Cardiac output as a potential risk factor for abnormal brain aging.
Cardiac output as a potential risk factor for abnormal brain aging.
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DOI：
10.3233/jad-2010-100081
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Jefferson AL
中科院分区：
文献类型：
--
作者：
Jefferson AL
心力衰竭是一种临床有用的模型，可以用来了解心功能障碍与老年人神经解剖和神经心理变化的关系，理论上是因为全身低灌流扰乱了大脑灌流，导致了临床脑损伤。这篇综述综述了更多的最新数据，这些数据表明，在没有心力衰竭或严重心肌病的情况下，轻微的心功能障碍或较低的正常心功能水平与认知和神经成像标记物异常脑老化有关。还需要更多的工作，但这些关联表明，心输出量减少可能是阿尔茨海默病(AD)和通过神经血管过程的传播或恶化、血栓形成导致的微血栓和AD神经病理过程的异常脑老化的风险因素。这种机制途径是在一个理论模型的背景下讨论的，该模型假设心输出量和异常脑老化(即，全身血流量减少扰乱脑血流动态平衡)之间存在直接的损伤途径，从而导致临床脑损伤，而与心功能障碍和异常脑老化的共同危险因素无关。
Heart failure has served as a clinically useful model for understanding how cardiac dysfunction is associated with neuroanatomic and neuropsychological changes in aging adults, theoretically because systemic hypoperfusion disrupts cerebral perfusion, contributing to clinical brain injury. This review summarizes more recent data suggesting that subtle cardiac dysfunction or low normal levels of cardiac function, as quantified by cardiac output, are related to cognitive and neuroimaging markers of abnormal brain aging in the absence of heart failure or severe cardiomyopathy. Additional work is required, but such associations suggest that reduced cardiac output may be a risk factor for Alzheimer’s disease (AD) and abnormal brain aging through the propagation or exacerbation of neurovascular processes, microembolism due to thrombosis, and AD neuropathological processes. Such mechanistic pathways are discussed in the context of a theoretical model that posits a direct pathway of injury between cardiac output and abnormal brain aging (i.e., reduced systemic blood flow disrupts cerebral blood flow homeostasis), contributing to clinical brain injury, independent of shared risk factors for both cardiac dysfunction and abnormal brain aging.