title: The effect of fluvastatin on fibrinolytic factors in patients with hypercholesterolemia.
abstract: Several studies have shown cardiovascular benefit in treating hypercholesterolemia with HMG-CoA reductase inhibitor. However, in addition to the lowering of cholesterol, the beneficial effects of this inhibitor reflect other pharmacological activities. Whether these beneficial effects are partly mediated by changes in fibrinolytic factors remains to be proven, since clinical studies on the effects of HMG-CoA reductase inhibitors on fibrinolytic factors have not yielded consistent results. The purpose of this study was to evaluate the effects of fluvastatin on fibrinolytic factors in hypercholesterolemic patients. After 6 weeks on a low-fat, low-cholesterol diet, 23 outpatients known to have primary hypercholesterolemia with low density lipoprotein cholesterol (LDL-C) > or = 130 mg/dl with at least 2 risk factors or fasting LDL-C > or = 160 mg/dl were selected for the study. Venous blood samples were collected at baseline and at 8 weeks after fluvastatin therapy (40 mg/day) to measure of tissue plasminogen activator (t-PA), plasminogen activators inhibitor-1 (PAI-1), fibrinogen, D-dimer and lipid profile. After 8 weeks of therapy, fluvastatin reduced serum cholesterol by 11% (261.9 mg/dl vs 233.2 mg/dl, P < 0.01) and LDL-C by 22% (191.9 mg/dl vs 149.3 mg/dl, P < 0.01). D-dimer was significantly decreased (0.38 ng/L vs 0.28 ng/L, P = 0.02) and tPA, PAI-1 and fibrinogen tended to decrease after therapy. Fluvastatin therapy improved fibrinolytic profile; the result of this study may in part explain the benefit of HMG-CoA reductase inhibitor on cardiovascular system other than lipid lowering.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
authors.forename: T H
authors.initials: TH
authors.lastname: Lin
authors.forename: C H
authors.initials: CH
authors.lastname: Huang
authors.forename: W C
authors.initials: WC
authors.lastname: Voon
authors.forename: H W
authors.initials: HW
authors.lastname: Yen
authors.forename: H M
authors.initials: HM
authors.lastname: Lai
authors.forename: H Y
authors.initials: HY
authors.lastname: Liang
authors.forename: Y H
authors.initials: YH
authors.lastname: Lu
authors.forename: K T
authors.initials: KT
authors.lastname: Lee
authors.forename: C S
authors.initials: CS
authors.lastname: Lee
authors.forename: W T
authors.initials: WT
authors.lastname: Lai
authors.forename: S H
authors.initials: SH
authors.lastname: Sheu
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis / Q000187:drug effects*; D000077340:Fluvastatin; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy*; D007211:Indoles / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D005229:Fatty Acids, Monounsaturated; D005338:Fibrin Fibrinogen Degradation Products; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D000077340:Fluvastatin; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator