Cardiac involvement in COVID-19: cause or consequence of severe manifestations?

TLDR: In this paper, a large body of evidence strongly suggested that cardiac involvement could potentially be one of these prognostic factors, and several hypotheses have been raised for the cardiovascular abnormalities observed, especially in severely ill patients.

Abstract: Since the inception of the COVID-19 pandemic, the identification of factors associated with unfavourable outcomes has been a topic of intense investigation. With limited disease-specific therapies, early stratification of those at highest risk of complications can guide who needs intensive clinical monitoring and supportive management. The large body of evidence in the early phases of the pandemic strongly suggested that cardiac involvement could potentially be one of these prognostic factors, and several hypotheses have been raised for the cardiovascular abnormalities observed, especially in severely ill patients. Markers of acute myocardial injury have been reported in up to one-fifth of patients with COVID-19,1 and several mechanisms have been implicated: (a) direct myocardial injury due to viral invasion of cardiomyocytes; (b) systemic inflammatory response and cytokine storm; (c) increased cardiometabolic demand associated with acute hypoxic respiratory failure; (d) increased vascular shear stress precipitating plaque rupture in the setting of a prothrombotic state; (e) deleterious cardiovascular effects of empirical drug regimens; (f) critical electrolyte disturbances. These disease-related mechanisms may be exacerbated by underlying cardiac disease and increase risk of adverse outcomes.1 The present study by Singh et al 2 brings a significant contribution to this growing body of evidence. Fifty-two patients recovered from COVID-19 (one-third with intensive care admission and one-fifth requiring mechanical ventilation) underwent a comprehensive imaging protocol with gadolinium and manganese-enhanced MRI, with 23 additionally undergoing CT coronary angiography for evaluation of underlying coronary artery disease. They were compared with 10 healthy controls and 26 volunteers propensity matched for cardiovascular morbidity. COVID-19-recovered patients demonstrated impaired left (LV) and right (RV) ventricular systolic function, elevated myocardial T1 values and extracellular volume fraction, and reduced myocardial manganese uptake compared with healthy controls. In contrast, when comparing with comorbidity-matched volunteers, patients with COVID-19 had preserved LV function but reduced RV systolic function …