI-related category.” Under these rules, a household can be only ONE or TWO. 18 NYCRR 360-4.2.

See DAB Household Size Chart. Married persons can sometimes be ONE or TWO depending on arcane rules, which can force a Medicare beneficiary to be limited to the income limit for ONE person even though his spouse who is under 65 and not disabled has no income, and is supported by the client applying for an MSP. EXAMPLE.

Bob's Social Security is $1300/month. He is age 67 and has Medicare. His wife, Nancy, is age 62 and is not disabled and does not work.

Under the old rule, Bob was not eligible for an MSP because his income was above the Income limit for One, even though it was well under the Couple limit. In 2010, NYS DOH modified its rules so that all married individuals will be considered a household size of TWO. DOH GIS 10 MA 10 Medicare Savings Program Household Size, June 4, 2010.

This rule for household size is an exception to the rule applying SSI budgeting rules to the MSP program. Under these rules, Bob is now eligible for an MSP. When is One Better than Two?.

Of course, there may be couples where the non-applying spouse's income is too high, and disqualifies the applying spouse from an MSP. In such cases, "spousal refusal" may be used SSL 366.3(a). (Link is to NYC HRA form, can be adapted for other counties).

3. The Three Medicare Savings Programs - what are they and how are they different?. 1.

Qualified Medicare Beneficiary (QMB). The QMB program provides the most comprehensive benefits. Available to those with incomes at or below 100% of the Federal Poverty Level (FPL), the QMB program covers virtually all Medicare cost-sharing obligations.

Part B premiums, Part A premiums, if there are any, and any and all deductibles and co-insurance. QMB coverage is not retroactive. The program’s benefits will begin the month after the month in which your client is found eligible.

** See special rules about cost-sharing for QMBs below - updated with new CMS directive issued January 2012 ** See NYC HRA QMB Recertification form ** Even if you do not have Part A automatically, because you did not have enough wages, you may be able to enroll in the Part A Buy-In Program, in which people eligible for QMB who do not otherwise have Medicare Part A may enroll, with Medicaid paying the Part A premium (Materials by the Medicare Rights Center). 2. Specifiedl Low-Income Medicare Beneficiary (SLMB).

For those with incomes between 100% and 120% FPL, the SLMB program will cover Part B premiums only. SLMB is retroactive, however, providing coverage for three months prior to the month of application, as long as your client was eligible during those months. 3.

Qualified Individual (QI-1). For those with incomes between 120% and 135% FPL, and not receiving Medicaid, the QI-1 program will cover Medicare Part B premiums only. QI-1 is also retroactive, providing coverage for three months prior to the month of application, as long as your client was eligible during those months.

However, QI-1 retroactive coverage can only be provided within the current calendar year. (GIS 07 MA 027) So if you apply in January, you get no retroactive coverage. Q-I-1 recipients would be eligible for Medicaid with a spend-down, but if they want the Part B premium paid, they must choose between enrolling in QI-1 or Medicaid.

They cannot be in both. It is their choice. DOH MRG p.

19. In contrast, one may receive Medicaid and either QMB or SLIMB. 4.

Four Special Benefits of MSPs (in addition to NO ASSET TEST). Benefit 1. Back Door to Medicare Part D "Extra Help" or Low Income Subsidy -- All MSP recipients are automatically enrolled in Extra Help, the subsidy that makes Part D affordable.

They have no Part D deductible or doughnut hole, the premium is subsidized, and they pay very low copayments. Once they are enrolled in Extra Help by virtue of enrollment in an MSP, they retain Extra Help for the entire calendar year, even if they lose MSP eligibility during that year. The "Full" Extra Help subsidy has the same income limit as QI-1 - 135% FPL.

However, many people may be eligible for QI-1 but not Extra Help because QI-1 and the other MSPs have no asset limit. People applying to the Social Security Administration for Extra Help might be rejected for this reason. Recent (2009-10) changes to federal law called "MIPPA" requires the Social Security Administration (SSA) to share eligibility data with NYSDOH on all persons who apply for Extra Help/ the Low Income Subsidy.

Data sent to NYSDOH from SSA will enable NYSDOH to open MSP cases on many clients. The effective date of the MSP application must be the same date as the Extra Help application. Signatures will not be required from clients.

In cases where the SSA data is incomplete, NYSDOH will forward what is collected to the local district for completion of an MSP application. The State implementing procedures are in DOH 2010 ADM-03. Also see CMS "Dear State Medicaid Director" letter dated Feb.

