Journal of vascular surgery · 2002
The contribution of plaque and arterial remodeling to de novo atherosclerotic luminal narrowing in the femoral artery.
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Vink Aryan, Schoneveld Arjan H, Borst Cornelius, Pasterkamp Gerard
Аннотация
BACKGROUND: Atherosclerotic luminal narrowing is caused by plaque growth and arterial remodeling. In peripheral arteries, a role for constrictive remodeling in luminal narrowing has been recognized, but the impact on lumen decrease has not yet been assessed. We studied to what extent arterial remodeling and plaque formation contribute to luminal narrowing in the superficial femoral artery.
METHODS: Elderly subjects (n = 79) were studied. Post mortem, pressure-fixed femoral arteries (n = 125) were dissected and divided into 0.5-cm segments (n = 3266). In each cross section, we measured lumen area, plaque area, and the area encompassed by the internal elastic lamina (IEL area). For each artery, the cross section with the least amount of plaque was considered the reference segment. In cross sections with a decrease in lumen area compared with the reference, we determined the contributions of both plaque increase and IEL area change.
RESULTS: A decrease in lumen area was found in 2193 cross sections. In cross sections with >50% lumen stenosis, plaque increase (accompanied by IEL area increase) fully explained lumen decrease in 80 of 280 cross sections (29%). In the remaining 200 of 280 cross sections (71%), both plaque increase and IEL area decrease contributed to lumen stenosis. In 57 of 280 cross sections (20%), IEL area decrease was the major determinant of lumen decrease, dominating over plaque increase. In 143 of 280 cross sections (51%), plaque increase was the major determinant, dominating over IEL area decrease.
CONCLUSION: The results of this post mortem study suggest that in a substantial part (20%) of severely stenotic lesions in the femoral artery, constrictive remodeling, not plaque size, is the major determinant of lumen decrease. Further serial studies are needed to confirm these results.
METHODS: Elderly subjects (n = 79) were studied. Post mortem, pressure-fixed femoral arteries (n = 125) were dissected and divided into 0.5-cm segments (n = 3266). In each cross section, we measured lumen area, plaque area, and the area encompassed by the internal elastic lamina (IEL area). For each artery, the cross section with the least amount of plaque was considered the reference segment. In cross sections with a decrease in lumen area compared with the reference, we determined the contributions of both plaque increase and IEL area change.
RESULTS: A decrease in lumen area was found in 2193 cross sections. In cross sections with >50% lumen stenosis, plaque increase (accompanied by IEL area increase) fully explained lumen decrease in 80 of 280 cross sections (29%). In the remaining 200 of 280 cross sections (71%), both plaque increase and IEL area decrease contributed to lumen stenosis. In 57 of 280 cross sections (20%), IEL area decrease was the major determinant of lumen decrease, dominating over plaque increase. In 143 of 280 cross sections (51%), plaque increase was the major determinant, dominating over IEL area decrease.
CONCLUSION: The results of this post mortem study suggest that in a substantial part (20%) of severely stenotic lesions in the femoral artery, constrictive remodeling, not plaque size, is the major determinant of lumen decrease. Further serial studies are needed to confirm these results.