Secondary Prevention of Coronary Heart Disease

Abstract

Areduction in low-density lipoprotein (LDL) cholesterol lowers coronary heart disease (CHD) by 24% to 31% in subjects with prevalent CHD; this reduction occurs with the use of several statins, including simvastatin1 and pravastatin.2 3 Additional reductions in CHD could come from further reductions in LDL cholesterol, as was suggested by the Post Coronary Artery Bypass Graft clinical trial (POST CABG).4 An alternative approach is to attempt to reduce triglyceride levels and to raise levels of high-density lipoprotein (HDL) cholesterol. The role of triglyceride levels in relation to CHD and the possible use of fibric acids in the reduction of CHD are controversial. Although initial meta-analyses challenged the possible independent role of triglycerides in relation to CHD,5 one recent carefully performed meta-analyses supported triglyceride levels as an independent predictor of CHD.6 Another potential issue is that the atherogenicity of elevated triglyceride levels may vary. Brunzell et al7 reported that subjects with familial hypertriglyceridemia are at a reduced risk for CHD than subjects with familial combined hyperlipidemia.7 In the Mevacor Atherosclerosis Regression Study (MARS),8 subjects with elevated levels of triglycerides rich in apoCIII had a very rapid progression of atherosclerosis. The misclassification of key variables, such as triglyceride levels, reduces the significance of relations in longitudinal studies, and it may also affect clinical trials by allowing the inclusion of subjects with, for example, elevated triglyceride levels but a low risk of CHD. The direct measurement of apoB may improve the selection of patients in clinical trials.9 The use of fibric acids in the treatment of CHD has been controversial, both because of questions of safety and because of questions of efficacy. In a World Health Organization (WHO) study,10 clofibrate therapy was associated with a significant reduction in major coronary events; however, the …