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.