THE ROLE OF VIRAL INFECTIONS IN THE DEVELOPMENT OF ISCHEMIC HEART DISEASE

Abstract

 Ischemic heart disease (IHD) remains the leading cause of morbidity and mortality worldwide, accounting for a substantial proportion of global cardiovascular deaths. Despite significant advances in pharmacological therapy, interventional cardiology, and preventive strategies, the burden of IHD continues to rise, particularly in low- and middle-income countries. Traditionally, the pathogenesis of IHD has been associated with well-established risk factors such as hypertension, dyslipidemia, diabetes mellitus, smoking, and obesity. However, in recent years, increasing attention has been directed toward the role of infectious agents—especially viral pathogens—as important contributors to cardiovascular disease development and progression.A growing body of evidence suggests that viral infections may act as both triggers and modulators of ischemic events. Respiratory viruses, including influenza, enteroviruses, and most notably severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have been associated with a wide spectrum of cardiovascular complications. These complications range from acute myocardial injury and myocarditis to more chronic manifestations such as endothelial dysfunction, accelerated atherosclerosis, and ischemic heart disease. The COVID-19 pandemic has particularly highlighted the systemic nature of viral infections and their profound impact on cardiovascular health.The mechanisms underlying the association between viral infections and IHD are complex and multifactorial. One of the central pathways involves systemic inflammation, characterized by the activation of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and other mediators. This inflammatory response contributes to endothelial injury, destabilization of atherosclerotic plaques, and increased thrombogenicity, thereby facilitating the development of acute coronary syndromes.