"Acute Myocardial Infarction in the Time of COVID-19": A Review of Biological, Environmental, and Psychosocial Contributors

Coronavirus disease 2019 (COVID-19) has quickly become a worldwide health crisis. Although respiratory disease remains the main cause of morbidity and mortality in COVID patients, myocardial damage is a common finding. Many possible biological pathways may explain the relationship between COVID-19 and acute myocardial infarction (AMI). Increased immune and inflammatory responses, and procoagulant profile have characterized COVID patients. All these responses may induce endothelial dysfunction, myocardial injury, plaque instability, and AMI. Disease severity and mortality are increased by cardiovascular comorbidities. Moreover, COVID-19 has been associated with air pollution, which may also represent an AMI risk factor. Nonetheless, a significant reduction in patient admissions following containment initiatives has been observed, including for AMI. The reasons for this phenomenon are largely unknown, although a real decrease in the incidence of cardiac events seems highly improbable. Instead, patients likely may present delayed time from symptoms onset and subsequent referral to emergency departments because of fear of possible in-hospital infection, and as such, may present more complications. Here, we aim to discuss available evidence about all these factors in the complex relationship between COVID-19 and AMI, with particular focus on psychological distress and the need to increase awareness of ischemic symptoms.