Coronavirus Disease 2019 (COVID-19) and Cardiac Injury—Reply

In Reply The issue of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been an important topic from the beginning of the coronavirus disease 2019 (COVID-19) pandemic. Our preliminary investigation demonstrated that myocardial injury is prevalent and associated with worse outcomes in hospitalized patients with COVID-19.¹ With the global outbreak of COVID-19, increasing data focusing on the association of SARS-CoV-2 infection with heart injury have confirmed various pathophysiological hypotheses. The potential mechanisms of myocardial injury in patients with COVID-19, based on our data and evidence from others, include acute myocardial infarction, myocarditis, inflammatory response, acute heart failure, hypoxemia, pulmonary embolism, and even stress cardiomyopathy. These conditions can coexist in the same patients.

Myocardial injury is a common phenomenon in patients with COVID-19, which is the key evidence that SARS-CoV-2 infection can affect the heart. Its prevalence rate was 19.7% in our report of 416 hospitalized patients with COVID-19.¹ Recently, a meta-analysis summarized that at least 8.0% of patients with COVID-19 experienced acute myocardial injury, and the rate was roughly 13-fold higher in patients with severe disease treated in the intensive care unit compared with patients without severe disease.²

Various possible pathophysiological mechanisms are widely speculated and gradually confirmed by clinical data. With regard to the cause of myocardial injury, direct viral invasion of the heart similar to pulmonary infection has been hypothesized because angiotensin-converting enzyme 2, proposed as a receptor for SARS-CoV-2, is also extensively expressed in myocardium. Although the first pathological study with limited sample and methodology did not document SARS-CoV-2 infection of cardiomyocytes,³ it is still a reasonable speculation that direct viral myocardial infection may exist because clinical cases resembling myocarditis have been reported.⁴ Systemic inflammatory responses with pneumonia can lead to nonischemic myocardial impairment, especially in the presence of preexisting cardiovascular diseases. Moreover, coronary atherosclerotic plaques with increased inflammatory activity are prone to rupture with subsequent cardiac impairment. A large proportion of myocardial injuries are attributed to type I and II myocardial infarction, defined as thrombosis caused by plaque rupture and caused by the imbalance of myocardial oxygen supply and demand,⁵ respectively. This would be caused by the combined effects of inflammation, cardiovascular comorbidities, and other risk factors (eg, older age). There is also the possibility of noncoronary myocardial injury⁶ and stress cardiomyopathy, which may be caused by a severe emotional stress and/or physical injury under public health emergencies. The cardiovascular adverse effects of various antiepidemic drugs should also not be ignored.

In conclusion, as the underlying mechanisms of myocardial injury are varied in patients with COVID-19, comprehensive cardiovascular examinations after balancing the risk of infection are crucial for differential diagnosis and precise treatment. In addition to acute myocardial injury, as a larger number of patients are discharged, the long-term cardiovascular consequences of COVID-19 will require further follow-up studies.

Corresponding Author: Bo Yang, MD, PhD, Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Rd, Wuchang District, Hubei 430060, China (yybb112@whu.edu.cn).

Published Online: July 8, 2020. doi:10.1001/jamacardio.2020.2456

Conflict of Interest Disclosures: None reported.