Cardiovascular Disorders and COVID-19: Difference between revisions

Revision as of 12:35, 12 June 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]

Overview

Complications

Acute Coronary Syndromes

Heart Failure

Cardiogenic Shock

Myocarditis

Pericarditis

Arrhythmias

Pathophysiology:

Respiratory disease is the main target of Covid-19. One-third of patients with the severe disease also reported other symptoms including arrhythmia. (1) Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. 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.(1,2,3) The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and endothelial cells. (4)

References

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 ===Arrhythmias===
+==== Pathophysiology: ====
+Respiratory disease is the main target of Covid-19. One-third of patients with the severe disease also reported other symptoms including arrhythmia. (1) Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. 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.(1,2,3) The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and endothelial cells. (4)
 ==References==