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Central blood pressure and hypertension.

During the 20th century, the brachial artery auscultatory method of blood pressure (BP) measurement has been the major basis for our understanding of clinical hypertension. First, the height of systolic (S) and diastolic (D) BP was used to define cardiovascular (CV) risk. Second, BP reduction by drug treatment was shown to be associated with a substantial decrease of CV risk in several varieties of high BP, including systolic hypertension in the elderly.1,2 However, drug treatment often reduced DBP more than SBP, resulting in increased pulse pressures (PP) and the related arterial stiffness. An associated increase in coronary risk was also observed.1,3 Because PP and arterial stiffness did not respond readily to drug treatment and was made even less responsive by aging, it has been suggested and shown that mechanical factors such as PP, arterial stiffness, and wave reflections, preferably measured by central (aortic or carotid) BP, should be fully investigated. Because the majority of the studies used noninvasive peripheral BPs the need arose for invasive methods to verify and validate central BP measurement in the evaluation of CV risk.4

In the present issue of this journal, Jankowski et al5 established, in a 4.5-year follow-up of 1109 patients undergoing coronary angiography, that central BP was a significant and independent predictor of CV risk, as potent as cardiac ejection fraction and more powerful than brachial sphygmomanometric measurements. For these coronary patients, the pulsatile …