F031: Atorvastatin and vitamin C on endothelial function of hypercholesterolemic patients

Abstract

The aims of present study were to test in a group of hypercholesterolemic outpatients the effects of vitamin C and atorvastatin treatment on endothelium-dependent and endothelium-independent vasodilation. The responses of the forearm vasculature to acetylcholine (ACh) (7.5, 15 and 30 μg/min), sodium nitroprusside (SNP) (0.8, 1.6, 3.2 μg/min) and L-NMMA (2, 4, 8 μmol/min) were evaluated in 12 normal volunteers (seven men and five women, aged 20 to 45 years), and in 18 hypercholesterolemic patients (ten men and eight women, aged 20 to 46 years) at baseline and after one month of atorvastatin (10 mg/day) treatment. Similarly, we evaluated the antioxidant effects of vitamin C (24 mg/min) at baseline and after lipid-lowering therapy. Drugs were infused into the brachial artery, and forearm blood flow (FBF) was measured by strain-gauge plethysmography. At baseline, the response to ACh was significantly attenuated in hypercholesterolemics vs controls: at the highest dose (30 μg/min), FBF was 27.0 ± 3.4 vs 11.5 ± 1.9 mL 100 mL tissue⁻¹ min⁻¹ respectively (p < 0.0001). No significant differences were found between groups during SNP infusion. The atorvastatin treatment significantly improved ACh-stimulated FBF: at highest dose the FBF increased to 14.9 ± 1.5 mL 100 mL tissue⁻¹ min⁻¹ (p < 0.0001). Similarly, the L-NMMA endothelial effects were significantly potentiated by lipid-lowering treatment, suggesting the improvement of basal nitric oxide. Vitamin C increased ACh-vasodilation in the same way before and after atorvastatin treatment. The endothelial dysfunction in hypercholesterolemics is due to an oxidative stress, and atorvastatin rapidly improves both basal and stimulated endothelium-dependent vasodilation.

Hypercholesterolemia, endothelium, atorvastatin, atherosclerosis, vitamin C