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Conventional risk factors (especially high arterial pressure, elevated cholesterol and glucose levels, and cigarette smoking) are useful predictors of morbid atherosclerotic and hypertensive events, and their control variably reduces the incidence of events. However, both the ability to predict risk and the ability to reduce it by modification of established risk factors are limited. These limitations occur in part because the progression from risk factor exposure to morbid events depends on the variable likelihood that individuals exposed to the same risk factors will progress through two stages: the development of asymptomatic or "preclinical" anatomic and functional cardiovascular disease in response to standard risk factors and other variables, and the precipitation of morbid events by progression of preclinical disease or by the action of additional "triggering" mechanisms in the presence of preclinical disease. Advances in diagnostic methodology now make possible accurate noninvasive detection in many asymptomatic individuals of preclinical disease such as left ventricular hypertrophy, carotid atherosclerosis, and renal dysfunction. Progress in elucidating stimuli to left ventricular hypertrophy and systemic atherosclerosis suggests that focusing research separately on these two stages of disease evolution is a fruitful strategy. The closer relation of measures of preclinical disease than risk factors with the subsequent risk of complications indicates that their detection improves clinical risk stratification. However, critical testing of whether clinical outcome is improved or treatment cost is lowered by basing antihypertensive or antihyperlipidemic treatment decisions in part on the presence of preclinical cardiovascular disease is needed before this strategy is adopted on a widespread scale.

Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events.