Mack W J, Ducruet A F, Hickman Z L, Zurica J, Starke R M, Garrett M C, Komotar R J, Quest D O, Solomon R A, Heyer E J, Sander Connolly E
Department of Neurological Surgery, Columbia University Medical Center, New York, NY 10032, USA.
Acta Neurochir (Wien). 2008 Aug;150(8):779-84; discussion 784. doi: 10.1007/s00701-008-1618-6. Epub 2008 Jun 23.
Previous studies have demonstrated that elevated pre-operative monocyte count is an independent predictor of acute neurocognitive decline following carotid endarterectomy (CEA). Monocyte chemoattractant protein-1 (MCP-1), secreted by human endothelial and monocyte-like cells, is a potent mediator of inflammation and mononuclear cell trafficking. This study examines the relationship between peri-operative serum MCP-1 elevation and post-operative neurocognitive injury following CEA.
Fifty-two patients undergoing CEA and 67 lumbar laminectomy (LL) controls were administered a battery of five neuropsychological tests pre-operatively and on post-operative day 1 (POD 1). Change in individual test scores from baseline to POD 1 were converted into Z-score and used to develop a point system quantifying the degree of neurocognitive dysfunction relative to change within the LL group. Neurocognitive injury following CEA was defined as a score greater than 2 standard deviations above mean total deficit scores of LL controls. Serum MCP-1 levels were measured pre-operatively and on POD 1 by enzyme-linked immunosorbent assay.
Mean percent MCP-1 elevation was higher for the 13 injured CEA patients (147.7 +/- 32.4%) in our cohort compared to 39 age- and sex-matched uninjured CEA patients (76.0 +/- 16.5%). In unconditional multivariate logistic regression analysis, percent elevation in serum MCP-1 level was associated with neurocognitive injury one day after CEA (OR = 2.19, 95% CI = 1.13-4.26, P = 0.021, for a 100% elevation from pre-operative levels).
Peri-operative elevations in serum MCP-1 levels correlate with acute neurocognitive dysfunction following CEA. These data implicate an inflammatory mechanism in the pathogenesis of Ischaemic neurocognitive decline.
既往研究表明,术前单核细胞计数升高是颈动脉内膜切除术(CEA)后急性神经认知功能下降的独立预测因素。人内皮细胞和单核细胞样细胞分泌的单核细胞趋化蛋白-1(MCP-1)是炎症和单核细胞运输的有效介质。本研究探讨CEA围手术期血清MCP-1升高与术后神经认知损伤之间的关系。
对52例行CEA的患者和67例腰椎椎板切除术(LL)对照者在术前及术后第1天(POD 1)进行一系列五项神经心理学测试。将个体测试分数从基线到POD 1的变化转换为Z分数,并用于建立一个评分系统,以量化相对于LL组内变化的神经认知功能障碍程度。CEA后神经认知损伤定义为得分高于LL对照组平均总缺陷分数2个标准差以上。术前及POD 1采用酶联免疫吸附测定法测量血清MCP-1水平。
与39例年龄和性别匹配的未发生神经认知损伤的CEA患者(76.0±16.5%)相比,我们队列中13例发生神经认知损伤的CEA患者的MCP-1平均升高百分比更高(147.7±32.4%)。在无条件多因素逻辑回归分析中,血清MCP-1水平升高百分比与CEA术后1天的神经认知损伤相关(术前水平升高100%时,OR = 2.19,95%CI = 1.13 - 4.26,P = 0.021)。
CEA围手术期血清MCP-1水平升高与急性神经认知功能障碍相关。这些数据提示炎症机制在缺血性神经认知功能下降的发病机制中起作用。