A variety of epidemiologic, biochemical, and experimental studies have established a direct relationship between low density lipoprotein (LDL) cholesterol concentration and the risk of developing ischemic heart disease. An even stronger inverse relationship has been demonstrated between high density lipoprotein (HDL) cholesterol and the risk of ischemic heart disease (1HD). Both of these associations reflect underlying relationships to atherogenesis. The mechanism by which elevated LDL levels lead to cholesterol ester deposition in arterial smooth muscle cells and/or macrophages is not clear. A causal relationship between low HDL levels and accelerated atherogenesis has not yet been established. Factors which increase plasma LDL concentration or reduce HDL concentration, with a consequent increase in the theoretical risk of coronary atherosclerosis, include obesity, physical inactivity, cigarette smoking, and progestin-containing oral contraceptives. Recent reports have added to this list widely used antihypertensive agents, such as thiazide diuretics and beta-blocking agents. The mechanisms and pathophysiologic significance of such drug-induced changes in lipoprotein levels are not clear. Until more information is available, however. it would seem prudent to avoid, whenever possible, any antihypertensive which in a given patient substantially lowers the HDL/LDL ratio