ABSTRACT
Acute myocardial ischemia during coronavirus disease 2019 (COVID-19) infection can occur in two forms of acute myocardial infarction type І and II. In acute myocardial infarction type І, infection can cause inflammation, and inflammation causes the secretion and increase of cytokines such as interleukin 1, 6, and 8, as well as tumor necrosis factor (TNF) in the circulation. This mechanism causes the secretion of collagenase from activated macrophages, and the results of these reactions is a precursor to plaque rupture, increased coagulation, and thrombus formation. This mechanism causes acute myocardial infarction type І on atherosclerotic plaque. In these patients, primary percutaneous coronary intervention (PCI) is the treatment of choice, contrary to the initial theory that lytic therapy was the main treatment. In COVID conditions, the primary PCI time increases from 120 minutes to 180 minutes, and if the primary PCI takes more than 180 minutes, then lytic therapy is recommended. In acute myocardial infarction type II, patients usually do not have angina clinically, troponin rises slightly (less than 2 times normal), and do not have electrocardiogram changes as a sign of ischemia. However, patients with coronary heart disease have persistent chest pain with or without myocardial necrosis. During COVID-19 infection, due to release of interleukin, tumor necrosis alpha, and catecholamine, as well as hypoxia, acidosis, hypertension and/or hypotension, oxygen delivery and myocardial oxygen demand become disturbed, so acute myocardial infarction type II may occur. Supportive therapies are performed in these patients, and the treatment of acute underlying disease such as treatment with steroidal anti-inflammatory drugs and antiviral drugs is the main treatment. © 2021 Isfahan University of Medical Sciences(IUMS). All rights reserved.