At #AHA21, I co-chaired a featured session with Dr. Mina Chung from the Cleveland Clinic in which the principal investigators of AHA-funded studies on COVID-19 and cardiovascular disease presented their preliminary findings in a “rapid fire” approach. Several of these translational research studies provide important new insights into mechanisms of cardiac injury in COVID-19. Two autopsy studies highlighted the finding that cardiac microthrombi appear to be the dominant cardiac feature of COVID-19.
Microthrombi were associated with markers of systemic inflammation, with pathological evidence of endothelial cell damage and a prothrombotic endothelial cell profile. Moreover, the endothelial cell activation appeared to be induced by hypoxia, providing a link between the respiratory and cardiac complications of COVID-19. A different study found that platelets can take up SARS-CoV-2 as part of their immune function, which may contribute to the propensity for arterial thrombosis seen in COVID-19. A study of endomyocardial biopsies from patients with COVID-19 and myocardial injury (i.e., elevated troponin levels) found decreased gene expression of angiotensin converting enzyme (ACE) 2 (a protective pathway) and increased expression of ACE (a harmful pathway) as compared with controls. There also was evidence for upregulated expression of inflammatory and thrombosis genes.