Coronary artery disease remains a major cause of death in the United States. Most epidemiologic data indicate that elevated high-density lipoprotein cholesterol decreases and increasing low-density lipoprotein cholesterol increases the risk of coronary artery disease. To attribute all coronary artery disease to these two variables, however, appears oversimplistic. Many patients with coronary artery disease have “normal” fasting lipid profiles and, in some studies, the majority of subjects with coronary artery disease had cholesterol levels less than 239 mg%. These findings suggest other contributing factors. Recent interest has focused on the changes in lipoproteins that occurespite substantial declines in cardiovascular disease mortality over the last four decades in the U.S. and most of Western Europe, 489,340 deaths were attributed to coronary heart disease (CHD) in the U.S. in 1990 and it is estimated that 6,230,000 Americans have a history of myocardial infarction, angina pectoris, or both , Based on observations in animal models of atherosclerosis, the careful study of patients and families with inherited lipoprotein disorders, the consistency of epidemiologic studies, and the more recent results of inter-vention studies, it is now well accepted that hypercho-lesterolemia and, in particular elevated low-density lipoprotein cholesterol (LDL-C), is causally related to the development of atherosclerosis and remains a significant risk factor for progression of disease even in patients with documented CHD. Furthermore, it is now clear that lowering such elevated cholesterol levels by diet, pharmacologic therapy, or other means favorably alters the natural history of CHD and, as a result, national guidelines for the treatment of hypercholesterolemia have been issued . There are also strong epidemiologic data indicating that elevated high-density lipoprotein cholesterol (HDL-C) decreases the risk of CHD at any given level of LDL-in the postprandial period, changes not re-flected in previous studies in which the lipid levels were determined in the “fasting state.” This article reviews metabolism of endogenous and exogenous triglyceride-rich lipoproteins and possible associations between changes in postprandial plasma lipids and coronary artery disease. © 1994 by Williams and Wilkins.