(Circulation. 2000;102:21.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Israeli Society for Prevention of Heart Attacks, Tel-Hashomer, Israel.
Correspondence to the BIP Study Group, Coordinating Center/S. Behar, MD, Neufeld Cardiac Research Institute, Sheba Medical Center, Tel-Hashomer 52621, Israel. E-mail behar{at}post.tau.ac.il
BackgroundCoronary 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 ResultsIn 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.
ConclusionsBezafibrate 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.
Key Words: lipids prevention cardiovascular diseases triglycerides lipoproteins, HDL bezafibrate
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S. Fazio and M. F. Linton Apolipoprotein AI as Therapy for Atherosclerosis: Does the Future of Preventive Cardiology Include Weekly Injections of the HDL Protein? Mol. Interv., December 1, 2003; 3(8): 436 - 440. [Abstract] [Full Text] [PDF] |
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I. Goldenberg, M. Jonas, A. Tenenbaum, V. Boyko, S. Matetzky, A. Shotan, S. Behar, and H. Reicher-Reiss Current Smoking, Smoking Cessation, and the Risk of Sudden Cardiac Death in Patients With Coronary Artery Disease Arch Intern Med, October 27, 2003; 163(19): 2301 - 2305. [Abstract] [Full Text] [PDF] |
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W. H Reinhart Fibrinogen - marker or mediator of vascular disease? Vascular Medicine, August 1, 2003; 8(3): 211 - 216. [Abstract] [PDF] |
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C.M. Ballantyne Raising high-density lipoprotein cholesterol: where are we now? Eur. Heart J. Suppl., June 1, 2003; 5(suppl_D): D17 - D25. [Abstract] [PDF] |
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P. Barter Review: Reconsidering the value of fibrates: lessons from the trials The British Journal of Diabetes & Vascular Disease, May 1, 2003; 3(3): 162 - 167. [Abstract] [PDF] |
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M. Evans, A. Roberts, and A. Rees Pharmacological management of hyperlipidaemia The British Journal of Diabetes & Vascular Disease, May 1, 2003; 3(3): 204 - 210. [Abstract] [PDF] |
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