PubMed · 5470094
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1970-09-12. Clofibrate.. https://pubmed.ncbi.nlm.nih.gov/5470094/
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AIM: To find out from published reports whether the tendency of coronary heart disease (CHD) to progress can be retarded by lowering total and LDL cholesterol concentrations. METHODS: After a data-base search a meta-analysis was undertaken of all those randomized, controlled and angiographically documented studies which contained informations about the effect of cholesterol reduction on the course of CHD over a period of at least 2 years. A total of 12 studies covering 3781 patients met the stated criteria. RESULTS: The different lipid-lowering measures (usually drugs) achieved a statistically significant reduction of the number of patients with progression of the coronary angiographic findings and a significant increase in the number of those with actual regression. The number of coronary incidents, such as myocardial infarction, unstable angina, sudden cardiac death, necessary aortocoronary bypass operations or percutaneous transluminal coronary angioplasty was lower by 34% in the groups with measures to influence cholesterol metabolism than in the untreated groups. In the studies in which coronary arteriograms were evaluated quantitatively there was an annual increase in the mean degree of stenosis of 1.01% in the untreated and 0.37% in the treated groups. CONCLUSIONS: The difference in the increase of the mean degree of stenosis is probably not only important because of the resulting haemodynamic changes in myocardial perfusion. The quantitatively only slightly increased trend towards progression in the untreated groups can be interpreted as a marker for an active process of atherogenesis with a tendency of plaques to break off and of plaque thromboses.
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BACKGROUND: Lowering the blood cholesterol level may reduce the risk of coronary heart disease. This double-blind study was designed to determine whether the administration of pravastatin to men with hypercholesterolemia and no history of myocardial infarction reduced the combined incidence of nonfatal myocardial infarction and death from coronary heart disease. METHODS: We randomly assigned 6595 men, 45 to 64 years of age, with a mean (+/- SD) plasma cholesterol level of 272 +/- 23 mg per deciliter (7.0 +/- 0.6 mmol per liter) to receive pravastatin (40 mg each evening) or placebo. The average follow-up period was 4.9 years. Medical records, electrocardiographic recordings, and the national death registry were used to determine the clinical end points. RESULTS: Pravastatin lowered plasma cholesterol levels by 20 percent and low-density-lipoprotein cholesterol levels by 26 percent, whereas there was no change with placebo. There were 248 definite coronary events (specified as nonfatal myocardial infarction or death from coronary heart disease) in the placebo group, and 174 in the pravastatin group (relative reduction in risk with pravastatin, 31 percent; 95 percent confidence interval, 17 to 43 percent; P < 0.001). There were similar reductions in the risk of definite nonfatal myocardial infarctions (31 percent reduction, P < 0.001), death from coronary heart disease (definite cases alone: 28 percent reduction, P = 0.13; definite plus suspected cases: 33 percent reduction, P = 0.042), and death from all cardiovascular causes (32 percent reduction, P = 0.033). There was no excess of deaths from noncardiovascular causes in the pravastatin group. We observed a 22 percent reduction in the risk of death from any cause in the pravastatin group (95 percent confidence interval, 0 to 40 percent; P = 0.051). CONCLUSIONS: Treatment with pravastatin significantly reduced the incidence of myocardial infarction and death from cardiovascular causes without adversely affecting the risk of death from noncardiovascular causes in men with moderate hypercholesterolemia and no history of myocardial infarction.