title: Does lowering of cholesterol levels influence functional properties of large arteries?
abstract: Hypercholesterolaemia is a risk factor for atherosclerosis and induces endothelial dysfunction. Endothelial dysfunction may increase vascular tone and arterial stiffness and as a consequence may decrease arterial distensibility (DC) and arterial compliance (CC). It is hypothesized that lipid-lowering therapy may enhance DC and CC. Therefore, the present study investigates the effect of lipid-lowering therapy with pravastatin on the haemodynamics, DC and CC of the elastic common carotid artery (CCA), and the muscular femoral (FA) and brachial (BA) arteries in patients with primary hypercholesterolaemia. After an 8-week placebo run-in period with a low-cholesterol diet, 19 patients with total cholesterol concentrations of between 6.5 and 9.0 mmol.l-1 and triglyceride concentrations < 4 mmol.l-1 entered a double-blind placebo controlled crossover study. Patients received pravastatin 40 mg o.d. or placebo, each for 8 weeks. Throughout the study the lipid-lowering diet was continued. With pravastatin, total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglycerides were decreased (total cholesterol 26%, LDL-C 35%, triglycerides 16%), while high-density lipoprotein cholesterol (HDL-C) was not changed. Other laboratory values remained within the normal range. Blood pressure, heart rate, cardiac function and systemic vascular resistance were not influenced by pravastatin. Compared to placebo, diameter, distensibility and compliance of all arteries were not statistically significantly changed with pravastatin. These data suggest that, in patients with mild to moderate primary hypercholesterolaemia, short-term lowering of plasma cholesterol does not alter the haemodynamics and vessel wall properties of large arteries.
authors.affiliation: Department of Pharmacology, Cardiovascular Research Institute Maastricht, University of Limburg, The Netherlands.
authors.forename: M
authors.initials: M
authors.lastname: Kool
authors.forename: F
authors.initials: F
authors.lastname: Lustermans
authors.forename: H
authors.initials: H
authors.lastname: Kragten
authors.forename: H
authors.initials: H
authors.lastname: Struijker Boudier
authors.forename: A
authors.initials: A
authors.lastname: Hoeks
authors.forename: R
authors.initials: R
authors.lastname: Reneman
authors.forename: H
authors.initials: H
authors.lastname: Rila
authors.forename: I
authors.initials: I
authors.lastname: Hoogendam
authors.forename: L
authors.initials: L
authors.lastname: Van Bortel
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001158:Arteries / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002784:Cholesterol / Q000097:blood* / Q000378:metabolism; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013997:Time Factors
chemical_list: D002784:Cholesterol