Brachial arterial pressure to assess cardiovascular structural damage: an overview and lessons from clinical trials

J Nephrol. Jan-Feb 2008;21(1):23-31.

Abstract

Epidemiological studies have emphasized the relationship between blood pressure (BP) and the incidence of cardiovascular diseases. Severity of hypertension was in the past judged on the basis of diastolic BP. More recent epidemiological studies have directed attention to systolic pressure as a better guide to cardiovascular and all-cause mortality. Traditionally, hypertension was appreciated by measures of BP recorded in peripheral arteries, usually brachial artery which was assumed to reflect pressures in all parts of arterial system. All these studies neglected that peripheral systolic BP differs from pressure recorded in the aorta and central arteries. While mean and diastolic pressures are almost constant along the arterial tree, due to the stiffness and geometric heterogeneity of large arteries and the timing and magnitude of wave reflections systolic BP and pulse pressure are amplified from the aorta to peripheral arteries, and brachial systolic BP only indirectly reflects the systolic BP in the aorta and central arteries. Several recent studies have shown that the effects of antihypertensive drugs are not the same in peripheral and central arteries, fact which could account for different effects of various drugs on end-organ damage, such as regression of left ventricular hypertrophy. Moreover, it has been shown that aortic and central artery pressure (or their determinants) are stronger predictors of end-organ damage and cardiovascular outcome than conventionally measured brachial pressure. These studies have focused the attention on the physical properties of large arteries and on the way they influence the level of systolic and pulse pressures along the arterial tree.

Publication types

  • Review

MeSH terms

  • Aorta / physiology*
  • Blood Pressure Determination
  • Blood Pressure*
  • Brachial Artery / physiology*
  • Cardiovascular Diseases / etiology
  • Cardiovascular Diseases / physiopathology*
  • Clinical Trials as Topic
  • Humans
  • Hypertension / complications