title: Influence of low HDL on progression of coronary artery disease and response to fluvastatin therapy.
abstract: BACKGROUND--Patients with coronary artery disease (CAD) commonly have low HDL cholesterol (HDL-C) and mildly elevated LDL cholesterol (LDL-C), leading to uncertainty as to whether the appropriate goal of therapy should be lowering LDL-C or raising HDL-C. METHODS AND RESULTS--Patients in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) had mildly to moderately elevated LDL-C; many also had low HDL-C, providing an opportunity to compare angiographic progression and the benefits of the HMG-CoA reductase inhibitor fluvastatin in patients with low versus patients with higher HDL-C. Of the 339 patients with biochemical and angiographic data, 68 had baseline HDL-C <0.91 mmol/L (35 mg/dL), mean 0.82+/-0.06 mmol/L (31. 7+/-2.2 mg/dL), versus 1.23+/-0.29 mmol/L (47.4+/-11.2 mg/dL) in patients with baseline HDL-C >/=0.91 mmol/L. Among patients on placebo, those with low HDL-C had significantly more angiographic progression than those with higher HDL-C. Fluvastatin significantly reduced progression among low-HDL-C patients: 0.065+/-0.036 mm versus 0.274+/-0.045 mm in placebo patients (P=0.0004); respective minimum lumen diameter decreases among higher-HDL-C patients were 0. 036+/-0.021 mm and 0.083+/-0.019 mm (P=0.09). The treatment effect of fluvastatin on minimum lumen diameter change was significantly greater among low-HDL-C patients than among higher-HDL-C patients (P=0.01); among low-HDL-C patients, fluvastatin patients had improved event-free survival compared with placebo patients. CONCLUSIONS--Although the predominant lipid-modifying effect of fluvastatin is to decrease LDL-C, patients with low HDL-C received the greatest angiographic and clinical benefit.
authors.affiliation: Baylor College of Medicine, Houston, Tex. 77030, USA. cmb@bcm.tmc.edu
authors.forename: C M
authors.initials: CM
authors.lastname: Ballantyne
authors.forename: J A
authors.initials: JA
authors.lastname: Herd
authors.forename: L L
authors.initials: LL
authors.lastname: Ferlic
authors.forename: J K
authors.initials: JK
authors.lastname: Dunn
authors.forename: J A
authors.initials: JA
authors.lastname: Farmer
authors.forename: P H
authors.initials: PH
authors.lastname: Jones
authors.forename: J R
authors.initials: JR
authors.lastname: Schein
authors.forename: A M
authors.initials: AM
authors.lastname: Gotto
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000175:diagnosis / Q000209:etiology / Q000401:mortality; D015906:Angioplasty, Balloon, Coronary; D001053:Apolipoproteins / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D004311:Double-Blind Method; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage*; D005260:Female; D000077340:Fluvastatin; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D007211:Indoles / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000209:etiology / Q000401:mortality; D016019:Survival Analysis