Secondary Prevention by Raising HDL Cholesterol and Reducing Triglycerides in Patients With Coronary Artery Disease

Ovid Technologies (Wolters Kluwer Health) - Tập 102 Số 1 - Trang 21-27 - 2000
D. Brunner1,2, J Agmon1,2, Elieser Kaplinsky1,2, I Bär1,2, Solomon Behar1,2, Avraham Caspi1,2, Uri Goldbourt1,2, E Graff1,2, Yehezekiel Kaplinsky1,2, Kishon1,2, Henrietta Reicher-Reiss1,2, Avraham Shotan1,2, J. Vollmar1,2, J Waysbort1,2
1Boehringer Mannheim GmbH, Mannheim, Germany
2Center/S. Behar, MD, Neufeld Cardiac Research Institute, Sheba Medical Center, Tel-Hashomer 52621, Israel.

Tóm tắt

Background —Coronary heart disease patients with low high-density lipoprotein cholesterol (HDL-C) levels, high triglyceride levels, or both are at an increased risk of cardiovascular events, but the clinical impact of raising HDL-C or decreasing triglycerides remains to be confirmed. Methods and Results —In a double-blind trial, 3090 patients with a previous myocardial infarction or stable angina, total cholesterol of 180 to 250 mg/dL, HDL-C ≤45 mg/dL, triglycerides ≤300 mg/dL, and low-density lipoprotein cholesterol ≤180 mg/dL were randomized to receive either 400 mg of bezafibrate per day or a placebo; they were followed for a mean of 6.2 years. The primary end point was fatal or nonfatal myocardial infarction or sudden death. Bezafibrate increased HDL-C by 18% and reduced triglycerides by 21%. The frequency of the primary end point was 13.6% on bezafibrate versus 15.0% on placebo ( P =0.26). After 6.2 years, the reduction in the cumulative probability of the primary end point was 7.3%, ( P =0.24). In a post hoc analysis in the subgroup with high baseline triglycerides (≥200 mg/dL), the reduction in the cumulative probability of the primary end point by bezafibrate was 39.5% ( P =0.02). Total and noncardiac mortality rates were similar, and adverse events and cancer were equally distributed. Conclusions —Bezafibrate was safe and effective in elevating HDL-C levels and lowering triglycerides. An overall trend in a reduction of the incidence of primary end points was observed. The reduction in the primary end point in patients with high baseline triglycerides (≥200 mg/dL) requires further confirmation.

Từ khóa


Tài liệu tham khảo

10.1016/S0368-1319(62)80014-3

10.1111/j.0954-6820.1987.tb03356.x

10.1056/NEJM199006143222403

10.1161/atvb.17.1.107

10.1016/0021-9150(77)90157-5

10.1161/atv91.11.1.1987999

Assmann G, Schulte H, Cullen P. New and classical risk factors: the Munster Heart Study (PROCAM). Eur J Med Res. 1997;2:237–242.

10.1093/oxfordjournals.aje.a115130

10.1097/00043798-199604000-00014

Berge KG Canner PL. Coronary drug project: experience with niacin: Coronary Drug Project Research Group. Eur J Clin Pharmacol. 1991;40(suppl 1):S49–S51.

10.1161/01.CIR.85.1.37

10.1056/NEJM199511163332001

10.1056/NEJM199811053391902

10.1056/NEJM199610033351401

Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344:1383–1389.

10.1001/jama.279.20.1615

10.1161/circ.86.3.1516196

10.1016/0002-9149(93)90905-R

10.1016/S0021-9258(18)47383-8

10.5551/jat1994.3.81

Auwerx J Schoonjans K Fruchart JC et al. Transcriptional control of triglyceride metabolism: fibrates and fatty acids change the expression of the LPL and apoC-III genes by activating the nuclear receptor PPAR. Atherosclerosis. 1995;124(suppl):S29–S37.

10.1161/circ.98.19.2088

Goldbourt U Brunner D Behar S et al for the BIP study group. Baseline characteristics of patients participating in the Bezafibrate Infarction Prevention (BIP) study. Eur Heart J. 1998;19(suppl H):H42–H47.

10.1093/clinchem/18.6.499

SAS Institute Inc. SAS/STAT User’s Guide. Version 6. 4th ed. Cary NC: SAS Institute Inc; 1987.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, National Cholesterol Education Program. Second report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). Circulation. 1994;89:1329–1445.

10.1056/NEJM199908053410604

10.1161/circ.96.7.2137

10.1016/S0140-6736(96)91343-4