AGING AND COGNITION AFTER CARDIAC SURGERY

越来越多的老年患者接受心脏手术，预计这一趋势将持续下去。这种手术的一个非常常见和令人不安的后果是认知功能的恶化。这种损伤在医院中可高达83%，并且在30%或更多的患者中持续超过一年。老年患者尤其容易受到这种神经认知后果的影响。这种认知功能障碍的原因被认为是在心脏手术中发生的脑栓塞的结果。认知功能障碍的原因被认为是在心脏手术中发生的脑栓塞的结果，这是无法预防的，因此必须开发保护大脑的策略。在低温体外循环过程中，利用红细胞压积的优势促进血液流动，并避免输血的不良后果，已成为心脏外科手术的标准做法。目前尚不清楚这种血液稀释（血液携氧能力降低50%）是否会导致脑损伤和认知障碍。我们将检验通过限制体外循环期间血液稀释量来保持血液携带氧的能力，从而提高脑保护的假设。将对370例患者进行前瞻性随机试验，其中一半患者将被分配到中度血液稀释组（血细胞比容大于或等于27%-治疗组），另一半患者将被分配到深度血液稀释组（血细胞比容15-18%-当前实践组）。手术后第一年认知功能的变化将在两组之间进行比较。第二个目的是确定神经胶质（s100 β）和神经元（神经元特异性烯醇化酶）脑损伤的血清标志物是否能预测认知功能的变化。脑损伤标志物与认知变化的正相关将允许早期检测，并支持认知变化是脑缺血结果的假设。在本研究中获得的新知识将立即转移到临床实践中，并可以减轻认知障碍的严重程度。有关脑保护的新信息也将适用于包括中风在内的所有缺血性脑综合征。

Elderly patients are increasingly undergoing cardiac surgery and this trend is forecasted to continue. A very common and disturbing consequence of this surgery is deterioration in cognitive function. This impairment can be as high as 83% in the hospital and continue in up to 30% or more of patients for over a year. Elderly patients are particularly susceptible to this neurocognitive consequence of life- preserving surgery. This cause of cognitive dysfunction is postulate to be a result of cerebral emboli that occur during cardiac surgery. The cause of cognitive dysfunction is postulated to be a result of cerebral emboli that occur during cardiac surgery, which are impossible to prevent, and therefore strategies to protect the brain must be developed. It has become standard practice in cardiac surgery to allow the hematocrit advantages to blood flow during hypothermic cardiopulmonary bypass and fear of adverse consequences of transfusion. It is not known whether this hemodilution (50% reduction in oxygen carrying capacity of the blood) contributes to brain injury and cognitive impairment. We will test the hypothesis that preserving oxygen carrying capacity of the blood by limiting the amount of hemodilution during cardiopulmonary bypass improves cerebral protection. A prospective, randomized trial in 370 patients will be conducted in which half of the patients will be assigned to moderate hemodilution (hematocrit of greater than or equal to 27%-treatment group) and other half to profound hemodilution (hematocrit 15-18%-current practice group). Change in cognitive function over the first year after surgery will be compared between the groups. A secondary aim is to determine if serum markers of glial (S100beta) and neuronal (neuron-specific enolase) brain injury predict the changes in cognitive function. A positive association of brain injury markers with cognitive change will allow earlier detection and support the hypothesis that the cognitive changes are a result of brain ischemia. New knowledge gained in this study would be immediately transferred to clinical practice and could reduce the severity of cognitive impairment. The new information regarding cerebral protection would also have application in all ischemic brain syndromes including stroke.