Pulse pressure - A review of mechanisms and clinical relevance

Citation
Am. Dart et Ba. Kingwell, Pulse pressure - A review of mechanisms and clinical relevance, J AM COL C, 37(4), 2001, pp. 975-984
Citations number
116
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
37
Issue
4
Year of publication
2001
Pages
975 - 984
Database
ISI
SICI code
0735-1097(20010315)37:4<975:PP-ARO>2.0.ZU;2-9
Abstract
The goal of this study was to review the origin, clinical relevance and tre atment 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 circula tion. hn increased stiffness of the aorta and large arteries leads to an in crease in PP through a reduction in arterial compliance and effects on wave reflection. A number of factors are known to influence arterial wall behav ior and, therefore, PP. In addition to the effects of aging and blood press ure on arterial wall elasticity, there is some evidence that atherosclerosi s, per se, amplifies these effects. Thus, the relationship between PP and c oronary disease may be bidirectional. A number of dietary and lifestyle int erventions have been shown to modify large artery behavior. These include a erobic exercise training and consumption of n-3 fatty acids. Conversely, st rength 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 concomitan t change in blood pressure, and to a lesser degree, heart rate. However a n umber 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. (J Am Coll Cardiol 2 001;37:975-84) (C) 2001 by the American College of Cardiology.