Download Basis and implications of change in arterial pressure with age

Vascular Medicine 2000; 5: 209–211
Editorial
Basis and implications of change in arterial pressure with
age
Seen from a pathophysiological perspective, the classical
contemporary clinical approach to arterial pressure is lamentably simplistic. We measure the extremes of the arterial
pressure pulse wave in a peripheral (brachial) artery, label
these as systolic and diastolic, and classify as hypertensive
those individuals whose systolic or diastolic pressures persistently exceed certain levels.
The first problem with this approach was tackled by
George Pickering1 some 50 years ago by pointing out that
cardiovascular events and death are related in a graded way
to systolic or diastolic pressure. To Pickering, there was no
such thing as hypertension, just high(er) blood pressure.
This theme was re-emphasized by MacMahon2 in the initial
twenty-first century New England Journal of Medicine editorial on arterial pressure.
The second problem is that clinicians have focused on
systolic and diastolic pressures according to the notion attributed to MacKenzie3 that systolic pressure is a measure
of cardiac strength, and diastolic pressure is a measure of
arteriolar tone. Such a notion was initially dispelled by the
Framingham investigators,4 and then finally laid to rest by
the SHEP investigators,5 who confirmed the evil of elevated
systolic pressure and the benefits of reducing this with
active therapy, even when diastolic pressure was normal.
But a third problem has recently been exposed in the
classic interpretation of diastolic pressure. The Framingham
investigators have shown that over the age of 50 years for
a given systolic pressure, diastolic pressure is inversely
related to cardiovascular events and death,6 so that pulse
pressure (systolic–diastolic) is the most robust predictor of
cardiovascular events. These views receive independent
verification from other studies.7–9 But the most recent
analysis from Framingham shows that males under the age
of 40 years – those most strongly represented in actuarial
and some epidemiological studies – pulse pressure is
inversely, not directly, related to coronary events.10
The only way to resolve all these issues is to take a fresh
look at the arterial system, and to apply appropriate pathophysiological principles.11,12 Surely this is warranted if the
conventional clinical approach has created so much confusion. An example of such an approach is contained in
this editorial, which considers the changes in arterial pressure that occur with age, and explains their relationship with
underlying mechanisms and to the risk of subsequent
events.
A longitudinal study of the original Framingham cohort
has clarified the changes in brachial blood pressure that
occur above the age of 40 years.13 Diastolic pressure rises
until 50 years of age, then falls progressively. Mean pressure rises until 50 years of age, then remains relatively constant. Systolic pressure rises with increasing years from the
age of 40, while pulse pressure shows the greatest change,
increasing markedly, especially over the age of 50. The Framingham study is complemented by others14–16 which show
 Arnold 2000
further information from people under the age of 40 years.
From childhood, brachial systolic and pulse pressures
increase markedly with bodily growth to age 17,14 whereafter systolic pressure remains relatively constant until the
age of 40 years, while pulse pressure appears to decrease
between 17 and 40 years of age.15,16 Mean and diastolic
pressures rise progressively between 17 and 40 years of
age.16
These aging changes in brachial blood pressure can only
be explained from studies of the arterial pressure pulse
wave. With aging, from childhood, there is gradual and progressive abbreviation in the travel time of the pulse wave
from ascending aorta to femoral artery. This is measured
as pulse wave velocity (distance between recording sites ⫼
delay between wave feet) and shown to increase from
⬍5 m/s under the age of 10 to ⬎10 m/s over the age of
60.11,12 Such a gradual and progressive increase in aortic
wave velocity is due to progressive stiffening of the aorta
and central, predominantly elastic arteries with age. Such
stiffening causes change in the arterial pressure pulse waves
themselves. In young, fully grown adults, wave reflection
is manifest in the central aorta as a secondary boost to
pressure during diastole; in older adults as a consequence of
faster wave velocity, this echo returns earlier and augments
pressure during systole rather than diastole.10–12,16 Such
augmentation, caused by aortic stiffening, is the principal
cause of increased systolic pressure, of decreasing diastolic
pressure, and increasing pulse pressure over the age of 50.11
The very slight increase in mean pressure with age is
attributable to increased peripheral resistance consequent
on apoptosis and decreased tissue vascularity (i.e. fewer
blood vessels rather than decreased vascular calibre).11
But why does brachial systolic pressure remain constant
between the ages of 17 and 40 years, and why does brachial
pulse pressure fall between 17 and 40 years? The answer
is to be had from consideration of wave transmission from
the ascending aorta to the brachial artery. In adolescence,
when the body is fully grown, the normal pressure pulse is
markedly amplified in the upper limb such that systolic and
pulse pressures in the brachial artery are 15–20 mmHg
higher than in the aorta.17 With aging, and aortic stiffening,
such amplification is reduced and brachial systolic pressure
approximates (i.e. is usually within 5 mmHg of) aortic systolic pressure.11,12
Amplification of the pulse wave in the upper limb17
explains the constancy of brachial systolic pressure between
the ages of 17 and 40 years, and the decrease in pulse pressure over this period.11 Such amplification also explains
much of the controversy in interpretation of systolic, diastolic and pulse pressures in young compared with older
individuals. Systolic and pulse pressures in young individuals are unreliable guides to central aortic systolic and pulse
pressures,11 and so are (predictably) less useful for epidemiological purposes than diastolic pressure.10 These points
1358-863X(00)VM321ED
210 MF O’Rourke
help explain why diastolic pressure appeared so useful in
actuarial studies; most individuals taking up insurance policies on first entering the workforce were in their early 20s
when examined medically and when blood pressure was
recorded.
