Evaluation of the vascular remodeling markers elastin, vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor receptor 2 (VEGFR2), and nitric oxide in patients with varicose veins.

INTRODUCTION: Varicose veins are a recurrent condition resulting from chronic valve failure, which can lead to blood reflux. The veins become dilated and tortuous due to increased venous pressure. Structural abnormalities of the vein wall, along with vascular dysfunction, contribute to disease progression. Alterations in elastin content, nitric oxide (NO) levels, and zinc (Zn) homeostasis have also been implicated in the pathophysiology of varicose vein development and progression.

MATERIAL AND METHODS: The study involved 180 individuals, divided into three groups. The first group consisted of 60 patients with severe varicose veins, the second group comprised 60 patients with moderate varicose veins, and the control group consisted of 60 clinically healthy patients. Venous blood specimens were drawn from the arm of all participants to analyze biochemical and inflammatory markers related to varicose vein disease, including vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor receptor 2 (VEGFR2), NO, elastin, zinc, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR).

RESULTS: Baseline blood test values were higher in individuals with mild and severe varicose veins than in healthy controls. The following metrics were substantially higher in people with moderate to severe varicose veins than in healthy controls: VEGF-A (160.089 ±63.762 ng/l, 77.106 ±12.964 ng/l, vs. 65.196 ±19.975 ng/l, p < 0.001), VEGFR2 (4.008 ±1.380 ng/ml, 1.256 ±0.390 ng/ml vs. 1.201 ±0.266 ng/ml, p < 0.001), NO (94.215 ±17.831 μmol/l, 66.589 ±12.528 μmol/l vs. 65.160 ±15.267 μmol/l, p < 0.001) and ELA (25.893 ±4.277 μg/ml, 26.264 ±8.661 μg/ml vs. 6.142 ±2.286 μg/ml, p < 0.045). The findings revealed increased levels of inflammatory markers, including CRP and ESR. Additionally, the affected group was found to have higher levels of Zn. These findings demonstrate that varicose vein disease is associated with chronic inflammation and disorders of angiogenesis. Elastin was also noted to be more sensitive to this condition, which helps determine when varicose vein disease first appears.

CONCLUSIONS: The research indicated that increased zinc concentrations, VEGF-A, VEGFR2, NO, and elastin signify compromised angiogenesis and venous wall elasticity in individuals with varicose veins. The inflammatory and molecular alterations are linked to compromised vascular function. This condition is exacerbated by elevated inflammatory markers (CRP and ESR), indicating that chronic inflammation plays a significant role in the disease etiology. Consequently, these markers may be viable targets for assessment and treatment intervention in the early stages of varicose veins.