18, 2010 Benefit 2. MSPs Automatically Waive Late Enrollment Penalties for Part B Generally one must enroll in Part B within the strict enrollment periods after turning age 65 or after 24 months of Social Security Disability. An exception is if you or your spouse are still working and insured under an employer sponsored group health plan, or if you have End Stage Renal Disease, and other factors, see this from Medicare Rights Center.

If you fail to enroll within those short periods, you might have to pay higher Part B premiums for life as a Late Enrollment Penalty (LEP). Also, you may only enroll in Part B during the Annual Enrollment Period from January 1 - March 31st each year, with Part B not effective until the following July. Enrollment in an MSP automatically eliminates such penalties...

For life.. Even if one later ceases to be eligible for the MSP. AND enrolling in an MSP will automatically result in becoming enrolled in Part B if you didn't already have it and only had Part A.

See Medicare Rights Center flyer. Benefit 3. No Medicaid Lien on Estate to Recover MSP Benefits Paid Generally speaking, states may place liens on the Estates of deceased Medicaid recipients to recover the cost of Medicaid services that were provided after the recipient reached the age of 55.

Since 2002, states have not been allowed to recover the cost of Medicare premiums paid under MSPs. In 2010, Congress expanded protection for MSP benefits. Beginning on January 1, 2010, states may not place liens on the Estates of Medicaid recipients who died after January 1, 2010 to recover costs for co-insurance paid under the QMB MSP program for services rendered after January 1, 2010.

The federal government made this change in order to eliminate barriers to enrollment in MSPs. See NYS DOH GIS 10-MA-008 - Medicare Savings Program Changes in Estate Recovery The GIS clarifies that a client who receives both QMB and full Medicaid is exempt from estate recovery for these Medicare cost-sharing expenses. Benefit 4.

SNAP (Food Stamp) benefits not reduced despite increased income from MSP - at least temporarily Many people receive both SNAP (Food Stamp) benefits and MSP. Income for purposes of SNAP/Food Stamps is reduced by a deduction for medical expenses, which includes payment of the Part B premium. Since approval for an MSP means that the client no longer pays for the Part B premium, his/her SNAP/Food Stamps income goes up, so their SNAP/Food Stamps go down.

Here are some protections. Do these individuals have to report to their SNAP worker that their out of pocket medical costs have decreased?. And will the household see a reduction in their SNAP benefits, since the decrease in medical expenses will increase their countable income?.

The good news is that MSP households do NOT have to report the decrease in their medical expenses to the SNAP/Food Stamp office until their next SNAP/Food Stamp recertification. Even if they do report the change, or the local district finds out because the same worker is handling both the MSP and SNAP case, there should be no reduction in the household’s benefit until the next recertification. New York’s SNAP policy per administrative directive 02 ADM-07 is to “freeze” the deduction for medical expenses between certification periods.

Increases in medical expenses can be budgeted at the household’s request, but NYS never decreases a household’s medical expense deduction until the next recertification. Most elderly and disabled households have 24-month SNAP certification periods. Eventually, though, the decrease in medical expenses will need to be reported when the household recertifies for SNAP, and the household should expect to see a decrease in their monthly SNAP benefit.

It is really important to stress that the loss in SNAP benefits is NOT dollar for dollar. A $100 decrease in out of pocket medical expenses would translate roughly into a $30 drop in SNAP benefits. See more info on SNAP/Food Stamp benefits by the Empire Justice Center, and on the State OTDA website.

Some clients will be automatically enrolled in an MSP by the New York State Department of Health (NYSDOH) shortly after attaining eligibility for Medicare. Others need to apply. The 2010 "MIPPA" law introduced some improvements to increase MSP enrollment.

See 3rd bullet below. Also, some people who had Medicaid through the Affordable Care Act before they became eligible for Medicare have special procedures to have their Part B premium paid before they enroll in an MSP. See below.

WHO IS AUTOMATICALLY ENROLLED IN AN MSP. Clients receiving even $1.00 of Supplemental Security Income should be automatically enrolled into a Medicare Savings Program (most often QMB) under New York State’s Medicare Savings Program Buy-in Agreement with the federal government once they become eligible for Medicare. They should receive Medicare Parts A and B.

