Journal
JOURNAL OF VASCULAR SURGERY
Volume 45, Issue 3, Pages 516-522Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jvs.2006.11.011
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Objective: The best way to manage both symptomatic and asymptomatic severe carotid stenoses has been thoroughly demonstrated by large randomized clinical trials, but less is known about the natural history and management of the contralateral asymptomatic internal carotid artery (ICA). This prospective study was undertaken to determine whether disease progressed in the contralateral ICA of patients who had undergone carotid endarterectomy (CEA) and were followed up clinically and by duplex ultrasound (US) scan. Methods. The contralateral asymptomatic ICAs of 599 patients who had undergone CEA for severe carotid disease over a 10-year period were followed up clinically and with duplex US scan at I month and then every 6 months. ICA stenosis was classified as mild (30%-49%), moderate (50%-69%), severe (70%-99%), or occlusion. Progression was defined as an increase in ICA stenosis of 50% or more for ICAs with a less than 50% baseline lesion or as an increase to a higher category if the baseline stenosis was 50% or more. End points of the study were the incidence of contralateral disease progression and late neurologic events. Kaplan-Meier analysis was used to estimate freedom from disease progression and from neurologic events. The relationship between progression and risk factors was also analyzed. Results. Overall, disease progressed in 25.2% of patients (151/599) after a mean follow-up of 4.1 years. Disease progressed in 34.3% of patients (101/294) with mild stenosis vs 47.9% of patients with moderate stenosis (47/99; P=.016). Three additional patients with mild lesions at baseline progressed to severe lesions. The median time to progression was 29.8 months for mild and 18.5 months for moderate stenoses (P =.033). The rate of late neurologic events referable to the contralateral ICA was 3.2% (19/599) for the entire series and 4.8%.(19/392) for patients with a 30% or greater ICA stenosis: these included 4 (0.7%) strokes and 15 (2.5%) transient ischernic attacks. All but 3 events (16.3%; 16/98) occurred in patients with disease progression from moderate to severe stenosis. Overall, 53 late CEAs were performed. Conclusions. This prospective analysis has shown that disease progression in contralateral asymptomatic ICAs after CEA is relatively common in patients with a diseased ICA at the baseline and strongly supports duplex US surveillance, approximately every 6 months, in patients with-more than mild disease. A baseline lesion is significantly predictive of progression to severe stenosis, and progression from moderate to severe stenosis is strongly associated with neurologic clinical events. No demographic or clinical factor proved useful in identifying patients likely to experience disease progression.
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