Download Influence of aging on arterial compliance

Journal of Human Hypertension (1998) 12, 583–586
 1998 Stockton Press. All rights reserved 0950-9240/98 $12.00
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Influence of aging on arterial compliance
LM Van Bortel and JJ Spek
Department of Pharmacology, Cardiovascular Research Institute Maastricht, Maastricht University, PO
Box 616, 6200 MD Maastricht, The Netherlands
With aging, pulse pressure increases. A high pulse
pressure has been recognised as an important cardiovascular risk factor. The increase in pulse pressure with
aging is mainly due to a decrease in large artery compliance. Compliance and distensibility are large artery
wall properties. Compliance is the buffering capacity of
the vessel. Distensibility reflects much more the elasticity of the artery. Compliance is related to distensibility
and arterial diameter. These large artery wall properties
can be measured non-invasively using new echo-tracking techniques. With these techniques it has been
shown that the elasticity (distensibility) and the buffering capacity (compliance) of the common carotid artery
is decreasing with aging, while diameter of the artery
increases. This increase in diameter might be a compen-
sating mechanism to limit the decrease in compliance.
There are indications that the effect of aging on large
artery wall properties may not be similar at all vascular
territories. A decrease in compliance leads to a high
pulse pressure and isolated systolic hypertension. The
drug of choice for the treatment of isolated systolic
hypertension should increase large artery compliance
with no, or only minor effect on resistance vessels. This
would lead to a decrease in pulse pressure without
decreasing mean blood pressure. As a result, systolic
but not diastolic blood pressure decreases. It appears
that nitrates better than other anti-hypertensive drugs
can decrease pulse pressure. They therefore have been
advocated for the treatment of isolated systolic hypertension.
Keywords: arterial compliance; aging; pulse pressure
Introduction
Blood pressure (BP) is generally known as systolic
(SBP) and a diastolic (DBP) pressure, but BP can also
be seen as a mean arterial pressure (MAP) and a
pulse pressure oscillating around this mean arterial
pressure. For a given cardiac output (CO), MAP—
the static component of the BP—is determined by
the systemic vascular resistance (SVR), as shown by
the formula:
MAP = CO × SVR.
Systemic vascular resistance is determined by resistance vessels, which are predominantly small
arteries, arterioles and capillaries (Table 1). The
pulse pressure—the dynamic component of the
BP—is mainly determined by stroke volume, the
timing of reflected pulse waves, and the compliance
of arterial capacitance vessels, which are predominantly large arteries.1 These large arteries have a
particular function. Apart from the conduit function, during systole large arteries have to temporTable 1 Determinants of blood pressure
Components
Mean arterial
pressure
Pulse pressure
nature
static
dynamic
main determinant
vessels
resistance vessels:
arterioles
capillaries
capacitance
vessels: large
arteries
Correspondence: LM Van Bortel
arily store the flow jet coming from the heart in
order to get a more continuous tissue perfusion. This
storing or buffering function is reflected by the compliance of the large artery. Compliance is defined as
the change in volume of the artery per unit of pressure [⌬V/⌬P].2 Compliance, together with systemic
vascular resistance, is considered the major determinant of the afterload on the heart.2 Distensibility—
the other large artery wall property—is defined as
the relative change in volume of the artery per unit
of pressure [⌬V/V/⌬P].3 Distensibility is considered
as a major determinant of the stress on the vessel
wall and might be important in processes such as
aging and atherosclerotic disease.4 Nowadays large
artery wall properties can be measured non-invasively.
Non-invasive measurement of large
artery wall properties in man
In man, different aspects of arterial wall properties
(distensibility and compliance) can be measured, ie,
total, regional and local compliance.4
Total arterial compliance (C) of the arterial tree
has been estimated from stroke volume (SV) and
pulse pressure (⌬P) by the formula ⌬P = SV/C.5
However, this formula is incomplete, since apart
from compliance of large vessels and stroke volume,
other factors, such as early reflected pulse waves,6–8
can influence pulse pressure. Nowadays new
approaches for the measurement of total arterial
compliance are being proposed.
