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During carotid endarterectomy (CEA) the internal carotid artery is cross-clamped for a period of several minutes. This maneuver may cause cerebral hypoperfusion and/or impairment of the blood-brain barrier (BBB) even in cases where clinical signs are absent. The aim of the present study was to examine whether such alterations could be detected by monitoring the cerebral marker S-100B protein concentrations during and after CEA in the serum. Twenty-five consecutive patients (17 M/8 F, mean age: 64.2 years, range 47-79 years) undergoing elective CEA at our department were studied. All of these patients were without perioperative neurological deficit. Intraoperative samples were collected from internal jugular and peripheral venous blood: 1) before carotid cross-clamping; 2) immediately before declamping; 3) after clamp release. Postoperative samples were taken from peripheral blood at 6 and 24 h, respectively. S-100B was assayed in sera using an immunoluminometric technique. During carotid cross-clamping, S-100B protein concentrations in the ipsilateral jugular serum significantly (p < 0.02) increased to pre-clamp values. After declamping, however, S-100B returned to the baseline level. No differences were seen between the responses of hypertensive and normotensive patients. There was no correlation between carotid occlusion time and S-100B protein concentrations. In the peripheral venous serum no significant changes in S-100B concentrations were detected during or after CEA. We presume that the elevation of S-100B protein concentration during CEA in patients with no neurological deficits indicates the transient opening of the BBB elicited by carotid cross-clamping.

Objective: Although the association between vulnerable lesions and cardiovascular events is well established, little is known about their relationship to postsurgery restenosis. To address this issue, we initiated a prospective, nonrandomized study to examine the femoral plaques on both sides in patients who were undergoing eversion carotid endarterectomy (CEA) and were longitudinally followed-up for early restenosis development. Methods: The final analysis enrolled 321 patients (189 women) with a median age of 67.0 years (interquartile range, 59.0-73.0 years), who underwent eversion CEA (2005 to 2007). Using duplex ultrasound scanning, we evaluated 321 common femoral atherosclerotic lesions on the day before CEA. A quantitative scale was used to grade the size of plaques as grade 1, one or more small plaques (<20 mm 2 ); grade 2, moderate to large plaques; and grade 3, plaques giving flow disturbances. The plaque morphology in terms of echogenicity was graded as echolucent, 1; predominantly echolucent, 2; predominantly echogenic, 3; echogenic 4; or calcified, 5. The plaque surface was categorized as smooth, irregular, or ulcerated. The patients underwent carotid duplex ultrasound imaging at 6 weeks and at 6, 12, and 24 months after CEA. Mann-Whitney U test, 2 test, and multivariate logistic regression were used for statistical evaluation. Results: Internal carotid artery restenosis of >50% was detected in 33 patients (10.28%) in the operated region. Neither the size (grade 1, P ‫؍‬ .793; grade 2, P ‫؍‬ .540; grade 3, P ‫؍‬ .395) nor the surface characteristics of the femoral plaques (smooth, P ‫؍‬ .278; irregular, P ‫؍‬ .281; ulcerated, P ‫؍‬ .934) were significantly different between the patients with and without carotid restenosis. Echolucent-predominantly echolucent femoral lesions were an independent predictor of recurrent carotid stenosis (adjusted odds ratio, 5.63; 95% confidence interval, 2.14-10.89; P < .001). Conclusion: Ultrasound evaluation of femoral plaque morphology before CEA can be useful for identifying patients at higher risk for carotid restenosis. ( J Vasc Surg 2010;51:345-50.)Eversion endarterectomy of the carotid artery (CEA) is a generally accepted elective surgical method in both symptomatic and asymptomatic patients with significant internal carotid artery (ICA) stenosis. Despite of the best surgical care, recurrent stenosis has been reported to occur in 1% to 36% of patients. 1 Stoney and String 2 were the first to classify carotid restenoses into two distinct types: lesions occurring Յ2 years after CEA were attributed to intimal hyperplasia and thereafter, to recurrent atherosclerosis.Multiple inflammatory mediators, including growth factors and cytokines, have been postulated to play different roles to trigger the neointimal response. 3 Similarly, inflammation is involved in all stages of the atherosclerotic process, from the initiation of the fatty streak to the final stage of plaque rupture. 4 Histologic findings have revealed that high-risk vulnerable lesions have a thin fibrous ca...

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Our present findings indicate that sTM may be adsorbed to the atherosclerotic plaques or inflamed endothelium in carotid arteries. The pathological significance of this adsorption remains to be determined.