Rationale to Treat
The weight of evidence from primary and secondary prevention clinical trials indicates that reduction of low-density lipoprotein cholesterol (LDLC) levels by diets, drugs, or other means can decrease the incidence of fatal and nonfatal myocardial infarction. A series of angiographic trials have demonstrated that reduced mortality and morbidity from LDL-C reduction are attributable, at least in part, to stabilization and regression of coronary atherosclerosis in both native vascular beds and venous bypass grafts. These studies provide the rationale for treatment of hyperlipoproteinemia with the goal of preventing coronary heart disease. Evidence from human clinical trials is supported by an extensive series of experiments in atherosclerotic animals of many species, including nonhuman primates. This review of treatment rationale summarizes evidence from human mortality and morbidity-based trials, human angiographic trials, and experimental animal models.
KeywordsFamilial Hypercholesterolemia Nonfatal Myocardial Infarction Coronary Artery Lesion Atherogenic Diet Coronary Drug Project
Unable to display preview. Download preview PDF.
- Clarkson TB, Bond MG et al. (1984) A study of atherosclerosis regression in Macaca mulatta: V. Changes in abdominal aorta and carotid and coronary arteries from animals with atherosclerosis induced for 38 months and then regressed for 24 or 48 months at plasma cholesterol concentrations of 300 or 200 mg/dl. Exp Mol Pathol 41: 96–118PubMedCrossRefGoogle Scholar
- Dayton S, Pearce ML et al. (1969) A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation 40 [Suppl II]: 1–63Google Scholar
- Erikson U, Helmius G et al. (1983) Measurement of atherosclerosis by arteriography and microdensitometry. Model and clinical investigations. In: Schettler G, Gotto AM et al. (eds) Atherosclerosis VI. Springer, Berlin Heidelberg New York, p 197Google Scholar
- Fritz KE, Augustyn JM et al. (1975) Effect of moderate diet and clofibrate on regression of swine atherosclerosis. Circulation 52: 11–16Google Scholar
- Malinow MR (1980) Atherosclerosis. Regression in nonhuman primates. Circulation 46: 311–320Google Scholar
- Ost RC, Stenson S (1967) Regression of peripheral atherosclerosis during therapy with high doses of nicotinic acid. Scand J Clin Lab Invest [Suppl] 99: 241–245Google Scholar
- Research Committee (1965) Low-fat diet in myocardial infarction: a controlled trial. Lancet I: 501–504Google Scholar
- Research Committee to the Medical Research Council (1968) Controlled trial of soya-bean oil in myocardial infarction. Lancet 1: 693–700Google Scholar
- Stary HC (1972) Progression and regression of experimental atherosclerosis in rhesus monkeys. In: Goldsmith EF, Morr-Hankowsky J (eds) Medical primatology. Karger, Basel, p 356Google Scholar
- Tucker CF, Catsulis C et al. (1971) Regression of early cholesterol-induced aortic lesions in rhesus monkeys. Am J Pathol 65: 494–502Google Scholar
- Vesselinovitch D, Wissler RW et al. (1978) The effect of diets with or without cholestryamine on the lesion components of atherosclerotic plaques. Fed Proc 37: 835Google Scholar
- Wissler RW, Vesselinovitch D et al. (1975) Regression of severe atherosclerosis in cholestryamine treated rhesus monkeys with or without a low fat, low-cholesterol diet. Circulation 52:15–16Google Scholar