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À propos de : Relation between coronary artery remodelling (compensatory dilatation) and stenosis in human native coronary arteries        

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  • Relation between coronary artery remodelling (compensatory dilatation) and stenosis in human native coronary arteries
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Abstract
  • OBJECTIVES. To investigate the contribution of plaque size and vessel remodelling to coronary artery stenosis and to assess the role of vessel shrinkage (negative remodelling) across a wide range of lesions. DESIGN. Postmortem study of coronary remodelling in perfusion fixed hearts. SUBJECTS. 24 men and 24 women who died suddenly with coronary artery disease. MAIN OUTCOME MEASURES. Percentage stenosis, percentage plaque burden, percentage remodelling, and arc of normal vessel were measured and related to age, sex, smoking status, and history of hypertension. RESULTS. There was a positive relation between percentage stenosis and percentage plaque burden (r = 0.6, p < 0.0001) and an inverse relation between percentage stenosis and percentage remodelling (r = -0.4, p < 0.0001). Multilinear regression modelling showed that luminal stenosis = 1.0 (plaque burden) − 0.4 (vessel remodelling). Remodelling was greater in lesions that would not have been significant at angiography (⩽ 25% stenosis) than in the remaining lesions (25.9 (26)% v10.0 (21.1)%, p < 0.0001, respectively) and was reduced in segments with circumferential plaques (12.7 (24.5)% v20.7 (24.3)% in eccentric plaques, p = 0.001). Remodelling did not correlate with age, sex, or smoking. Negative remodelling was present in 62 lesions with a stenosis > 25% versus 10 lesions with ⩽ 25% stenosis (p < 0.0001). Lesions with negative remodelling had greater plaque burden and luminal stenosis and a reduced arc of normal segment. CONCLUSION. Outward arterial remodelling negates the stenosing effect of increasing plaque size. Significant coronary stenoses arise from a failure of this outward remodelling in the face of a large plaque burden. Coronary arterial remodelling is unrelated to sex or smoking and is plaque specific.
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  • 00402
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PubMed ID
  • 11454845



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