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.缺血性心脏病（Ischemic heart disease, IHD）仍是全球重大健康负担，亦是全球范围内发病率与死亡率最高的疾病。据当前流行病学数据显示，心血管疾病占全球总死亡人数的三分之一以上，其中IHD占比最高[1]。尽管在预防、诊断与治疗领域已取得显著进展，但IHD的发病率仍居高不下，尤其在中低收入国家，其心血管疾病危险因素的负担持续加重。 近年来，学界对病原体——尤其是病毒病原体——在心血管疾病发生与进展中的作用关注度与日俱增[4]。包括流感病毒、肠道病毒，以及最受关注的严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）在内的各类病毒感染，均被证实可对心血管系统产生直接与间接影响。此类影响涵盖急性心肌损伤、心肌炎，以及内皮功能障碍、动脉粥样硬化加速、缺血性心脏病等长期并发症[5]。 越来越多的研究证据表明，病毒感染可通过一系列复杂的病理生理交互机制，成为心肌缺血的强效触发因素。其中一条核心通路为以细胞因子介导的免疫反应为特征的全身性炎症，即常提及的“细胞因子风暴”，该反应可引发内皮损伤、斑块不稳定及血栓形成倾向升高。与此同时，病毒诱导的内皮功能障碍会通过降低一氧化氮生物利用度、促进血管收缩以及增强促凝活性，严重损害血管稳态[6]。 另一项关键机制为神经体液系统失调，尤以交感肾上腺系统激活为甚，该激活会导致循环儿茶酚胺水平升高，进而引发心肌氧需求增加、冠状动脉痉挛，并加重缺血性病理进程。