Atrial Fibrillation and Great Saphenous Vein Insufficiency: Exploration of Common Pathways in Hemodynamic Derangements and Systemic Inflammation.

Atrial fibrillation is the most prevalent type of arrhythmia globally, the incidence of atrial fibrillation continues to rise. Concurrently, as lifestyles modernize, the prevalence of saphenous varicose veins is also increasing significantly. Although both conditions have received considerable clinical attention, previous studies have primarily focused on independent investigations within their respective fields, leaving the potential association between these conditions relatively unexplored. In recent years, retrospective clinical analyses have shown that saphenous varicose veins may constitute a novel risk factor for the onset of atrial fibrillation-a breakthrough discovery that has opened a new dimension of cross-border dialogue in investigating disease mechanisms. Therefore, this study aimed to develop an innovative framework for the pathophysiological association between atrial fibrillation and saphenous varicose veins and to elucidate the associated underlying mechanisms from a multidimensional, evidence-based medical perspective. Available evidence suggests that hemodynamic changes in the lower extremity veins can directly affect right heart preload via central venous pressure transmission, thereby inducing atrial electrophysiological remodeling. Activation of the RAAS (renin-angiotensin-aldosterone system) is involved in venous wall remodeling and in the activation of inflammatory cytokine networks that promote atrial fibrosis. Autonomic dysfunction also exhibits shared pathological features in venous insufficiency and the neural remodeling associated with atrial fibrillation. Moreover, the bidirectional alterations in blood flow shear force may not only accelerate venous valve injury but also trigger abnormal electrical activity in atrial myocytes. The pathophysiological bridging hypothesis proposed in this study not only challenges the traditional single-system research paradigm, but also provides important implications for clinical intervention strategies. Indeed, by integrating a multidisciplinary chain of evidence, this paper systematically demonstrates the potential impact of peripheral venous lesions on cardiac electrophysiological activity, thereby adding a new dimension to screening and identifying a potential therapeutic target for the prevention of atrial fibrillation. These findings both deepen understanding of the nature of the two diseases and lay a theoretical foundation for establishing an integrated cardiovascular-peripheral vascular diagnostic and treatment model.