Hypertension, diabetes, and hypercholesterolemia are characterized by a red
uction in arterial distensibility and by accelerated atherosclerosis. Wheth
er arterial stiffening is an inherent feature of these conditions or just t
he consequence of the atherosclerotic clinical or subclinical lesions is no
t known, however. Our aim was to obtain information on this issue by direct
ly measuring, in humans, arterial distensibility both at the site of an ath
erosclerotic lesion and at the proximal normal site. In 10 patients (8 men;
mean +/- SEM age, 65.2 +/-3.4 years) affected by monolateral hemodynamic s
ignificant internal carotid artery stenosis, we measured arterial distensib
ility (Wall Track System; PIE Medical) bilaterally, both at the internal ca
rotid artery and at the common carotid artery level. In the common carotid
artery, measurements were made 3 cm below the bifurcation. In the affected
internal carotid artery, measurements were made at the plaque shoulder (wal
l thickness of 2 mm). Measurements were made in the contralateral internal
carotid artery at a symmetrical level. Arterial wall thickness was measured
in the same site of arterial distensibility. Arterial distensibility was l
ess in the internal than in the common carotid artery, with a marked reduct
ion at the plaque internal carotid artery level compared with the correspon
ding contralateral site (-45%, P <0.01). It was also less, however, in the
common carotid artery branching into the atherosclerotic internal carotid a
rtery than in the contralateral common carotid artery (-25%, P <0.05). Wall
thickness was similar in the 2 common carotid arteries and obviously great
er in the affected internal carotid artery than in the contralateral artery
. Arterial distensibility was markedly less in the internal carotid artery
where there was a plaque compared with the intact contralateral internal ca
rotid artery; it was also less, however, in the common carotid artery of th
e affected side in comparison with the contralateral common carotid artery.
This provides evidence that the effect of a plaque on arterial mechanical
properties is not limited to the actual plaque site but rather extends to a
considerable degree in a proximal direction.