COVID 19 and Heart

Abstract

virus, SARS-CoV-2 in severe form is associated with myocardial injury with features of myocarditis with ECG changes and increased level of troponin. But it involves myocardium at far more rate (24-33%) than influenza (around 1%). It is understood when we consider the pathophysiology of the way virus acts in the body. It utilizes Angiotensin Converting Enzyme 2 (ACE2) receptors to enter the cells. These receptors are abundant in the lungs and much expressed in the myocardium, endothelium. kidneys and GI tract. Following a few days of infection, it enters myocytes causing myocardial injury. This direct effect of the virus leads to focal myocardial damage and scar formation. Thus, in addition to immediate cause of arrhythmia, it remains as nidus of future arrhythmia. In the later stage of the diseases, when there is immune response with cytokine release, there is suppression of myocardium with onset of acute left ventricular failure. This process of myocardial suppression is transient with no residual damage to the myocardium in most cases.