A Real Pandora's Box in Pandemic Times: A Narrative Review on the Acute Cardiac Injury Due to COVID-19

Abstract

The intricate relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the cardiovascular system is an extensively studied pandemic topic, as there is an ever-increasing amount of evidence that reports a high prevalence of acute cardiac injury in the context of viral infection. In patients with Coronavirus disease 2019, COVID-19, a significant increase in serum levels of cardiac troponin or other various biomarkers was observed, suggesting acute cardiac injury, thus predicting both a severe course of the disease and a poor outcome. Pathogenesis of acute cardiac injury is not yet completely elucidated, though several mechanisms are allegedly involved, such as a direct cardiomyocyte injury, oxygen supply-demand inequity caused by hypoxia, several active myocardial depressant factors during sepsis, and endothelial dysfunction due to the hyperinflammatory status. Moreover, the increased levels of plasma cytokines and catecholamines and a significantly enhanced prothrombotic environment may lead to the destabilization and rupture of atheroma plaques, subsequently triggering an acute coronary syndrome. In the present review, we focus on describing the epidemiology, pathogenesis, and role of biomarkers in the diagnosis and prognosis of patients with acute cardiac injury in the setting of the COVID-19 pandemic. We also explore some novel therapeutic strategies involving immunomodulatory therapy, as well as their role in preventing a severe form of the disease, with both the short-term outcome and the long-term cardiovascular sequelae being equally important in patients with SARS-CoV-2 induced acute cardiac injury.

Keywords: COVID-19; biomarkers; cytokines; heart failure; myocardial injury.

Figure 1

Potential pathophysiological mechanisms of SARS-CoV-2 induced acute cardiac injury; acute coronary syndromes occur by destabilization and rupture of atheroma plaques with the consequent formation of a thrombus that causes occlusion of the artery responsible for heart attack [41]. Myocarditis can occur through direct myocardial injury and immune or autoimmune mechanisms [72,73,74]. Type 2 myocardial infarction occurs due to an imbalance between the need and supply of oxygen [12]. Sepsis-induced cardiomyopathy occurs due to myocytic apoptosis and cardiodepressant factors [82,83]. Stress-induced cardiomyopathy occurs through the cardiotoxic effect of catecholamines and is secondary to microvascular dysfunction [85]. Legend: STEMI: ST-elevation myocardial infarction; and N-STEMI: non-ST-elevation myocardial infarction.

Figure 2

The inflammatory cascade during SARS-CoV-2 infection. IL-1β is synthesized by macrophages, monocytes, and B lymphocytes, and has the ability to self-induce its production and stimulate the synthesis of IL-6 in macrophages, endothelial cells, and smooth muscle cells [12,96,97]. Further, IL-6 determines the liver synthesis of acute phase reactants and exerts a pro-coagulant effect by inducing tissue factor synthesis, also causing endothelial dysfunction by increasing vascular permeability [108,109,110]. Legend: IL-1β: Interleukin 1β; IL-6: Interleukin-6; and CRP: C reactive protein.