An understanding of the role of the aortic elastic properties indicate
s their relevance at several sites of cardiovascular function. Acting
as an elastic buffering chamber behind the heart (the Windkessel funct
ion), the aorta and some of the proximal large vessels store about 50%
of the left ventricular stroke volume during systole. In diastole, th
e elastic forces of the aortic wall forward this 50% of the volume to
the peripheral circulation, thus creating a nearly continuous peripher
al blood flow. This systolic-diastolic interplay represents the Windke
ssel function, which has an influence not only on the peripheral circu
lation but also on the heart, resulting in a reduction of left ventric
ular afterload and improvement in coronary blood flow and left ventric
ular relaxation. The elastic resistance (or stiffness), which the aort
a sets against its systolic distention, increases with aging, with an
increase in blood pressure, and with pathological changes such as athe
rosclerosis. This increased stiffness leads to an increase in systolic
blood pressure and a decrease in diastolic blood pressure at any give
n mean pressure, an increase in systolic blood velocity, an increase i
n left ventricular afterload, and a decrease in subendocardial blood s
upply during diastole, and must be considered a major pathophysiologic
al factor, for example, in systolic hypertension. The elastic properti
es of the aortic Windkessel can be assessed in vivo in humans in sever
al ways, most easily by measuring the pulse wave velocity along the ao
rta. The higher this velocity, the higher the elastic resistance, that
is, the stiffness. Other methods depend on assessment of the ratio be
tween pulse pressure and aortic volume changes (Delta P/Delta V), whic
h can be assessed noninvasively by ultrasonic or tomographic methods.
All assessments of vessel stiffness have to take into account the dire
ct effect of current blood pressure, and thus judgements about influen
ces of interventions rely on an unchanged blood pressure. Alternativel
y, to derive the ''intrinsic'' stiffness of the aortic wall one has to
correct for the effect of the blood pressure present. Recently report
s about pharmacologic influences on the elastic properties of the aort
a have emerged in the literature. Angiotensin-converting enzyme (ACE)
inhibitors and nitric oxide (NO) donors seem to directly reduce the el
astic resistance of the aorta. This effect, in addition to other effec
ts on blood pressure and the peripheral circulation, could have major
clinical relevance as an additional mechanism for unloading the left v
entricle, improving coronary circulation, and reducing the pulsatile s
tress of the arterial system.