Cardiovascular hazards of components of blood pressure.

Hypertension is an established highly prevalent, powerful, independent and modi®able promoter of cardiovascular disease. It damages and compromises the vascular supply to the heart, brain, kidneys and limbs. It also directly alters the structure and function of the myocardium by promoting left ventricular hypertrophy (LVH). Despite the acknowledged importance of hypertension as a promoter of cardiovascular disease, there is uncertainty about the relative importance of its various components. Since the beginning of the twentieth century, medical research was preoccupied with diastolic blood pressure as the chief hazard of hypertension [1±4]. Lately, the focus has shifted to the systolic and, most recently, the pulse pressure. In a review of the subject, Rutan et al. pointed out that after the Framingham Study, a large number of diverse prospective population-based investigations found that systolic blood pressure exerted a stronger in ̄uence than diastolic pressure [5]. Consideration of vascular haemodynamics suggests that pulse pressure plays a role in the contribution of hypertension to the development of cardiovascular disease. Diastolic blood pressure rises with peripheral arterial resistance and falls with increased central artery stiffness so the relative contributions of these opposing forces determine the diastolic and, ultimately, the pulse pressure. Usually, pulse pressure and systolic blood pressure are highly correlated because both components rise with increases in vascular resistance and large artery stiffness. However, when assessed individually in the Framingham Study, increments in pulse pressure at particular systolic pressures were associated with a greater risk of coronary heart disease (CHD) than were increments in systolic blood pressure at ®xed pulse pressure [6]. It appears that despite the high correlation of pulse pressure with systolic pressure, pulse pressure predominates in predicting CHD because of the contribution of the strong pulsatile stress in subjects with discordantly low diastolic blood pressure. Whether this also applies to myocardial hypertrophy is more conjectural, but LVH is an important phenomenon in the evolution of hypertension on the path to myocardial infarction and heart failure. Increased pulsatile load plays a dominant role in clinical disease, large artery atherosclerosis, vascular remodelling of small resistance arteries, LVH and eventually heart failure. Prediction of cardiac hypertrophy from high pulse pressure and low diastolic pressure has been reported [7,8].