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__NOTOC__
'''Acute Myocardial Injury'''
{{COVID-19 associated Heart Failure}}
'''For patient information, click [[Xyz (patient information)|here]]'''


{{CMG}}; {{AE}} {{Mitra}}
Thank you for your great work!
There are only a few comments which may help you to improve the page.
*Your name does not redirect to your “user page”. You may fix this.
*Create redirects to the page (including all the synonyms).
*Follow abc format throughout the page. For example, complete age, gender, race in “epidemiology and demographics”. Also, complete physical examination, x-ray, CT, MRI, … sections. If you have no data to put there, link the readers to corresponding pages, the same that you have done for treatment. There are several blank paragraphs on your page, please do the same for all of them.
*Include “Differentiating ((Page name)) from other Diseases” and make a table for differential diagnosis.
*Please be careful to paraphrase sentences that you use from other sources to avoid plagiarism. Some sentences are exactly the same as in “UpToDate”. Please change them.
*You may add a figure to your page, in particular for the pathophysiology section. Also, Make a table for differential diagnosis.


{{SK}}
'''
Myocarditis and pericarditis''' (2 pages)


Thank you for your great work!


There are only a few comments which may help you to improve the page
• In myocarditis page, I think some of the redirects and links should be to the COVID-related pages rather than general pages. For example, in differential diagnosis, linking to COVID-associated acute coronary syndrome or heart failure is more logical rather than ACS or heart failure. But for pericarditis page, you've used links greatly.
• Follow abc format throughout the page. You have most parts of the template but still, some are missing, like primary prevention and secondary prevention.
• In historical perspective, present data for COVID-associated myocarditis or pericarditis, not the COVID-19 itself. In myocarditis page, you may begin with that famous Italian case report presenting the first case of COVID-19 myocarditis (doi:10.1001/jamacardio.2020.1096).
• In overview sections of both pages, also use COVID-19-associated myocarditis or pericarditis, rather than COVID-19 itself.
• Please make a table for differential diagnosis.


'''Acute coronary syndrome'''


Thank you for your great work!


There are only a few comments which may help you to improve the page.
• Please reconsider the “Classification” section. I think it is not relevant to talk about the reduction in the incidence of MI during the COVID-19 outbreak, rather we should talk about the occurrence of COVID-associated acute coronary syndrome. Although these data are also given in ACS section of “UptoDate” but our wikidoc approach (according to the template) and personal preferences of Dr. Gibson are different, so it makes this section less relevant to our COVID-19 page. 
• Pathophysiology also seems off-topic in most parts. For example in this sentence: The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial” you are not going to talk about the myocardial injury in COVID-19. Please focus on ACS, not myocardial injury. You can use type I and II ischemia to extend the pathophysiology section. 
• I think the “causes” section also needs revision. You’re giving data on classification; you can move this to the classification section. In addition, according to the universal definition of MI, we have 5 types of MI, even though I and II have been suggested for the pathophysiology of MI in COVID-19.
• Follow abc format throughout the page. All sections should be completed.
• Please make a table for differential diagnosis.




__NOTOC__
'''Arrhythmia'''
{{COVID-19 associated Heart Failure}}
Thank you for your great work!
'''For patient information, click [[Xyz (patient information)|here]]'''


{{CMG}}; {{AE}} {{Mitra}}
There are only a few comments which may help you to improve the page.
• Please delete unused sentences from the template.
• In pathophysiology, more data is given on pathophysiology of myocardial injury than arrhythmia in COVID-19 and makes the reader confused. For example Type 1 and type 2 pneumocytes exhibit ACE 2 receptors in the lung. Studies report that coronary endothelial cells in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the renin-angiotensin system. Or In COVID-19 patients, excessive ranges of circulating cytokines, especially interleukin (IL)-6 is related to in-hospital death.[9]  etc.
• Prolong QT Interval, Atrial Arrhythmia, and Ventricular Arrhythmia are not considered symptoms. You may transfer them to the ECG section or other more related sections.
• Please make a table for differential diagnosis.


{{SK}}


==[[Heart Failure overview|Overview]]==
'''Cardiogenic shock'''


*Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
Thank you for your great work!
*Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.