Regional compliance describes compliance in an
arterial segment. It can be calculated from arterial
volume and distensibility. Regional distensibility is
Influence of aging on arterial compliance
LM Van Bortel and JJ Spek
584
mainly measured using pulse wave velocity. Distensibility and pulse wave velocity are inversely
related.9 In the literature pulse wave velocity has
been regularly mentioned as a measure of arterial
compliance, instead of distensibility. Arterial volume is more difficult to assess since vascular diameter is not constant over the arterial segment.
Local distensibility and compliance can be
assessed by the development of new echo-tracking
techniques.10,11 These devices can accurately measure diameter (d) and stroke change in diameter (⌬d)
of various large arteries. The device developed by
Hoeks and coworkers12 consists of a commercially
available echo-imager and a computer with a builtin data acquisition system. First, the artery of interest is scanned in B-mode. Then, a line perpendicular
to the arterial wall is chosen and a registration is
made in M-mode during about 5 sec. From this registration, radiofrequency signals are captured and
stored in the computer. After registration, the computer shows a first radiofrequency signal. The investigator has to mark the regions of interest: the
anterior and the posterior wall. Then, the computer
will process all radiofrequency signals. As a result
an image of the movement of the anterior wall and
of the posterior wall of the artery is displayed. From
diameter, change in diameter during the heart cycle
and pulse pressure, vessel wall properties, can be
calculated.
Assuming that during the heart cycle arteries predominantly change in diameter and hardly in
length, cross-sectional compliance (CC)—defined as
arterial compliance per unit of length (L)—can be
used as an estimate of local compliance. Cross-sectional compliance is the change in cross-sectional
area of the vessel (⌬A) per unit of pressure:
CC = ⌬V/L/⌬P = ⌬A/⌬P ⬇ ␲.d.⌬d/(2.⌬P).
Similarly, distensibility coefficient (DC) can be
defined as the relative change in the cross-sectional
area of the vessel (⌬A/A) per unit of pressure:
DC = ⌬A/A/⌬P ⬇ 2.⌬d/d/⌬P.
Compared to other techniques, the strength of these
echo-tracking techniques is that: (1) both distensibility and compliance can be calculated; and
(2) different arterial territories can be investigated.
Whereas the device accurately measures diameter
and stroke change in diameter, the weakness of this
method is that accurate non-invasive assessment of
the pulse pressure at the site of the arterial wall
movement registration might sometimes be difficult.
In contrast to MAP, pulse pressure is not equal in
large arteries.6 As a consequence, using the pulse
pressure in one artery as a surrogate for the pulse
pressure in the target artery might be erroneous. To
overcome these problems, pulse pressure assessment using applanation tonometry has recently been
proposed.13 Alternatively, calculation of the pulse
pressure of a central artery using amplitude and contour of the pressure wave of a peripheral artery may
also be promising.14
Effect of aging on large artery
compliance
With aging especially SBP increases,15,16 while DBP
does not increase or even tend to decrease.15 This
leads to an increase in pulse pressure, which has
been shown to be an important cardiovascular risk
factor.17–19 This pulse pressure amplification with
aging is due to large artery stiffening. Different factors may contribute to this stiffening; for example, a
decreased connective tissue elasticity, atherosclerosis and a decrease in smooth muscle relaxation.20
Large artery stiffening results in a decrease in large
artery compliance and early reflected pulse waves.
Early reflected pulse waves originate on the one
hand from reflection sites being closer to the heart
and on the other hand by a higher pulse wave velocity due to the increase in arterial stiffness.
It has been shown that with aging, compliance of
large arteries decreases.21,22 For the common carotid
artery, this decrease in compliance was due to a
more pronounced decrease in distensibility (the
elasticity) of the artery with an increase in diameter.22 So, it appears that the increase in diameter
with aging might be a compensation for the decrease
in elasticity of the artery in order to limit the
decrease in compliance.
