Arterial remodelling is a potentially important component in atherogenesis
aimed at delaying the development of significant lumen compromise. Current
knowledge on this phenomenon is mainly restricted to experimental evaluatio
ns and a few postmortem studies. We used high-resolution duplex ultrasound
to study 5-year changes (1990 to 1995) in vessel geometry in a large random
sample of the general population (Bruneck Study). Carotid arteries free of
atherosclerosis and wall thickening preserved a normal size to high ages.
In contrast, common and internal carotid arteries with elevated intima-medi
a thickness (greater than or equal to 50th percentile) experienced marked a
ge-dependent dilation that started already in the 5th decade and continuous
ly accelerated thereafter (structural ageing). Vessel diameters were subjec
t to complex regulation involving morphometric characteristics, sex, wall t
hickness, hypertension, LDL cholesterol levels, and alcohol consumption. Va
scular remodelling secondary to incident or slowly progressive (mural) athe
rosclerosis included local compensation and a generalised dilation response
of vascular segments not primarily affected. Adaptive enlargement at the s
ite of active atherogenesis effectively preserved a near-normal lumen in mo
st instances. The current study identified a second main type of plaque gro
wth, characterized by episodic marked increase in lesion volume probably on
the basis of plaque thrombosis. In this setting, we did not observe maximu
m but insufficient compensation but instead usually observed no compensatio
n at all. Failure of vascular remodelling and marked expansion in plaque si
ze acted synergistically in producing significant lumen compromise. The cur
rent prospective survey describes fundamental principles and various facets
of arterial remodelling and vascular biology in the general population (in
vivo). Vessel geometry was subject to marked temporal changes and showed a
correspondingly complex (multifactorial) and dynamic regulation. Vascular
remodelling emerged as an important compensatory process in human atherogen
esis, which crucially contributed to the determination of lumen obstruction
. Efficacy and failure of compensation primarily depended on the type and p
athomechanisms of underlying atherogenesis and only in second instance on p
laque size and location.