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Willem E. Hellings, MD; Frans L. Moll, MD, PhD; Jean-Paul P. M. De Vries, MD, PhD; Rob G. A. Ackerstaff, MD, PhD; Kees A. Seldenrijk, MD, PhD; Rosemarie Met, MD; Evelyn Velema, BSc; Wouter J. M. Derksen, MD; Dominique P. V. De Kleijn, PhD; Gerard Pasterkamp, MD, PhD

JAMA. 2008;299(5):547-554.

Context  Previous studies have assessed the predictive value of clinical and angiographic parameters for development of restenosis after vascular interventions. The composition of the atherosclerotic plaque at the intervention site has not been evaluated as a marker for restenosis.

Objective  To investigate the relationship between atherosclerotic plaque histology and the occurrence of restenosis after carotid endarterectomy.

Design, Setting, and Patients  The Athero-Express study is a longitudinal vascular biobank study that includes the collection of atherosclerotic plaques of patients undergoing primary carotid endarterectomy. Five hundred patients were prospectively followed up between April 1, 2002, and March 14, 2006, to assess carotid artery restenosis measured by duplex ultrasound 1 year after the intervention.

Main Outcome Measures  Risk of carotid restenosis in relation to predefined histological characteristics (macrophage and smooth muscle cell infiltration, collagen, calcifications, intraplaque bleeding, luminal thrombus, and lipid core size), adjusted for clinical characteristics (multivariate logistic regression analysis).

Results  At 1 year, 85 patients (17%) developed 50% or greater restenosis, including 40 patients (8%) who developed 70% or greater restenosis of the target vessel. Patients whose histological examination of the plaque revealed marked macrophage infiltration (n = 286) had a lower risk than those with none or minor macrophage infiltration (n = 214) of developing 50% or greater restenosis (risk difference, 11.5% vs 24.3%; adjusted odds ratio [OR], 0.43; 95% confidence interval [CI], 0.26-0.72) and a lower risk of developing 70% or greater restenosis (risk difference, 4.5% vs 12.6%; adjusted OR, 0.36; 95% CI, 0.17-0.74). Patients (n = 177) with a plaque having a large lipid core size (>40%) had a lower risk than those (n = 94) with a plaque having a lipid core size of less than 10% of developing 50% or greater restenosis (risk difference, 11.3% vs 25.5%; adjusted OR, 0.40; 95% CI, 0.19-0.81) and a lower risk of developing 70% or greater restenosis (risk difference, 5.6% vs 14.9%; adjusted OR, 0.42; 95% CI, 0.17-1.04), independent of clinical characteristics.

Conclusions  Plaque composition is an independent predictor of restenosis after carotid endarterectomy. The dissection of a lipid-rich, inflammatory plaque is associated with reduced risk of restenosis.

Author Affiliations: Department of Vascular Surgery (Drs Hellings and Moll) and Experimental Cardiology Laboratory (Drs Met, Derksen, De Kleijn, and Pasterkamp, and Ms Velema), University Medical Center, Utrecht, the Netherlands; and Departments of Vascular Surgery (Dr De Vries), Clinical Neurophysiology (Dr Ackerstaff), and Pathology (Dr Seldenrijk), St Antonius Hospital, Nieuwegein, the Netherlands.

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