THE ROLE OF ENDOTHELIAL DYSFUNCTION IN DEEP VEIN THROMBOSIS: A MULTI-CENTER STUDY

Abstract

Deep vein thrombosis (DVT) is a multifactorial condition with significant morbidity and mortality, often resulting from a complex interplay between hemodynamic changes, coagulation abnormalities, and endothelial dysfunction. While the contributions of stasis and hypercoagulability are well established, the role of endothelial dysfunction in DVT pathogenesis remains underexplored. This multi-center study aimed to investigate the mechanistic contribution of endothelial dysfunction to DVT through comprehensive biomarker analysis and vascular assessment. A total of 412 patients with ultrasound-confirmed DVT and 200 age- and sex-matched controls were enrolled. Biomarkers of endothelial injury (circulating endothelial cells, endothelial microparticles), vasodilation (nitric oxide), inflammation (VCAM-1, IL-6, TNF-α, CRP), oxidative stress (MDA, SOD), and senescence (β-galactosidase activity, p16INK4a) were evaluated. Both non-invasive imaging and statistical analysis were used to discover what predicts DVT. Patients with DVT had much greater levels of endothelial cells, microparticles, VCAM-1 and pro-inflammatory cytokines (IL-6, TNF-α and CRP) than the controls (p < 0.001). There was clear oxidative stress since MDA levels in the DVT group were higher than in the non-DVT group. An increase in senescence markers implies that vascular aging may play a new role in triggering thrombus development. Flow-mediated dilation and the tone of the arteries were significantly lower in people with DVT, as found by functional assessments. Analysis of several factors showed that VCAM-1, IL-6, MDA and p16INK4a are powerful factors linked to DVT (p < 0.001). It is clear from these findings that dysfunction of the vascular endothelium, caused by inflammation, free radicals and aging, has a key role in developing DVT. Recognizing these biomarkers may lead to better therapies and better ways to assess disease risk in patients.