AGING AND COGNITION AFTER CARDIAC SURGERY

越来越多的老年患者接受心脏手术，预计这一趋势将继续下去。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。这种损害在医院中可能高达83%，并且在高达30%或更多的患者中持续一年以上。老年患者特别容易受到这种维持生命手术的神经认知后果的影响。这种认知功能障碍的原因被认为是心脏手术期间发生的脑栓塞的结果。认知功能障碍的原因被认为是心脏手术期间发生的脑栓塞的结果，这是不可能预防的，因此必须制定保护大脑的策略。在心脏手术中，允许红细胞压积有利于低温体外循环期间的血流，并且担心输血的不良后果，这已成为标准做法。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。我们将检验这一假设，即在体外循环期间通过限制血液稀释量来保持血液的携氧能力，可改善脑保护。将在370例患者中进行一项前瞻性随机试验，其中一半患者将被分配至中度血液稀释（红细胞压积大于或等于27%-治疗组），另一半患者将被分配至深度血液稀释（红细胞压积15-18%-当前实践组）。将比较两组术后第一年认知功能的变化。第二个目的是确定胶质细胞（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可预测认知功能的变化。脑损伤标志物与认知变化的正相关性将允许更早地检测并支持认知变化是脑缺血的结果的假设。本研究中获得的新知识将立即转移到临床实践中，并可降低认知障碍的严重程度。关于脑保护的新信息也将应用于所有缺血性脑综合征，包括中风。

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.