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J Am Coll Cardiol, 2001; 37:975-984
© 2001 by the American College of Cardiology Foundation
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REVIEW ARTICLE

Pulse pressure—a review of mechanisms and clinical relevance

Anthony M. Dart, BA, DPhil, BM, BCh, FRCPa and Bronwyn A. Kingwell, BSc, PhDa

a Alfred Baker Medical Unit, Alfred Hospital and Baker Medical Research Institute, Melbourne, Australia

Manuscript received March 21, 2000; revised manuscript received November 10, 2000, accepted December 13, 2000.

Reprint requests and correspondence: Dr. A. M. Dart, Alfred Baker Medical Unit, Alfred Hospital, Commercial Road, Prahran, Victoria, Australia 3181
a.dart{at}alfred.org.au

The goal of this study was to review the origin, clinical relevance and treatment of pulse pressure (PP). Elevated PP is increasingly being recognized as a risk factor for cardiovascular, particularly coronary, disease. Pulse pressure is discussed in terms of both Windkessel and distributive models of the arterial circulation. Pulse pressure arises from the interaction of cardiac ejection (stroke volume) and the properties of the arterial circulation. An increased stiffness of the aorta and large arteries leads to an increase in PP through a reduction in arterial compliance and effects on wave reflection. A number of factors are known to influence arterial wall behavior and, therefore, PP. In addition to the effects of aging and blood pressure on arterial wall elasticity, there is some evidence that atherosclerosis, per se, amplifies these effects. Thus, the relationship between PP and coronary disease may be bidirectional. A number of dietary and lifestyle interventions have been shown to modify large artery behavior. These include aerobic exercise training and consumption of n-3 fatty acids. Conversely, strength training is associated with an increase in arterial stiffness and a higher PP. The effects of antihypertensive medication have been extensively studied, but many studies are difficult to interpret because of concomitant change in blood pressure, and to a lesser degree, heart rate. However a number of studies do suggest direct arterial wall effects, particularly for angiotensin-converting enzyme inhibitors. A distributed compliance model of the arterial circulation provides a framework for understanding the causes, effects and potential treatment of elevations in PP.

Abbreviations and Acronyms
  ACE = angiotensin-converting enzyme
  C = compliance
  DBP = diastolic blood pressure
  LV = left ventricle or left ventricular
  PP = pulse pressure
  PWV = pulse wave velocity
  SBP = systolic blood pressure
  SV = stroke volume




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