Systolic and diastolic blood pressure are generally considered to be the ex
clusive mechanical factors 'that predict cardiovascular risk in normotensiv
e and hypertensive populations. However, these 2 measures give an incomplet
e picture when evaluating risk for cardiovascular events. Rather, one must
consider the entire blood pressure curve when assessing risk.
The blood pressure curve has 2 components: the mean arterial pressure and t
he pulse pressure. Both components of the blood pressure curve also vary wh
ich age. Abnormalities of the large arteries predominate over abnormalities
of the small arteries in the elderly, causing a predominant increase in pu
lse pressure. This pattern is also observed in persons with diabetes and in
those with end-stage renal disease.
As a result of these changes, the shapes of the blood pressure curves from
older patients and younger ones are very different, despite the same mean,
arterial pressure. Mean arterial pressure has recently been shown to be a p
redictor of risk for events involving the cerebral vessels, the coronary ve
ssels, and the kidney. Pulse pressure has an additional effect on cardiovas
cular mortality: it is an independent predictor of cardiac death and, to a
lesser extent, stroke death, particularly in women over the age of 55.
It is possible to reverse pulsatile arterial hemodynamics in patients with
hypertension, particularly with the use of angiotensin-converting enzyme (A
CG) inhibitors. Several techniques are available to measure arterial stiffn
ess, for which pulse pressure is a surrogate.
ACE inhibition with perindopril has been shown to increase the diameter of
muscular arteries in patients with hypertension, demonstrating a drug-induc
ed effect on the arterial wall. Furthermore, there was an additional improv
ement in brachial artery compliance at the end of 12 months with perindopri
l treatment.