Acute Coronary Syndrome in the COVID-19 Era-Differences and Dilemmas Compared to the Pre-COVID-19 Era

Abstract

The COVID-19 pandemic has led to numerous negative implications for all aspects of society. Although COVID-19 is a predominant lung disease, in 10-30% of cases, it is associated with cardiovascular disease (CVD). The presence of myocardial injury in COVID-19 patients occurs with a frequency between 7-36%. There is growing evidence of the incidence of acute coronary syndrome (ACS) in COVID-19, both due to coronary artery thrombosis and insufficient oxygen supply to the myocardium in conditions of an increased need. The diagnosis and treatment of patients with COVID-19 and acute myocardial infarction (AMI) is a major challenge for physicians. Often the presence of mixed symptoms, due to the combined presence of COVID-19 and ACS, as well as possible other diseases, nonspecific changes in the electrocardiogram (ECG), and often elevated serum troponin (cTn), create dilemmas in diagnosing ACS in COVID-19. Given the often-high ischemic risk, as well as the risk of bleeding, in these patients and analyzing the benefit/risk ratio, the treatment of patients with AMI and COVID-19 is often associated with dilemmas and difficult decisions. Due to delays in the application of the therapeutic regimen, complications of AMI are more common, and the mortality rate is higher.

Keywords: COVID-19; acute coronary syndrome; before COVID and COVID era; dilemmas in COVID-19; myocardial injury.

Figure 1

Different types of ACS in COVID-19. Legend: SARS-CoV-2—severe acute respiratory syndrome coronavirus 2; ACS—acute coronary syndrome; UA—unstable angina; AMI—acute myocardial infarction; ACS-NNOCA—acute coronary syndrome with normal or near-normal coronary arteries; INOCA—ischemia with non-obstructive coronary artery disease; MINCA—myocardial infarction with normal coronary arteries; MINOCA—myocardial infarction with non-obstructive coronary artery disease; NSTEMI—non-ST elevation myocardial infarction; STEMI—ST elevation myocardial infarction.

Figure 2

Possible mechanisms of myocardial injury in patients with COVID-19. Legend: IL 6—interleukin 6; IL 1—interleukin 1; IL 17—interleukin 17; TNF-alpha—tumor necrosis factor-alpha; CRP—C-reactive protein; RAAS—renin–angiotensin–aldosterone system; CVD—cardiovascular disease.