A current review of COVID-19 for the cardiovascular specialist

Abstract

Although coronavirus disease 2019 (COVID-19) predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to ~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19.

Figure 1

The interplay of COVID-19 and cardiovascular disease includes the common presence of underlying cardiovascular risk factors and conditions as well as the acute consequences of COVID-19.

Figure 2

Representation of the possible mechanisms of acute myocardial injury related to COVID-19. A, Myocarditis; (B) type 2 MI (left) and type I MI (right); (C) contraction bands in stress cardiomyopathy; (D) microvascular dysfunction from microthrombi and endothelial injury; and (E) cytopathic injury in cytokine storm.

Figure 3

COVID-19 for the cardiologist: Monitoring for cardiovascular complications and supportive management. PT,  prothrombin time; PTT,  partial thromboplastin time; TTE,  transthoracic echocardiogram; cMRI,  cardiac magnetic resonance imaging; CT-PE, computed tomography  pulmonary angiogram; MCS,  mechanical circulatory support; GDMT,  guideline-directed medical therapy.