(Circulation. 2000;102:1186.)
© 2000 American Heart Association, Inc.
Current Perspective |
Arterial Remodeling
Mechanisms and Clinical Implications
From the Division of Cardiovascular Medicine, Stanford University Medical Center, Stanford, Calif (M.R.W., A.C.Y.); Department of Cardiology, Utrecht University Medical Center, Utrecht, the Netherlands (G.P., C.B.); and Interuniversity Cardiology Institute of the Netherlands, Utrecht.
Correspondence to Dr Michael R. Ward, Division of Cardiovascular Medicine, Stanford University Medical Center, 300 Pasteur Dr, Stanford CA 94305-5218. E-mail: mrward@stanford.edu
Key Words: KEY WORDS: remodeling • atherosclerosis • hemodynamics • angioplasty • transplantation
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Introduction |
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The presentation of coronary atherosclerosis can be gradual, because of progressive flow-limiting stenosis and exertional angina, or dramatic, with plaque rupture and thrombosis causing unstable angina, myocardial infarction, or sudden death. The importance of arterial remodeling, or persistent change in vessel size, has recently become apparent in both situations. Arterial remodeling, not plaque size, has been identified as the primary determinant of lumen size in the presence of stable lesions. Similarly, luminal stenosis in transplant vasculopathy and with restenosis after angioplasty occur mainly because of inward remodeling rather than plaque growth. However, recent evidence also suggests that adequate outward remodeling may be associated with an increased risk of plaque rupture, the underlying cause of acute coronary syndromes and sudden cardiac death.
The term "arterial remodeling" has previously been used
to describe any change in vessel wall structure. More recently,
however, it has been used specifically to refer to a change in vessel
size (or cross-sectional area within the external elastic lamina), and
it is on this entity that this review is focused. Inward remodeling
denotes a reduction in vessel size. Outward remodeling denotes an
increase in vessel size. Various other terms are used in the literature
(the Table
). When outward remodeling is present but
insufficient to prevent luminal stenosis, it is referred to as
inadequate outward remodeling.
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Remodeling as a Primary Determinant of Lumen Size |
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It has been known for more than a century1 that blood vessels enlarge to accommodate increasing flow to the organ downstream (eg, during natural growth or in left
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