title: The impact of atherosclerotic arterial remodeling on percentage of luminal stenosis varies widely within the arterial system. A postmortem study.
abstract: Luminal stenosis can be based on large atherosclerotic plaques in compensatory enlarged segments or on relatively little plaques in shrunken segments. In the present study, the contribution of plaque formation and remodeling to luminal narrowing was compared among six types of arteries prone to symptomatic atherosclerosis. Cross-sections (n = 5195) were obtained at regular intervals from 329 arteries. For each artery, the cross-section that contained the least amount of plaque was considered to be the reference. For each cross-section, the percentage of lumen area decrease was expressed as a percentage of the lumen area at the reference site (luminal stenosis). Similarly, the area encompassed by the internal elastic lamina (IEL area) was expressed as a percentage of the IEL area at the reference site (relative IEL area). All cross-sections were categorized in three groups: relative IEL area > 105% (enlargement), 95% to 105% (no remodeling), and < 95% (shrinkage). The prevalence of enlargement (50% to 75%) was significantly higher compared with shrinkage (8% to 25%). Shrinkage was observed most frequently in the femoral arteries (25%) and infrequently in the renal arteries (8%). For all types of arteries, the relative IEL area correlated negatively with luminal stenosis (P < .001). Regression analysis of relative IEL area on luminal stenosis, however, showed significant differences in the first-order regression coefficients among artery types. On average, plaque increase was more compensated for by enlargement in the coronary, common carotid, and renal arteries compared with the arteries obtained from the lower extremities. Anatomic regional differences were observed in the impact of arterial wall remodeling on percent luminal stenosis in de novo atherosclerotic lesions.
authors.affiliation: Department of Cardiology, Utrecht University Hospital, The Netherlands. g.pasterkamp@hli.azu.nl
authors.forename: G
authors.initials: G
authors.lastname: Pasterkamp
authors.forename: A H
authors.initials: AH
authors.lastname: Schoneveld
authors.forename: W
authors.initials: W
authors.lastname: van Wolferen
authors.forename: B
authors.initials: B
authors.lastname: Hillen
authors.forename: R J
authors.initials: RJ
authors.lastname: Clarijs
authors.forename: C C
authors.initials: CC
authors.lastname: Haudenschild
authors.forename: C
authors.initials: C
authors.lastname: Borst
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001158:Arteries / Q000473:pathology*; D001161:Arteriosclerosis / Q000473:pathology*; D017536:Carotid Artery, Common / Q000473:pathology; D016893:Carotid Stenosis / Q000473:pathology; D003324:Coronary Artery Disease / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D005260:Female; D005263:Femoral Artery / Q000473:pathology; D006801:Humans; D007083:Iliac Artery / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009928:Organ Specificity; D012077:Renal Artery / Q000473:pathology