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