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Abstract

Population studies have shown that systolic blood pressure (SBP) rises linearly from adolescence through old age, whereas diastolic blood pressure (DBP) levels off at age 50 and decreases after age 60. Thus, pulse pressure (PP), the gap between SBP and diastolic blood pressure (DBP) begins to increase from age 50-59 years with acceleration of this increase from age 60 onward. The Framingham Heart Study examined the relationship between BP and coronary heart disease (CHD) risk as a function of age. In the younger age group (<50 years old), DBP was a more powerful predictor of CHD risk than was SBP. Recent studies using radial artery waveform recorded non-invasively by applantion tonometry have shown that peripheral amplification of SBP from the aorta to the brachial artery decreases as peripheral DBP increases in the under age 50s, but not in older subjects. This may explain why peripheral DBP is a better predictor of risk than peripheral SBP in younger subjects. Thus, both small vessel resistance and altered pulse wave reflection are important hemodynamic mechanisms in hypertension of the young. With aging, however, the Framingham studies showed that the best predictor of CHD risk shifted from DBP to SBP and by age 60 to PP. Much evidence suggests that PP is a surrogate marker for large artery stiffness. Thus, CHD risk in the middle-aged and elderly is more related to the pulsatile stress of large artery stiffness during systole than the steady stress of vascular resistance during diastole. Furthermore, the greatest burden of hypertension-related CHD occurs in the middle-aged and elderly, in whom wide PP isolated systolic hypertension predominates.

Hypertension, aging, pulse pressure, coronary disease
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© American Journal of Hypertension, Ltd. 2001
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