==[[Heart Failure historical perspective|Historical Perspective]]==
There are only a few comments which may help you to improve the page.
• I think for historical perspective you can find more prior cases. The case you are mentioning was not actually the first case of cardiogenic shock in COVId-19, it was the first who showed viral particles in the myocardial biopsy.
• Please follow the abc format. You have so many missing sections.
• This page was a short page (with limited data) and most sections have overlap with other pages, but you may extend some parts and link different sections to corresponding pages.
• Nothing is written regarding the use of ECMO in COVID-19 patients.
• According to Dr. Gibson’s feedback, all pages should have a table for differential diagnosis.


==[[Heart Failure classification|Classification]]==
'''Sudden cardiac death'''


==[[Heart Failure pathophysiology|Pathophysiology]]==
Thank you for your great work!


*Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>   
There are only a few comments which may help you to improve the page.
**Acute exacerbation of chronic heart failure
**Acute myocardial injury (which in turn can be caused by several mechanisms)
**Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
**Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
**Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)


==[[Heart Failure causes|Causes]]==
• Please follow the abc format. You have so many missing sections.
• For example, for “Causes” you can add pulmonary embolism, MI, arrhythmias, etc. Dr. Gibson has also emphasized on adding “pulmonary embolism” as a cause of sudden cardiac death in COVID-19 patients.
• Most sentences on your page do not have appropriate citations.
• This page has overlap with other pages, mainly arrhythmia page, but you may extend some parts and link different sections to corresponding pages. Please try to link to COVID-19-related pages, rather than general pages, when possible. 
• According to Dr. Gibson’s feedback, all pages should have a table for differential diagnosis.


==[[Heart Failure differential diagnosis|Differentiating Heart Failure from other Diseases]]==
'''Spontaneous coronary artery dissection'''
Thank you for your great work!


==[[Heart Failure epidemiology and demographics|Epidemiology and Demographics]]==
There are only a few comments which may help you to improve the page.
 
• This page is inherently a short page due to limited data, but please try to add more COVID-19 related data rather than general SCAD. You may a few case reports of SCAD in COVID-19.
==[[Heart Failure risk factors|Risk Factors]]==
• Please follow the abc format. You have so many missing sections. For sections you have no data, use appropriate sentences from the template.  
 
• The page has no reference.
==[[Heart Failure screening|Screening]]==
 
==[[Heart Failure natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
 
 
==Diagnosis==
[[COVID-19-associated heart failurediagnostic study of choice|Diagnostic study of choice]] | [[COVID-19-associated heart failure history and symptoms|History and Symptoms]] | [[COVID-19-associated heart failure physical examination|Physical Examination]] | [[COVID-19-associated heart failure laboratory findings|Laboratory Findings]] | [[COVID-19-associated heart failure electrocardiogram|Electrocardiogram]] | [[COVID-19-associated heart failure x ray|X-Ray Findings]] | [[COVID-19-associated heart failure echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[COVID-19-associated heart failure CT scan|CT-Scan Findings]] | [[COVID-19-associated heart failure MRI|MRI Findings]] | [[COVID-19-associated heart failure other imaging findings|Other Imaging Findings]] | [[COVID-19-associated heart failure other diagnostic studies|Other Diagnostic Studies]]
 
 
 
====Electrocardiography (ECG)====
 
| [[Xyz x ray|X-Ray Findings]]
====Chest x-ray (CXR)====
*The Chest x-ray may show evidence of:
**Cardiomegaly
**Pulmonary congestion
**Increased pulmonary vascular markings.
*Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
| [[Heart Failure echocardiography and ultrasound|Echocardiography and Ultrasound]]
 
====Echocardiography====
*A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**Cardiac point-of-care ultrasound (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography
*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia
| [[Heart Failure CT scan|CT-Scan Findings]] | [[Heart Failure MRI|MRI Findings]] | [[Heart Failure other imaging findings|Other Imaging Findings]] | [[Heart Failure other diagnostic studies|Other Diagnostic Studies]]
====Cardiac biomarkers====
*Cardiac Troponins:
**Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>
*Natriuretic Peptides:
**Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.
 
