COMPENSATORY ENLARGEMENT IN CORONARY AND FEMORAL ARTERIES IS RELATED TO NEITHER THE EXTENT OF PLAQUE-FREE VESSEL WALL NOR LESION ECCENTRICITY - A POSTMORTEM STUDY

Citation
Jagm. Clarijs et al., COMPENSATORY ENLARGEMENT IN CORONARY AND FEMORAL ARTERIES IS RELATED TO NEITHER THE EXTENT OF PLAQUE-FREE VESSEL WALL NOR LESION ECCENTRICITY - A POSTMORTEM STUDY, Arteriosclerosis, thrombosis, and vascular biology, 17(11), 1997, pp. 2617-2621
Citations number
22
ISSN journal
10795642
Volume
17
Issue
11
Year of publication
1997
Pages
2617 - 2621
Database
ISI
SICI code
1079-5642(1997)17:11<2617:CEICAF>2.0.ZU;2-W
Abstract
Arteries may demonstrate compensatory enlargement in response to plaqu e accumulation. It has been proposed that enlargement is achieved by t he expansion of the nondiseased (plaque-free) vessel wall. In this stu dy, we assessed this hypothesis. Post mortem, 32 atherosclerotic coron ary arteries (left anterior descending, n=10; left circumflex, n=11; a nd right coronary, n=11) and 54 atherosclerotic femoral arteries were pressure fixed. Cross sections (coronary arteries, n=537; femoral arte ries, n=1602) were obtained for analysis every 2.5 mm for the coronary arteries and every 5.0 mm for the femoral arteries. From these cross sections, we determined the degree of remodeling and an eccentricity i ndex. Finally, we measured the extent of plaque-free vessel wall. The plaque-free vessel wall was defined as (1) no plaque present or (2) pl aque thickness <0.5 mm. A very weak, negative correlation was observed between the degree of remodeling and the extent of the plaque-free ve ssel wall (coronary arteries: no plaque r(2)=.13, P<.01; <0.5 mm plaqu e r(2)=.15, P<.05; femoral arteries: no plaque r(2)=.02, P<.01; <0.5 m m plaque r(2)=0.04, P<.01). The degree of remodeling did not correlate with the eccentricity index (coronary arteries r(2)=.002, P>.05 and f emoral arteries r(2)=.001, P>.05). Thus, compensatory enlarged segment s did not reveal a larger circumference of plaque-free vessel wall com pared with segments that failed to enlarge. This study provides no sup port for the hypothesis that nondiseased vessel-wall expansion is resp onsible for compensatory enlargement in atherosclerotic arteries.