Historically, stroke, heart failure and renal insufficiency were seen as the major complications of untreated hypertension. More recently, it has become evident that coronary heart disease is probably the most common outcome of this condition. Unlike the other complications of hypertension, coronary events have not been reduced in a meaningful fashion by traditional antihypertensive drug therapy. 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 without taking into account the other factors that contribute to atherosclerotic disease can have only limited protective effects. The coronary hypothesis in hypertension extends this reasoning into 3 separate components. First is an intrinsic tendency to excessive proliferative and hypertrophic activity in vascular tissue, presumably reflecting growth-promoting activity stimulated by increased endocrine and local paracrine effects; second is the impact of the commonly encountered concomitant risk factors, including high blood pressure, that exaggerate and accelerate development of the underlying atherosclerotic lesions; third are 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 effectively reduce the incidence of vascular endpoints. In younger patients, ongoing vascular proliferative changes and the impact of concomitant risk factors are equally as important as hemodynamic forces in producing coronary disease, and effective treatment must take all these issues into account.