The Heart in COVID-19: Primary Target or Secondary Bystander?

Abstract

In the throes of the current coronavirus disease-2019 (COVID-19) pandemic, interest has burgeoned in the cardiovascular complications of this virulent viral infection. As troponin, a biomarker of cardiac injury, often rises in hospitalized patients, its interpretation and actionability require careful consideration. Fulminant myocarditis due to direct viral infection can certainly occur, but in patients with increased oxygen demands due to tachycardia and fever and reduced oxygen delivery due to hypotension and hypoxemia, COVID-19 disease can cause myocardial injury indirectly. Cytokines released during the acute infection can elicit activation of cells within pre-existing atherosclerotic lesions, augmenting thrombotic risk and risk of ischemic syndromes. Moreover, microvascular activation by cytokines can cause not only myocardial injury but can also harm other organ systems commonly involved in COVID-19 infections including the kidneys. Dealing with the immense challenge of COVID-19, confronted with severely ill patients in dire straits with virtually no rigorous evidence base to guide our therapy, we must call on our clinical skills and judgment. These touchstones can help guide us in selecting patients who might benefit from the advanced imaging and invasive procedures that present enormous logistical challenges in the current context. Lacking a robust evidence base, pathophysiologic reasoning can help guide our choices of therapy for individual clinical scenarios. We must exercise caution and extreme humility, as often plausible interventions fail when tested rigorously. But act today we must, and understanding the multiplicity of mechanisms of myocardial injury in COVID-19 infection will help us meet our mission unsupported by the comfort of strong data.

Keywords: atherosclerosis; cytokines; endothelial cells; inflammation; sepsis; vascular biology.

© 2020 The Author.

Figures

Figure 1

Hypothetical Spectrum of Myocardial Involvement in COVID-19 This diagram represents the hypothetical spectrum of myocardial involvement in coronavirus disease-2019 (COVID-19). On the extreme left, a case of fulminant myocarditis could occur in an individual with no coronary artery atherosclerosis. On the extreme right, an individual could have an acute coronary syndrome because of severe pre-existing lesions triggered to cause an event due to the consequences of infection described in the text.

Figure 2

Inflammatory Infectious Processes Can Produce Systemic Effects That Can Promote Atherothrombotic Events and Myocardial Ischemia This diagram depicts how inflammatory infectious processes in remote locations including the lungs can produce systemic effects that can promote atherothrombotic events and myocardial ischemia and also evoke “echoes” within the plaque itself that can predispose toward plaque disruption or acute progression of the disease.

Figure 3

Physiologic Changes Associated With Acute Infection Affect Adversely Oxygen Supply and Demand This figure depicts how physiologic changes associated with infection can tip the balance between myocardial oxygen supply and demand to favor myocardial ischemia. See the text for details.

Figure 4

Infection Has Multiple Effects That May Impinge on the Cardiovascular System and Provoke Events In addition to the aspects detailed in Figures 1, 2, and 3, infection may predispose toward thrombosis and reduced fibrinolysis as explained in the text. The consequences of infection may also alter the function of macro- or microvascular endothelium and thus contribute to cardiovascular complications of coronavirus disease-2019.