ISCHEMIC HEART DISEASE AFTER VIRAL INFECTIONS: CURRENT INSIGHTS INTO PATHOGENESIS AND CLINICAL IMPLICATIONS

Ischemic heart disease (IHD) continues to represent a major global health burden and remains the leading cause of morbidity and mortality worldwide. According to contemporary epidemiological data, cardiovascular diseases account for more than one-third of all deaths globally, with IHD constituting the largest proportion[1]. Despite significant advances in prevention, diagnosis, and treatment, the incidence of IHD remains high, particularly in low- and middle-income countries, where the burden of cardiovascular risk factors continues to increase. In recent years, growing attention has been directed toward the role of infectious agents—particularly viral pathogens—in the initiation and progression of cardiovascular diseases [4]. Viral infections, including influenza, enteroviruses, and most notably severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have been shown to exert both direct and indirect effects on the cardiovascular system. These effects range from acute myocardial injury and myocarditis to long-term complications such as endothelial dysfunction, accelerated atherosclerosis, and ischemic heart disease[5].Accumulating evidence suggests that viral infections may act as potent triggers of myocardial ischemia through a complex interplay of pathophysiological mechanisms. One of the central pathways involves systemic inflammation characterized by a cytokine-mediated response, often referred to as a “cytokine storm,” which contributes to endothelial damage, plaque instability, and increased thrombogenicity. In parallel, viral-induced endothelial dysfunction plays a critical role in impairing vascular homeostasis by reducing nitric oxide bioavailability, promoting vasoconstriction, and enhancing procoagulant activity[6].Another important mechanism is the dysregulation of neurohumoral systems, particularly activation of the sympathoadrenal system, which leads to increased circulating catecholamines. This results in elevated myocardial oxygen demand, coronary vasospasm, and exacerbation of ischemic processes.