Vasodilatory Capacity of Forearm Resistance Vessels Is Augmented in Hypercholesterolemic Patients After Treatment with Fluvastatin

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Abstract
Atherosclerotic vessels are characterized by endothelial and structural abnormalities as indicated by an impaired vasodilation to metabolic requirements. To determine whether effective treatment of hypercholesterolemia may improve vasodilatory capacity of resis tance vessels, the authors examined the impact of 12 and 24 weeks of lipid-lowering therapy with the hepatic hydroxymethylglutaryl coenzyme A (HMG-CoA)-reductase inhibitor fluvastatin (40 to 80 mg/day) on the increment in forearm blood flow during reactive hyperemia in 24 hypercholesterolemic patients (mean age: 56 ±11 years; 15 men/9 women). Changes in forearm blood flow in response to reactive hyperemia were measured by venous occlusion plethysmography. Serum low-density lipoprotein (LDL)-cholesterol fell from 213 ±32 to 125 ±27 mg/dL (P<0.001) after 12 weeks and remained stable at a level of 125 ± 18 mg/dL after 24 weeks of treatment. Baseline forearm blood flow was similar before and after 12 and 24 weeks of therapy. In contrast, forearm blood flow at peak reactive hyperemia was greater at week 12 (37.0 ±22.9 mL/min/100 mL; P<0.05), and at week 24 (47.1 ±33.5 mL/min/100 mL; P<0.05) than at week 0 (30.5 ± 18.1 mL/min/100 mL). Compared with week 0 (defined as 100%), the percent change in forearm blood flow in response to reactive hyperemia was augmented at week 12 (171 ± 144%; P<0.05 vs week 0) and at week 24 (218 ±228%; P<0.05 vs week 0). Thus, the lowering of high serum LDL choles terol after short-term treatment with fluvastatin increased the blood flow responses during reactive hyperemia in forearm resistance vessels. These data indicate a beneficial effect of HMG-CoA reductase inhibition on structural wall properties of peripheral arteries in human atherosclerosis.