Abstract
Subclinical alterations of cerebral function can occur during or after carotid revascularization and can be detected by a variety of standard tests. This comparative study assessed the relationship among serum levels for two biochemical markers of cerebral injury, postoperative diffusion-weighted magnetic resonance imaging (DW-MRI), and neuropsychometric testing in patients undergoing carotid endarterectomy (CEA) or carotid artery stenting (CAS) for high-grade asymptomatic carotid stenosis. Forty-three consecutive asymptomatic patients underwent carotid revascularization by endarterectomy (CEA, 20) or stenting (CAS, 23). They were evaluated with DW-MRI and the Mini-Mental State Examination (MMSE) test preoperatively and <or=24 hours after carotid revascularization. Venous blood samples to assess serum levels of neuron-specific enolase (NSE) and S100beta protein were collected for each patient preoperatively and five times in a 24-hour period postoperatively and assayed using automated commercial equipment. The MMSE test was repeated at 6 months. The relationship between serum marker levels and neuropsychometric and imaging tests and differences between the two groups of patients were analyzed by chi(2) test, with significance at P < .05. No transient ischemic attacks or strokes were clinically observed. CAS caused more new subcortical lesions at postoperative DW-MRI and a significant decline in the MMSE postoperative score compared with CEA (P = .03). In CAS patients, new lesions at DW-MRI were significantly associated with a postoperative MMSE score decline >5 points (P = .001). Analysis of S100beta and NSE levels showed a significant increase at 24 hours in CAS patients compared with CEA patients (P = .02). The MMSE score at 6 months showed a nonsignificant increase vs the postoperative score in both groups. Biochemical markers measurements of brain damage combined with neuropsychometric tests and DW-MRI can be used to evaluate silent injuries after CAS. The mechanisms of rise in S100beta and NSE levels at 24 hours after CAS may be due to increased perioperative microembolization rather than to hypoperfusion. Further studies are required to assess the clinical significance of those tests in carotid revascularization.
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