Monotherapy with hMG‐CoA reductase inhibitors and secondary prevention in coronary artery disease
- 1 September 1996
- journal article
- review article
- Published by Wiley in Clinical Cardiology
- Vol. 19 (9) , 683-689
- https://doi.org/10.1002/clc.4960190903
Abstract
Although thrombolytic drugs, percutaneous transluminal coronary angioplasty, and coronary artery bypass grafting have provided major advances in the treatment of coronary artery disease, the use of lipid‐lowering drugs for secondary prevention has significantly reduced cardiovascular events in the population with coronary artery disease. Secondary prevention trials using HMG‐CoA reductase inhibitors include the Familial Atherosclerosis Treatment Study (FATS), the Monitored Atherosclerosis Regression Study (MARS), the Canadian Coronary Atherosclerosis Intervention Trial (CCAIT), the Asymptomatic Carotid Artery Progression Study (ACAPS), the Multi Anti‐Atheroma Study (MAAS), the Scandinavian Simvastatin Survival Study (4S), the Pravastatin Limitation of Atherosclerosis in Coronary Arteries (PLAC I), the Regression Growth Evaluation Statin Study (REGRESS), the Pravastatin Multinational Study, and the Pravastatin, Lipids, and Atherosclerosis in Carotids (PLAC II). Mean changes from baseline of lipid fractions in these trials included: total cholesterol 18 to 35% reduction low‐density lipoprotein (LDL) cholesterol 26 to 46% reduction high‐density lipoprotein (HDL) cholesterol 5 to 15% increase and triglyceride 7 to 22% reduction. Angiographic regression or lack of progression was statistically demonstrated in the FATS, MARS, CCAIT, MAAS, PLAC I, and REGRESS trials. Cardiovascular events decreased 25 to 92% in all trials, and there was a significant reduction in both cardiovascular and total mortality in the 4S. The greater reduction in cardiovascular events than in anatomic changes suggests that the HMG‐CoA reductase inhibitors stabilized the surface of plaques. Monotherapy with HMG‐CoA reductase inhibitors provides the clinical opportunity to modify the natural history of coronary artery disease.Keywords
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