title: Improvement of myocardial perfusion by short-term fluvastatin therapy in coronary artery disease.
abstract: Patients with hypercholesterolemia have impaired coronary and peripheral endothelial function. In patients with coronary artery disease, intracoronary acetylcholine infusion or mental stress causes paradoxical vasoconstriction, whereas lowering cholesterol restores endothelial function. The impact of lipid lowering by fluvastatin on myocardial perfusion in hypercholesterolemic patients with perfusion abnormalities was assessed by thallium-201 single photon-emission computed tomography (SPECT). A total of 22 patients were treated with fluvastatin (40 mg once daily) for 6 weeks, followed by 40 mg twice daily if low density lipoprotein cholesterol (LDL-C) levels were decreased by < or = 30%. During the 12-week treatment period, myocardial perfusion was measured by quantitative SPECT after standardized stress testing at baseline and after 12 weeks. Preliminary results for 17 male patients (mean age, 59.3 +/- 6.7 years) are presented here. LDL-C decreased from 191 +/- 26 to 146 +/- 28 mg/dL (p < 0.001). In ischemic segments myocardial perfusion increased by 30% (280 +/- 100 to 365 +/- 110 counts per matrix; p < 0.001). In normal segments perfusion increased by only 5% (451 +/- 74 to 473 +/- 69 counts per matrix; p < 0.005). The change in perfusion rate between ischemic and normal segments was significant (p < 0.005). In conclusion, LDL-C lowering with short-term fluvastatin therapy improved myocardial perfusion, especially in areas of ischemia. This suggests that improvement is due to functional restoration of coronary endothelium by fluvastatin, before anatomic regression of stenosis can occur following long-term treatment.
authors.affiliation: Department of Cardiology, Rudolf Virchow University Hospital, Free University of Berlin, Germany.
authors.forename: H W
authors.initials: HW
authors.lastname: Eichstädt
authors.forename: H
authors.initials: H
authors.lastname: Eskötter
authors.forename: I
authors.initials: I
authors.lastname: Hoffman
authors.forename: H W
authors.initials: HW
authors.lastname: Amthauer
authors.forename: G
authors.initials: G
authors.lastname: Weidinger
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D008078:Cholesterol, LDL / Q000097:blood; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000187:drug effects; D005080:Exercise Test; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D000077340:Fluvastatin; D006339:Heart Rate; D006801:Humans; D006903:Hydroxymethylglutaryl CoA Reductases / Q000008:administration & dosage / Q000627:therapeutic use*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006937:Hypercholesterolemia / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D007211:Indoles / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology; D013794:Thallium Radioisotopes; D015899:Tomography, Emission-Computed, Single-Photon; D014664:Vasodilation
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D013794:Thallium Radioisotopes; D000077340:Fluvastatin; D006903:Hydroxymethylglutaryl CoA Reductases