Cardiac output as a potential risk factor for abnormal brain aging.
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.
Jefferson
Angela L
AL
Department of Neurology, Alzheimer's Disease Center, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA. angelaj@bu.edu
D000375:Aging / Q000473:pathology*; D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology*; D001921:Brain / Q000503:physiopathology*; D002302:Cardiac Output / Q000502:physiology*; D006801:Humans; D012307:Risk Factors