• Han Zhu, June-Wha Rhee, Paul Cheng, Sarah Waliany, Amy Chang, Ronald M Witteles, Holden Maecker, Mark M Davis, Patricia K Nguyen, and Sean M Wu.
• Department of Medicine, Stanford University, Room G1120A, Lokey Stem Cell Building, 265 Campus Drive, Stanford, CA, 94305, USA.
• Curr Cardiol Rep. 2020 Apr 21; 22 (5): 32.

Purpose Of ReviewCoronavirus disease of 2019 (COVID-19) is a cause of significant morbidity and mortality worldwide. While cardiac injury has been demonstrated in critically ill COVID-19 patients, the mechanism of injury remains unclear. Here, we review our current knowledge of the biology of SARS-CoV-2 and the potential mechanisms of myocardial injury due to viral toxicities and host immune responses.Recent FindingsA number of studies have reported an epidemiological association between history of cardiac disease and worsened outcome during COVID infection. Development of new onset myocardial injury during COVID-19 also increases mortality. While limited data exist, potential mechanisms of cardiac injury include direct viral entry through the angiotensin-converting enzyme 2 (ACE2) receptor and toxicity in host cells, hypoxia-related myocyte injury, and immune-mediated cytokine release syndrome. Potential treatments for reducing viral infection and excessive immune responses are also discussed. COVID patients with cardiac disease history or acquire new cardiac injury are at an increased risk for in-hospital morbidity and mortality. More studies are needed to address the mechanism of cardiotoxicity and the treatments that can minimize permanent damage to the cardiovascular system.

35 keywords...

hide…