Abstract
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.
Highlights
At the end of 2019, the new coronavirus SARS-CoV-2 was identified as the cause of an acute respiratory infection and cause of a worldwide pandemic
The heart–brain axis shows close interaction, as depression and anxiety are related to a higher risk of CV events and mortality [118,119,120,121,122]. In this COVID-19 period, psychological load does not seem associated with CV disease exacerbation, but rather with a fall in hospital admissions
It has been observed that non-COVID-19 hospital admissions significantly decrease during the outbreak, likely due, almost in part, to changes in health care decisions and/or delays in hospital access [124]
Summary
At the end of 2019, the new coronavirus SARS-CoV-2 was identified as the cause of an acute respiratory infection and cause of a worldwide pandemic. There are many unclear issues related to the pathogenesis of the infection and the reasons underlying the extremely different clinical course, from asymptomatic to severe clinical manifestations, often carried out in a very short time period. The virus enters in several cell types, including cardiomyocytes following proteolytic cleavage of its S protein by a serine protease, and binding to the transmembrane angiotensin-converting enzyme 2 (ACE2) [1]. Whether it seems that pre-existing cardiovascular (CV) risk factors and disease may increase COVID-19 susceptibility, it has been observed that patients with CV disease may experience more severe symptoms of infection [2]. Public Health 2020, 17, 7371; doi:10.3390/ijerph17207371 www.mdpi.com/journal/ijerph
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