title: HMG CoA reductase inhibitors are related to improved systemic endothelial function in coronary artery disease.
abstract: Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase (statins) may enhance vascular endothelial function independent of their cholesterol lowering effect. To test this hypothesis, we surveyed two groups of patients (age 55+/-7, mean+/-SD) with coronary artery disease that were matched for age, blood pressure and serum lipid levels. Group 1 comprised 23 men without lipid-lowering medication and Group 2 included 22 patients with ongoing HMG CoA reductase inhibitor medication. Flow-mediated (endothelium-dependent) arterial dilatation (FMD) and nitrate-mediated (smooth muscle dependent) dilatation (NMD) were measured in the brachial artery using high resolution ultrasound. FMD was considerably higher in group 2 (4.3+/-2.6 vs. 2.6+/-2.8%; P<0.05). In multivariate regression model, statin use was the only significant (P<0.05) predictor of FMD. In all subjects, FMD correlated with statin dose (P<0.05 for trend). NMD was non-significantly higher in group 2 (11.4+/-5.0 vs. 9.0+/-4.2%, P=0. 08). We conclude that patients with established coronary artery disease on HMG CoA reductase inhibitor therapy have better vascular endothelial function than similar patients without the medication. These data provide further support for the idea that HMG CoA reductase inhibitors enhance endothelial function independent of their lipid-lowering effects. This may suggest that these drugs could be beneficial in secondary prevention of coronary artery disease regardless of the serum cholesterol concentration.
authors.affiliation: Department of Clinical Physiology, Turku University Central Hospital, Turku, Finland.
authors.forename: M J
authors.initials: MJ
authors.lastname: Järvisalo
authors.forename: J O
authors.initials: JO
authors.lastname: Toikka
authors.forename: T
authors.initials: T
authors.lastname: Vasankari
authors.forename: J
authors.initials: J
authors.lastname: Mikkola
authors.forename: J S
authors.initials: JS
authors.lastname: Viikari
authors.forename: J J
authors.initials: JJ
authors.lastname: Hartiala
authors.forename: O T
authors.initials: OT
authors.lastname: Raitakari
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000188:drug therapy*; D003331:Coronary Vessels / Q000187:drug effects* / Q000473:pathology; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012016:Reference Values; D014463:Ultrasonography; D014654:Vascular Patency
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors