Coronary disease is a frequent outcome of hypertension. Although clinical trials with conventional antihypertensive agents have shown that the incidence of other complications of hypertension, such as stroke or congestive heart failure, is reduced as predicted, they have failed to show the expected reductions in coronary events. A partial explanation may lie in the fact that hypertension typically consists of a syndrome of inherited metabolic and cardiovascular abnormalities, and treatment that focuses primarily on blood pressure control without taking into account other factors that contribute to atherosclerotic disease can have only limited protective effects. The coronary hypothesis in hypertension extends this reasoning into three separate components. First is an intrinsic tendency to excessive proliferative and hypertrophic activity within vascular tissue, presumably reflecting growth-promoting activity stimulated by increased endocrine and local paracrine effects; next is the impact of the commonly encountered concomitant risk factors, including high blood pressure, that exaggerate and accelerate development of underlying atherosclerotic lesions; and finally hemodynamic factors, including increased variability and sustained elevations of blood pressure, that can destabilize vascular lesions and precipitate acute events. Treatment of these hemodynamic factors in elderly patients whose underlying vascular changes are already well advanced is likely to reduce vascular endpoints effectively, but a broader-based therapeutic approach is required for younger patients, in whom the ongoing proliferative and risk factor aspects of their potential coronary disease must also be targeted.