| Literature DB >> 28688874 |
Ricardo Castro-Ferreira1, Rita Cardoso2, Adelino Leite-Moreira2, Armando Mansilha3.
Abstract
Chronic venous disease is a potentially prevalent and debilitating condition affecting millions of individuals, mostly in Western world. Predisposing genetic and environmental factors contribute to its development. However, the main etiology remains to be elucidated. An extensive literature search was conducted in Medline using the following key words algorithm: ("Chronic venous disease" OR "Chronic venous insufficiency" OR "varicose veins") AND ("endothelial dysfunction" OR "inflammation"). Besides being a multifactorial disease, it is now recognized that the hallmark of chronic venous disease pathophysiology likely remains in inflammation, possibly triggered by sustained venous hypertension and valvular incompetence. Shear stress changes are directly sensed by endothelial cells, leading to its activation and subsequent recruitment of leukocytes and release of proinflammatory agents. Dysfunctional endothelium has a pivotal role perpetuating the inflammatory cascade, with consequent pathological venous changes and chronic venous disease worsening. Endothelial dysfunction may be the central player in the link between varicose veins and deep vein thrombosis. In this article, we aim to analyze the crucial role of endothelial activation in the persistent inflammatory cycle that characterizes chronic venous disease.Entities:
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Year: 2017 PMID: 28688874 DOI: 10.1016/j.avsg.2017.06.131
Source DB: PubMed Journal: Ann Vasc Surg ISSN: 0890-5096 Impact factor: 1.466