Coronavirus disease 2019 (COVID-19) is mainly a respiratory disease, that can lead also to cardiovascular complications such as myocarditis, acute coronary syndromes, arrhythmias, heart failure, stroke, venous and arterial thromboembolism etc. Furthermore, cardiovascular patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have worse outcomes and higher risk of death(1). Myocardial injury can be caused by myocardial ischemia or non-ischemic myocardial injury. Different mechanisms have been suggested: the affinity of SARS-CoV-2 to ACE2, widely expressed in the heart, the cytokine storm, activation of the sympathetic nervous system, myocardial damage induced by hypoxemia, anemia(2).
Chinese studies reported that between 7-20% of hospitalized patients with COVID-19 develop myocardial injury(3). These patients with myocardial injury usually associate higher levels of inflammatory biomarkers and a more severe pulmonary disease, necessitating noninvasive or invasive ventilation(4).
Patients with COVID-19 have a higher risk of acute coronary syndrome. An Italian study on 28 patients reported that acute ST-elevation myocardial infarction (STEMI) was the first clinical manifestation of COVID-19 in 85.7% of cases(5). Interesting, angiography did not find obstructive coronary artery disease in almost 40% of cases(5). In these cases, small-vessel involvement may be due to systemic vasculitis, microembolization or hypercoagulability. Very interesting, patients with nonobstructive coronary lesions had higher mortality rates than those with obstructive lesions. The delays in seeking medical care due to fear of COVID-19 during the pandemic may be responsible for a part of the cardiac deaths, by indirect mechanisms. The management of STEMI in patients with COVID-19 has been especially difficult, because of specific protocols from protection of staff, with additional time needed.
A study of 138 COVID-19 patients, hospitalized, has found that cardiac arrhythmias was the main complication (19.6% of cases), more common in patients admitted in the ICU(6). In patients with COVID-19, arrhythmias may be induced by direct viral invasion to myocardial cells, dyselectrolytemias, sympathetic hyperstimulation with electrical instability, systemic inflammation, or worsening of previous myocardial disturbances. The side effects of drug treatments used in patients with COVID-19 may also be responsible for arrhythmias. From 136 patients with COVID-19 who presented in-hospital cardiac arrest, 89.7% had asystole, 4.4% pulseless electrical activity, and only 5.9% a shockable rhythm(7).
Heart failure in the setting of COVID-19 may be induced by the exacerbation of an underlying cardiac disease or the onset of a cardiomyopathy, such as stress cardiomyopathy. Patients with COVID-19 and heart failure have a worse prognosis. A study of 191 COVID-19 patients in China has found that 23% of patients had the diagnosis of heart failure(8). Patients with COVID-19 may have elevated levels of brain natriuretic peptide (BNP) without significant ventricular dysfunction(9) .
Venous and arterial thromboembolism is an important and severe complication of COVID-19 and may contribute to the increased rates of death. An Italian study described an incidence of 7.7% of at least one thromboembolic event in hospitalized patients with COVID-1910. Ischemic stroke or systemic thrombosis have been reported in COVID-19 patients without predisposing factors(10). Pulmonary thromboembolism was the most common thromboembolic event in retrospective studies of COVID-19 and may contribute to the cardiac injury encountered in severe cases(10).
In conclusion, cardiovascular manifestations of COVID-19 range from mild elevations of serum troponin and/or BNP levels to life-threatening arrhythmias,pulmonary thromboembolism, fulminant myocarditis and acute heart failure with cardiogenic shock. The exact mechanisms are still unclear and most likely involve a combination of pathophysiological processes.