COVID-19 is associated with a hyperinflammatory state causing plaque disruption along with a pro-thrombotic milieu.[3], [6] In addition, the angiotensin-converting enzyme-2 (ACE-2) receptor present in cardiomyocytes could be a mediator of direct viral damage to the myocardium.[7] Accordingly, findings from a study have indicated that in the 7 days following COVID-19 diagnosis, the risk of myocardial infarction is roughly increased twofold.[8] Notably, the large increase in in-hospital mortality in our study was consistent regardless of the use of a historical or concurrent cohort. Here, ACE2 is linked to myocardial infarction.