Effects of monotherapy with an HMG-CoA reductase inhibitor on the progression of coronary atherosclerosis as assessed by serial quantitative arteriography. The Canadian Coronary Atherosclerosis Intervention Trial.
- 1 March 1994
- journal article
- clinical trial
- Published by Wolters Kluwer Health in Circulation
- Vol. 89 (3), 959-968
- https://doi.org/10.1161/01.cir.89.3.959
Abstract
BACKGROUND 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors are widely prescribed for hyperlipidemia, yet their effect on the evolution of coronary atherosclerosis has not been defined. METHODS AND RESULTS To address this issue, 331 patients with diffuse but not necessarily severe coronary atherosclerosis documented on a recent arteriogram and with fasting serum cholesterol between 220 and 300 mg/dL were enrolled in a randomized, double-blind, placebo-controlled trial. All patients received intensive dietary counseling. Lovastatin or placebo was begun at 20 mg/d and was titrated to 40 and 80 mg during the first 16 weeks to attain a fasting low-density lipoprotein (LDL) cholesterol < or = 130 mg/dL. The mean lovastatin dose was 36 mg/d. Coronary arteriography was repeated after 2 years. In 299 patients (90%), 3858 coronary segments containing 2309 stenoses were measured blindly on pairs of films with an automated computerized quantitative system. Total and LDL cholesterol decreased by 21 +/- 11% and 29 +/- 11%, respectively, in the lovastatin-treated group but changed by < 2% in placebo patients. The primary end point, coronary change score, defined as the per-patient mean of the minimum lumen diameter changes (follow-up minus baseline angiogram) for all lesions measured, excluding those < 25% on both films, worsened by 0.09 +/- 0.16 mm in the placebo group and by 0.05 +/- 0.13 mm in the lovastatin group (P = .01). Progression (a worsening in minimum diameter of one or more stenoses by > or = 0.4 mm) with no regression at other sites occurred in 48 of 146 lovastatin and 76 of 153 placebo patients (33% versus 50%, P = .003). New coronary lesions developed in 23 lovastatin and 49 placebo patients (P = .001). The beneficial effect of treatment was most pronounced in the more numerous, milder lesions and in patients whose baseline total or LDL cholesterol levels were above the group median. CONCLUSIONS Lovastatin slows the progression of coronary atherosclerosis and inhibits the development of new coronary lesions.Keywords
This publication has 20 references indexed in Scilit:
- Effect of cholesterol reduction by simvastatin on progression of coronary atherosclerosis: Design, baseline characteristics, and progress of the Multicenter Anti-Atheroma Study (MAAS)Controlled Clinical Trials, 1993
- Measuring progression and regression of coronary atherosclerosis in clinical trials: problems and progressThe International Journal of Cardiovascular Imaging, 1992
- Quantitative angiographic and statistical methods to assess serial changes in coronary luminal diameter and implications for atherosclerosis regression trialsThe American Journal of Cardiology, 1992
- Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' Atherosclerosis Regression Study (STARS)The Lancet, 1992
- Regression of Coronary Artery Disease as a Result of Intensive Lipid-Lowering Therapy in Men with High Levels of Apolipoprotein BNew England Journal of Medicine, 1990
- Effect of Partial Ileal Bypass Surgery on Mortality and Morbidity from Coronary Heart Disease in Patients with HypercholesterolemiaNew England Journal of Medicine, 1990
- Retardation of angiographic progression of coronary artery disease by nifedipineThe Lancet, 1990
- Clinical and angiographic correlates and prognostic significance of the coronary extent scoreThe American Journal of Cardiology, 1988
- Clinical and angiographic predictors of new total coronary occlusion in coronary artery disease: Analysis of 313 nonoperated patientsThe American Journal of Cardiology, 1984
- Clinical and Angiographic Factors Associated With Coronary Artery Disease Progression of Coronary Artery DiseaseJournal of the American College of Cardiology, 1984