Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:1491-1498
© 1999 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
The Natural Course of Atherosclerosis
Part II: Vascular Remodeling
From the Department of Neurology, Innsbruck University Hospital, Innsbruck, Austria
Correspondence to Dr J. Willeit, Department of Neurology, Innsbruck University Hospital, Anichstr. 35, A-6020 Innsbruck, Austria.
Abstract—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
evaluations 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-media
thickness (
50th percentile) experienced marked age-dependent dilation
that started already in the 5th decade and continuously accelerated
thereafter (structural ageing). Vessel diameters were subject to
complex regulation involving morphometric characteristics, sex, wall
thickness, hypertension, LDL cholesterol levels, and
alcohol consumption. Vascular remodelling secondary to incident or
slowly progressive (mural) atherosclerosis included
local compensation and a generalised dilation response of vascular
segments not primarily affected. Adaptive enlargement at the site of
active atherogenesis effectively preserved a near-normal lumen in most
instances. The current study identified a second main type of plaque
growth, characterized by episodic marked increase in lesion volume
probably on the basis of plaque thrombosis. In this setting, we did not
observe maximum but insufficient compensation but instead usually
observed no compensation at all. Failure of vascular remodelling
and marked expansion in plaque size acted synergistically in producing
significant lumen compromise. The current 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 atherogenesis, which crucially contributed to the determination
of lumen obstruction. Efficacy and failure of compensation primarily
depended on the type and pathomechanisms of underlying atherogenesis
and only in second instance on plaque size and location.
Key Words: atherosclerosis • vascular remodelling • vascular biology
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