Comprehensive Review of Cardiovascular Complications of Coronavirus Disease 2019 and Beneficial Treatments

Abstract

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 and was first reported in December 2019 in Wuhan, China. Since then, it caused a global pandemic with 212,324,054 confirmed cases and 4,440,840 deaths worldwide as of August 22, 2021. The disease spectrum of COVID-19 ranges from asymptomatic subclinical infection to clinical manifestations predominantly affecting the respiratory system. However, it is now evident that COVID-19 is a multiorgan disease with a broad spectrum of manifestations leading to multiple organ injuries including the cardiovascular system. We review studies that have shown that the relationship between cardiovascular diseases and COVID-19 is indeed bidirectional, implicating that preexisting cardiovascular comorbidities increase the morbidity and mortality of COVID-19, and newly emerging cardiac injuries occur in the settings of acute COVID-19 in patients with no preexisting cardiovascular disease. We present the most up-to-date literature summary to explore the incidence of new-onset cardiac complications of coronavirus and their role in predicting the severity of COVID-19. We review the association of elevated troponin with the severity of COVID-19 disease, which includes mild compared to severe disease, in nonintensive care unit compared to intensive care unit patients and in those discharged from the hospital compared to those who die. The role of serum troponin levels in predicting prognosis are compared in survivors and non-survivors. The association between COVID-19 disease and myocarditis, heart failure and coagulopathy are reviewed. Finally, an update on beneficial treatments is discussed.

FIGURE 1.

Flow diagram summarizing the method of selecting studies to review.

FIGURE 2.

SARS-CoV-2 infection is associated with new onset cardiovascular disease including heart failure, acute cardiac injury, myocardial infarction, myocarditis, arrhythmias, and coagulopathies. SARS-CoV-2 infects multiple organs mainly through the ACE-2 receptor. This could subsequently result in the development of cardiac injury with the following mechanisms: direct viral invasion of cardiomyocytes; renal function impairment leading to electrolyte abnormalities and water retention; inflammatory response and cytokine release; and respiratory damage, which causes increasing myocardial demand and hypoxia-induced oxidative stress. ACE-2 indicates angiotensin-converting enzyme 2; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2.