COVID-19
ACE2, the functional receptor of COVID-19 is expressed in the myocardium. Whether the use of the renin-angiotensin-aldosterone system inhibitors alters COVID-19 infection by upregulating ACE2 is under investigation. Similar to MERS-CoV and SARS-CoV, COVID-19 also causes acute cardiac injury in a subset of patients with corresponding elevated high-sensitivity cardiac troponin-I levels22 , 44 (Table 1). CK-MB and high-sensitivity cardiac troponin-I were higher in ICU patients, suggesting that myocardial injury is more likely present in patients with severe disease.45 , 46 As many as 7% of deaths in COVID-19 patients have been attributed to myocardial injury.47 Other cardiac manifestations include acute myocardial infarction, fulminant heart failure and dysrhythmias.48 In some studies, arrhythmia with COVID-19 infection was as high as 17%.20 , 45 It is also important to note various drug interactions and the arrhythmogenic potential of medications often used in these patients. Additionally, patients with preexisting cardiovascular disease and hypertension have been seen to suffer from more severe disease requiring critical care.48
Presenting symptoms range from mild chest pain with preserved ejection fraction to profound cardiovascular collapse requiring extracorporeal membrane oxygenation. Echocardiography may show a regional wall motion abnormality or global hypokinesis with or without pericardial effusion.49 , 50 Initial electrocardiogram may show low voltage QRS complexes in the limb leads, ST segment elevations in leads I, II, aVL, V2-V6 and PR elevation and ST depressions in aVR.49 , 50 There should be a low threshold for SARS-CoV-2 testing in patients presenting with signs of myopericarditis even in the absence of fever and respiratory symptoms.
Proposed mechanisms of cardiac injury in patients with COVID-19 include overexpression of ACE2 in patients with chronic cardiovascular disease, cytokine storm triggered by an imbalanced response by type 1 and type 2 helper cells, hypoxemia resulting in myocardial damage, plaque rupture, coronary vasospasm, or direct vascular injury.22 , 45 , 51 There may be a complex interplay between the accelerated immunologic dysregulation of the cytokines and T cells and the underlying cardiovascular or related metabolic conditions. Virally-induced systemic inflammation may also promote coronary plaque rupture and have a procoagulant effect necessitating the intensification of medical therapy.52