==Treatment==
[[Heart Failure medical therapy|Medical Therapy]]
 
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**Vasopressors and/or inotropes
**Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
*Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
 
| [[Heart Failure interventions|Interventions]] | [[Heart Failure surgery|Surgery]] | [[Heart Failure primary prevention|Primary Prevention]] | [[Heart Failure secondary prevention|Secondary Prevention]] | [[Heart Failure cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]
 
==Case Studies==
[[Xyz case study one|Case #1]]
 
[[Category: (name of the system)]]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
==[[Heart Failure overview|Overview]]==
 
*Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
*Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
 
==[[Heart Failure historical perspective|Historical Perspective]]==
 
==[[Heart Failure classification|Classification]]==
 
==[[Heart Failure pathophysiology|Pathophysiology]]==
 
*Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>   
**Acute exacerbation of chronic heart failure
**Acute myocardial injury (which in turn can be caused by several mechanisms)
**Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
**Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
**Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)
 
==[[Heart Failure causes|Causes]]==
 
==[[Heart Failure differential diagnosis|Differentiating Heart Failure from other Diseases]]==
 
==[[Heart Failure epidemiology and demographics|Epidemiology and Demographics]]==
 
==[[Heart Failure risk factors|Risk Factors]]==
 
==[[Heart Failure screening|Screening]]==
 
==[[Heart Failure natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
 
 
==Diagnosis==
[[COVID-19-associated heart failurediagnostic study of choice|Diagnostic study of choice]] | [[COVID-19-associated heart failure history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]]
 
 
 
| [[Xyz physical examination|Physical Examination]] | [[Heart Failure laboratory findings|Laboratory Findings]] | [[Heart Failure electrocardiogram|Electrocardiogram]]
 
====Electrocardiography (ECG)====
*There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
*These ECG findings may include:
**Low QRS Voltage
**Left ventricular hypertrophy
**Left atrial enlargement
**Left bundle branch block
**Poor R progression
**ST-T changes
| [[Xyz x ray|X-Ray Findings]]
====Chest x-ray (CXR)====
*The Chest x-ray may show evidence of:
**Cardiomegaly
**Pulmonary congestion
**Increased pulmonary vascular markings.
*Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
| [[Heart Failure echocardiography and ultrasound|Echocardiography and Ultrasound]]
 
====Echocardiography====
*A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
**Cardiac point-of-care ultrasound (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography
*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia
| [[Heart Failure CT scan|CT-Scan Findings]] | [[Heart Failure MRI|MRI Findings]] | [[Heart Failure other imaging findings|Other Imaging Findings]] | [[Heart Failure other diagnostic studies|Other Diagnostic Studies]]
====Cardiac biomarkers====
*Cardiac Troponins:
**Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>
*Natriuretic Peptides:
**Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.
 
==Treatment==
[[Heart Failure medical therapy|Medical Therapy]]
 
*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**Vasopressors and/or inotropes
**Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
*Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>
 
| [[Heart Failure interventions|Interventions]] | [[Heart Failure surgery|Surgery]] | [[Heart Failure primary prevention|Primary Prevention]] | [[Heart Failure secondary prevention|Secondary Prevention]] | [[Heart Failure cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]
 
==Case Studies==
[[Xyz case study one|Case #1]]
 
[[Category: (name of the system)]]

Revision as of 19:27, 11 July 2020

Acute Myocardial Injury

Thank you for your great work! There are only a few comments which may help you to improve the page.

  • Your name does not redirect to your “user page”. You may fix this.
  • Create redirects to the page (including all the synonyms).
  • Follow abc format throughout the page. For example, complete age, gender, race in “epidemiology and demographics”. Also, complete physical examination, x-ray, CT, MRI, … sections. If you have no data to put there, link the readers to corresponding pages, the same that you have done for treatment. There are several blank paragraphs on your page, please do the same for all of them.
  • Include “Differentiating ((Page name)) from other Diseases” and make a table for differential diagnosis.
  • Please be careful to paraphrase sentences that you use from other sources to avoid plagiarism. Some sentences are exactly the same as in “UpToDate”. Please change them.
  • You may add a figure to your page, in particular for the pathophysiology section. Also, Make a table for differential diagnosis.

Myocarditis and pericarditis (2 pages)

Thank you for your great work!