Clients who are already eligible for Medicare when they apply for Medicaid should be automatically assessed for MSP eligibility when they apply for Medicaid. (NYS DOH 2000-ADM-7 and GIS 05 MA 033). Clients who apply to the Social Security Administration for Extra Help, but are rejected, should be contacted &.

Enrolled into an MSP by the Medicaid program directly under new MIPPA procedures that require data sharing. Strategy TIP. Since the Extra Help filing date will be assigned to the MSP application, it may help the client to apply online for Extra Help with the SSA, even knowing that this application will be rejected because of excess assets or other reason.

SSA processes these requests quickly, and it will be routed to the State for MSP processing. Since MSP applications take a while, at least the filing date will be retroactive. Note.

The above strategy does not work as well for QMB, because the effective date of QMB is the month after the month of application. As a result, the retroactive effective date of Extra Help will be the month after the failed Extra Help application for those with QMB rather than SLMB/QI-1. Applying for MSP Directly with Local Medicaid Program.

Those who do not have Medicaid already must apply for an MSP through their local social services district. (See more in Section D. Below re those who already have Medicaid through the Affordable Care Act before they became eligible for Medicare.

If you are applying for MSP only (not also Medicaid), you can use the simplified MSP application form (theDOH-4328(Rev. 8/2017-- English) (2017 Spanish version not yet available). Either application form can be mailed in -- there is no interview requirement anymore for MSP or Medicaid.

See 10 ADM-04. Applicants will need to submit proof of income, a copy of their Medicare card (front &. Back), and proof of residency/address.

See the application form for other instructions. One who is only eligible for QI-1 because of higher income may ONLY apply for an MSP, not for Medicaid too. One may not receive Medicaid and QI-1 at the same time.

If someone only eligible for QI-1 wants Medicaid, s/he may enroll in and deposit excess income into a pooled Supplemental Needs Trust, to bring her countable income down to the Medicaid level, which also qualifies him or her for SLIMB or QMB instead of QI-1. Advocates in NYC can sign up for a half-day "Deputization Training" conducted by the Medicare Rights Center, at which you'll be trained and authorized to complete an MSP application and to submit it via the Medicare Rights Center, which submits it to HRA without the client having to apply in person. Enrolling in an MSP if you already have Medicaid, but just become eligible for Medicare Those who, prior to becoming enrolled in Medicare, had Medicaid through Affordable Care Act are eligible to have their Part B premiums paid by Medicaid (or the cost reimbursed) during the time it takes for them to transition to a Medicare Savings Program.

In 2018, DOH clarified that reimbursement of the Part B premium will be made regardless of whether the individual is still in a Medicaid managed care (MMC) plan. GIS 18 MA/001 Medicaid Managed Care Transition for Enrollees Gaining Medicare ( PDF) provides, "Due to efforts to transition individuals who gain Medicare eligibility and who require LTSS, individuals may not be disenrolled from MMC upon receipt of Medicare. To facilitate the transition and not disadvantage the recipient, the Medicaid program is approving reimbursement of Part B premiums for enrollees in MMC." The procedure for getting the Part B premium paid is different for those whose Medicaid was administered by the NYS of Health Exchange (Marketplace), as opposed to their local social services district.

The procedure is also different for those who obtain Medicare because they turn 65, as opposed to obtaining Medicare based on disability. Either way, Medicaid recipients who transition onto Medicare should be automatically evaluated for MSP eligibility at their next Medicaid recertification. NYS DOH 2000-ADM-7 Individuals can also affirmatively ask to be enrolled in MSP in between recertification periods.

IF CLIENT HAD MEDICAID ON THE MARKETPLACE (NYS of Health Exchange) before obtaining Medicare. IF they obtain Medicare because they turn age 65, they will receive a letter from their local district asking them to "renew" Medicaid through their local district. See 2014 LCM-02.

Now, their Medicaid income limit will be lower than the MAGI limits ($842/ mo reduced from $1387/month) and they now will have an asset test. For this reason, some individuals may lose full Medicaid eligibility when they begin receiving Medicare. People over age 65 who obtain Medicare do NOT keep "Marketplace Medicaid" for 12 months (continuous eligibility) See GIS 15 MA/022 - Continuous Coverage for MAGI Individuals.

Since MSP has NO ASSET limit. Some individuals may be enrolled in the MSP even if they lose Medicaid, or if they now have a Medicaid spend-down. If a Medicare/Medicaid recipient reports income that exceeds the Medicaid level, districts must evaluate the person’s eligibility for MSP.

