Many epidemiological studies have demonstrated the close relation between blood pressure and the subsequent development of cardiovascular disease. Blood pressure has characteristically been defined by its direct relation with cardiac output and peripheral resistance. In essential hypertension, the most consistent cause for an elevated blood pressure is an increase in peripheral resistance, rather than cardiac output. This increase in peripheral resistance, considered to be caused by arteriolar constriction, was shown in early physiologic experiments to be best represented by an increase in diastolic pressure.1Consequently, it was generally believed that the hazard of hypertension to the cardiovascular system was derived principally from the diastolic component of blood pressure. This viewpoint was subsequently reinforced by a number of therapeutic trials, showing the benefits of treating hypertension defined on the basis of elevated diastolic blood pressures. At the same time, systolic blood pressure was considered to reflect elasticity of the large arteries and any increases in systolic pressure were viewed as a natural and innocuous effect of increased stiffness of the aorta caused by aging. However, in recent years, the emphasis on increased peripheral resistance and elevated diastolic pressure as the principal determinants of cardiovascular outcome has been challenged. This is in part due to a reappraisal of the early studies and the emergence of new insights into the pathophysiological significance of increased arterial stiffness and its influence on blood pressure components, particularly systolic and pulse pressure.

As early as 1971, the Framingham study showed that although diastolic pressure was the major determinant of cardiovascular risk in men under 45 years of age, systolic blood pressure was the stronger risk factor in older men and in women of all ages.2 Since then, a meta-analysis of cohort studies3 has confirmed a continuous, graded, and independent association between systolic blood pressure …