Atrial fibrillation and peripheral varicose vein: Where is the connection?

Abstract

Dear Editor, Varicose vein is one of the most important health care problems in the World with respect to cardiovascular morbidity, mortality, and cosmetic concern as well and has been named to mention varicose veins of lower extremity. However, it has been recognized that peripheral varicose veins (PVV) might be a manifestation of systemic vascular or venous wall pathology rather than a localized disease of lower extremity peripheral venous territory. Association of PVV with other venous or vascular dilatations, namely varicocele, pelvic varicose veins, hemorrhoids, and coronary artery ectasia (CAE), has been reported with an increasing number of papers in literature. Therefore, PVV has been nominated as a member of dilating venous diseases or dilating vascular diseases. Pathophysiologic, epidemiologic, and clinical aspects of PVVin association with other dilating vascular diseases have been reviewed recently. Within this context, we have read the article published byHu et al.with great enthusiasm and interest. Briefly they have assessed the incidence rates and associates of atrial fibrillation (AF) in patients with and without PVV in their cohort. After controlling the confounding factors, they have found that patients with PVV have been found to be associated with significantly higher risk of AF (adjusted hazard ratio: 1.23, 95% CI: 1.03–1.45) compared to those without PVV. This is an interesting finding to be discussed in terms of pathophysiologic connections between the PVV and AF. Although the authors have commented on the atherosclerotic, thrombogenic, and inflammatory process as contributing factors to development of AF, we have further rationalities to explain the association of PVV with AF. We would like to focus on the concept of systemic vascular wall pathology as an underlying etiology of PVV or dilatation of any other vascular territory. The pathophysiologic process underlying dilating vascular diseases might have also involved the atrial tissue and therebymight havemade the atrial tissue prone toAF. Structural remodeling in atrial tissue characterized by disorganized deposition of extracellular matrix components has been known to facilitate the development of AF. Therefore, Hu et al.’s report has been a cornerstone for the association of AF with a distinct vascular pathology, that is, PVV. Although PVV is a remote pathology in regard to heart, that is, atriums, it is likely that the underlying pathology of PVV or dilating vascular diseases may also reside in the atrial wall tissue as well and plays a role in the development of AF. Further studies evaluating the association ofAFwith vascular pathology would improve our understanding not only in regard to PVVbut also in regard to dilating vascular diseases.