In contrast with actuarial studies, most recent clinical
studies and trials targeted people over the age of 40. Such
trials confirmed the greater importance of systolic over
diastolic pressure, and the overwhelming importance of
pulse pressure in older subjects.5,9,18–20 Such results are predictable on pathophysiological principles. In older individuals, brachial pressures approximate aortic pressure.11 The
pressure during systole in the aorta approximates that in
the left ventricle, and is the load against which the heart
must pump, the stimulus to left ventricular hypertrophy,
and the principal determinant of left ventricular myocardial
oxygen demand. Systolic central pressure is the highest
pressure that central arteries must withstand, and so is the
principal factor in arterial medial damage, aneurysm formation and arterial rupture.11 Predictably, systolic pressure in
older people is robustly associated with resulting cardiovascular events. The even more robust association of pulse
pressure with coronary events7–10,19,20 is explicable on the
basis of the reduction in aortic pressure throughout diastole,
and so the decrease in the capacity to perfuse even moderately narrowed coronary arteries.11 Such coronary perfusion
capacity is even more critical if, as a consequence of
ventricular hypertrophy, the systolic ejection period is
prolonged and the diastolic period compromised.11,21
The pathophysiological principles discussed here help to
explain many of the controversial issues raised initially:
• why there is no logical definition of hypertension
• why elevated arterial pressure constitutes a graded risk
• why central aortic systolic and pulse pressures rise progressively with age as a consequence of aortic stiffening,
while brachial values of systolic and pulse pressures are
exaggerated in young adults
• why brachial systolic, diastolic and pulse pressures
appear to carry different prognostic importance at different ages.
The pathophysiologic principles are also important with
respect to logical treatment of elevated blood pressure at
different ages. In Western societies, screening programs
and awareness, together with effective drugs, have virtually
conquered the problem of ‘diastolic hypertension’, at least
with respect to breaking the vicious circle of vasoconstriction and progressively increasing blood pressure.22 In older
people, ‘isolated systolic hypertension’ is now the most
commonly recognized problem and the acknowledged
cause of the modern epidemic of cardiac failure.23 In such
people, the underlying problem is not increased resistance
of peripheral arterioles, but dilation and rigidity of the aorta
and proximal elastic arteries, with early wave reflection
boosting aortic and left ventricular pressure. The most
effective drugs for such a condition should decrease aortic
stiffness (if this were possible), or if not, should reduce
the early wave reflection from peripheral sites that augment
aortic and left ventricular systolic pressure. Such reduction
in wave reflection can be accomplished by dilation of muscular conduit arteries (with drugs such as nitrates), or by
arteriolar dilation. Since arteriolar dilation, as achieved
with many hypertensive agents, also reduces mean and
Vascular Medicine 2000; 5: 209–211
diastolic pressure, there is a risk of ‘steal’ from vital organs,
especially the heart, and accentuation of myocardial ischaemia. Concentration on conduit artery dilation and the
reduction of large artery stiffening using drugs that have
arterial conduit actions like glyceryl trinitrate, may provide
more appropriate therapies than what is presently available
for the treatment of elevated systolic pressure in our
aging society.
Michael F O’Rourke
University of New South Wales
St Vincent’s Clinic
Victoria Street
Sydney, NSW 2010
Australia
References
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