Studies on local arterial wall properties also
revealed that large conduit arteries do not similarly
react to disease states and to changes in physiologic
conditions. Aging decreases elasticity of the common carotid artery.21,22 Such an effect was not found
in the femoral artery.21 Three other examples: (1) in
hypertension distensibility and compliance of elastic arteries decrease.23 However, compliance of the
radial artery did not decrease, probably compensating for the loss of compliance in elastic arteries.24
Compared to healthy subjects, in patients with
(2) mild hypercholesterolemia25 and in patients with
(3) uncomplicated insulin-dependent diabetes mellitus,26 arterial distensibility was lower at the femoral but not at the carotid artery. Studies on the
effects of aging were mainly investigating central
arteries in relatively small groups. These observations on local vessel wall properties in different
conditions suggest that a population study on the
effect of aging on different arterial territories could
reveal more detailed information on the effect of
aging on large artery wall properties. Such a study
is ongoing as part of the PheeCad study.27
Treatment of high pulse pressure
The effect of different anti-hypertensive drugs on
large artery compliance is shown in Table 2.28 Large
artery compliance can be increased by calciumantagonists, ACE-inhibitors, ␤-blocking agents with
vasodilating properties, and nitrates. Apart from
metoprolol, all ␤1-blockers also improve compliance. At higher doses ␤1-blockers lose selectivity.
This might be an explanation for the difference
between metoprolol (100 mg twice daily) and other
selective ␤1-blockers on large artery compliance.
Since a higher BP, by itself, may decrease arterial
distensibility,29 the beneficial effect of some anti-
Influence of aging on arterial compliance
LM Van Bortel and JJ Spek
Table 2 Effect of anti-hypertensive drugs on large artery compliance
Compliance increased
Compliance unchanged
ACE-inhibitors
Selective ␤1-blockers
␤-blockers with vasodilatory
action
Calciumantagonists
Some diuretics
Ketanserin
Nitrates
Non-selective ␤-blockers
Clonidine
Direct vasodilators
Urapidil
Some diuretics
hypertensive drugs on large artery compliance
might, in part, be due to the decrease in BP. Despite
a marked fall in BP, the nonselective ␤-blocker propranolol, direct vasodilators of the hydralazine
group and the centrally acting alpha2 agonist clonidine do not increase arterial compliance. The effect
of ␣-blocking agents is not clear. On the one hand
ketanserin (␣ + serotonin2-antagonist) improves
arterial compliance, while urapidil (␣-adrenoceptor
antagonist + central serotonin1A-agonist) does not.
Some authors did find an increase in distensibility
and/or
compliance
during
treatment
with
diuretics,30,31 while other authors did not.32 In general, diuretics containing thiazides improved compliance. Since most diuretics, used in hypertension,
show some vasodilatory effect—which might
improve large artery properties—only after 4 to 8
weeks, some studies might have been too short to
depict this effect. It is clear that the effect of different
anti-hypertensive drugs on large artery compliance
is not uniform.
With age structural changes cause a decrease in
distensibility and compliance of the carotid artery.
These structural changes may be responsible for an
altered effect of anti-hypertensive drugs in the elderly. For example, despite a larger fall in BP, vessel
wall properties were less increased in elderly (⭓60
years) than in young (⭐40 years) hypertensive
patients with verapamil 120 mg three times daily.4
A decrease in compliance with aging leads to an
increase in pulse pressure, thereby increasing SBP
and, to a smaller extent, decreasing DBP. In elderly
people this often leads to isolated systolic hypertension.
Classical anti-hypertensive drugs mainly decrease
systemic vascular resistance by dilating resistance
vessels. This results not only in a decrease in SBP,
but also in a decrease in DBP. A further decrease in
DBP may be harmful, especially in elderly patients
with coronary artery disease. Indeed, coronary
artery perfusion depends upon DBP. A further fall
in the normal DBP may alter coronary perfusion and
provoke cardiac ischaemia.
It has been suggested that, at least in part, the
J-shaped BP mortality curve might be due to elderly
subjects with coronary artery disease and a low
DBP.33
Thus, the drug of choice for the treatment of isolated systolic hypertension should increase large
artery compliance without decreasing systemic vascular resistance. Such a drug will decrease systolic
pressure without substantially changing diastolic
pressure. So far, such an ideal drug does not exist.
From all classical anti-hypertensive drugs, nitrates
have been shown to decrease SBP without important
change in diastolic pressure.34,35 They, therefore,
have been advocated for the treatment of isolated
systolic hypertension. Recently a new drug has been
shown to be more selective than nitrates to large
arteries than to resistance vessels in normal subjects.36 Such a drug may be very promising for the
treatment of isolated systolic hypertension.
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