08 OHIP/ADM-4 ​If you became eligible for Medicare based on disability and you are UNDER AGE 65, you are entitled to keep MAGI Medicaid for 12 months from the month it was last authorized, even if you now have income normally above the MAGI limit, and even though you now have Medicare. This is called Continuous Eligibility. EXAMPLE.

Sam, age 60, was last authorized for Medicaid on the Marketplace in June 2016. He became enrolled in Medicare based on disability in August 2016, and started receiving Social Security in the same month (he won a hearing approving Social Security disability benefits retroactively, after first being denied disability). Even though his Social Security is too high, he can keep Medicaid for 12 months beginning June 2016.

Sam has to pay for his Part B premium - it is deducted from his Social Security check. He may call the Marketplace and request a refund. This will continue until the end of his 12 months of continues MAGI Medicaid eligibility.

He will be reimbursed regardless of whether he is in a Medicaid managed care plan. See GIS 18 MA/001 Medicaid Managed Care Transition for Enrollees Gaining Medicare (PDF) When that ends, he will renew Medicaid and apply for MSP with his local district. Individuals who are eligible for Medicaid with a spenddown can opt whether or not to receive MSP.

(Medicaid Reference Guide (MRG) p. 19). Obtaining MSP may increase their spenddown.

MIPPA - Outreach by Social Security Administration -- Under MIPPA, the SSA sends a form letter to people who may be eligible for a Medicare Savings Program or Extra Help (Low Income Subsidy - LIS) that they may apply. The letters are. · Beneficiary has Extra Help (LIS), but not MSP · Beneficiary has no Extra Help (LIS) or MSP 6.

Enrolling in MSP for People Age 65+ who do Not have Free Medicare Part A - the "Part A Buy-In Program" Seniors WITHOUT MEDICARE PART A or B -- They may be able to enroll in the Part A Buy-In program, in which people eligible for QMB who are age 65+ who do not otherwise have Medicare Part A may enroll in Part A, with Medicaid paying the Part A premium. See Step-by-Step Guide by the Medicare Rights Center). This guide explains the various steps in "conditionally enrolling" in Part A at the SSA office, which must be done before applying for QMB at the Medicaid office, which will then pay the Part A premium.

See also GIS 04 MA/013. In June, 2018, the SSA revised the POMS manual procedures for the Part A Buy-In to to address inconsistencies and confusion in SSA field offices and help smooth the path for QMB enrollment. The procedures are in the POMS Section HI 00801.140 "Premium-Free Part A Enrollments for Qualified Medicare BenefiIaries." It includes important clarifications, such as.

SSA Field Offices should explain the QMB program and conditional enrollment process if an individual lacks premium-free Part A and appears to meet QMB requirements. SSA field offices can add notes to the “Remarks” section of the application and provide a screen shot to the individual so the individual can provide proof of conditional Part A enrollment when applying for QMB through the state Medicaid program. Beneficiaries are allowed to complete the conditional application even if they owe Medicare premiums.

In Part A Buy-in states like NYS, SSA should process conditional applications on a rolling basis (without regard to enrollment periods), even if the application coincides with the General Enrollment Period. (The General Enrollment Period is from Jan 1 to March 31st every year, in which anyone eligible may enroll in Medicare Part A or Part B to be effective on July 1st). 7.

What happens after the MSP approval - How is Part B premium paid For all three MSP programs, the Medicaid program is now responsible for paying the Part B premiums, even though the MSP enrollee is not necessarily a recipient of Medicaid. The local Medicaid office (DSS/HRA) transmits the MSP approval to the NYS Department of Health – that information gets shared w/ SSA and CMS SSA stops deducting the Part B premiums out of the beneficiary’s Social Security check. SSA also refunds any amounts owed to the recipient.

!. ) CMS “deems” the MSP recipient eligible for Part D Extra Help/ Low Income Subsidy (LIS). ​Can the MSP be retroactive like Medicaid, back to 3 months before the application?.

​The answer is different for the 3 MSP programs. QMB -No Retroactive Eligibility – Benefits begin the month after the month of the MSP application. 18 NYCRR § 360-7.8(b)(5) SLIMB - YES - Retroactive Eligibility up to 3 months before the application, if was eligible This means applicant may be reimbursed for the 3 months of Part B benefits prior to the month of application.

QI-1 - YES up to 3 months but only in the same calendar year. No retroactive eligibility to the previous year. 7.