There are only a few comments which may help you to improve the page • In myocarditis page, I think some of the redirects and links should be to the COVID-related pages rather than general pages. For example, in differential diagnosis, linking to COVID-associated acute coronary syndrome or heart failure is more logical rather than ACS or heart failure. But for pericarditis page, you've used links greatly. • Follow abc format throughout the page. You have most parts of the template but still, some are missing, like primary prevention and secondary prevention. • In historical perspective, present data for COVID-associated myocarditis or pericarditis, not the COVID-19 itself. In myocarditis page, you may begin with that famous Italian case report presenting the first case of COVID-19 myocarditis (doi:10.1001/jamacardio.2020.1096). • In overview sections of both pages, also use COVID-19-associated myocarditis or pericarditis, rather than COVID-19 itself. • Please make a table for differential diagnosis.

Acute coronary syndrome

Thank you for your great work!

There are only a few comments which may help you to improve the page. • Please reconsider the “Classification” section. I think it is not relevant to talk about the reduction in the incidence of MI during the COVID-19 outbreak, rather we should talk about the occurrence of COVID-associated acute coronary syndrome. Although these data are also given in ACS section of “UptoDate” but our wikidoc approach (according to the template) and personal preferences of Dr. Gibson are different, so it makes this section less relevant to our COVID-19 page. • Pathophysiology also seems off-topic in most parts. For example in this sentence: The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial” you are not going to talk about the myocardial injury in COVID-19. Please focus on ACS, not myocardial injury. You can use type I and II ischemia to extend the pathophysiology section. • I think the “causes” section also needs revision. You’re giving data on classification; you can move this to the classification section. In addition, according to the universal definition of MI, we have 5 types of MI, even though I and II have been suggested for the pathophysiology of MI in COVID-19. • Follow abc format throughout the page. All sections should be completed. • Please make a table for differential diagnosis.


Arrhythmia Thank you for your great work!

There are only a few comments which may help you to improve the page. • Please delete unused sentences from the template. • In pathophysiology, more data is given on pathophysiology of myocardial injury than arrhythmia in COVID-19 and makes the reader confused. For example Type 1 and type 2 pneumocytes exhibit ACE 2 receptors in the lung. Studies report that coronary endothelial cells in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the renin-angiotensin system. Or In COVID-19 patients, excessive ranges of circulating cytokines, especially interleukin (IL)-6 is related to in-hospital death.[9] etc. • Prolong QT Interval, Atrial Arrhythmia, and Ventricular Arrhythmia are not considered symptoms. You may transfer them to the ECG section or other more related sections. • Please make a table for differential diagnosis.


Cardiogenic shock

Thank you for your great work!

There are only a few comments which may help you to improve the page. • I think for historical perspective you can find more prior cases. The case you are mentioning was not actually the first case of cardiogenic shock in COVId-19, it was the first who showed viral particles in the myocardial biopsy. • Please follow the abc format. You have so many missing sections. • This page was a short page (with limited data) and most sections have overlap with other pages, but you may extend some parts and link different sections to corresponding pages. • Nothing is written regarding the use of ECMO in COVID-19 patients. • According to Dr. Gibson’s feedback, all pages should have a table for differential diagnosis.

Sudden cardiac death

Thank you for your great work!

There are only a few comments which may help you to improve the page.

• Please follow the abc format. You have so many missing sections. • For example, for “Causes” you can add pulmonary embolism, MI, arrhythmias, etc. Dr. Gibson has also emphasized on adding “pulmonary embolism” as a cause of sudden cardiac death in COVID-19 patients. • Most sentences on your page do not have appropriate citations. • This page has overlap with other pages, mainly arrhythmia page, but you may extend some parts and link different sections to corresponding pages. Please try to link to COVID-19-related pages, rather than general pages, when possible. • According to Dr. Gibson’s feedback, all pages should have a table for differential diagnosis.

Spontaneous coronary artery dissection Thank you for your great work!

There are only a few comments which may help you to improve the page. • This page is inherently a short page due to limited data, but please try to add more COVID-19 related data rather than general SCAD. You may a few case reports of SCAD in COVID-19. • Please follow the abc format. You have so many missing sections. For sections you have no data, use appropriate sentences from the template. • The page has no reference.