Structural brain alterations in heart failure: a review of the literature and implications for risk of Alzheimer’s disease

• Published in: Heart failure reviews Vol. 20; no. 5; pp. 561 - 571
• Main Authors: Alosco, Michael L., Hayes, Scott M.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-09-2015; Springer Nature B.V
• Subjects: Alzheimer Disease - epidemiology; Alzheimer Disease - pathology; Alzheimer Disease - physiopathology; Brain - pathology; Brain - physiopathology; Cardiology; Diffusion Tensor Imaging - methods; Heart Failure - epidemiology; Heart Failure - psychology; Humans; Magnetic Resonance Imaging - methods; Medicine; Medicine & Public Health; Neuropsychological Tests; Risk Assessment; Risk Factors; Heart failure; DTI; Alzheimer’s disease; MRI; Cerebrovascular disease; Medial temporal lobe
• ISSN: 1382-4147; 1573-7322
• DOI: 10.1007/s10741-015-9488-5

Cardiovascular disease is a recognized contributor to the pathogenesis of Alzheimer’s disease (AD). Heart failure (HF) is a cardiovascular subtype that can be used to model the contribution of cardiovascular disease to AD. Neuroimaging research indicates that HF patients exhibit a diverse range of structural brain alterations and epidemiological studies suggest HF may be an important risk factor for AD. The neural alterations observed in HF may overlap with those observed in AD and contribute to increased risk of AD in HF patients. To examine this possibility, we reviewed structural MRI studies in persons with HF. We examined subcortical brain regions affected in the early stages of AD (medial temporal lobes), as well as cortical alterations that typically occur in the later stages of AD. Our review indicates that patients with HF exhibit greater neural atrophy and white matter microstructural alterations of nearly every region of the Papez circuit (e.g., hippocampus, cingulate gyrus, thalamus, mammillary bodies, and fornix), as well-significant alterations in cortical and cerebellar regions. Based on animal research and past work in AD patients, the mechanisms for structural brain changes in HF may stem from reductions in cerebral blood flow subsequent to cardiac deficiency. This review supports the hypothesis that HF may contribute to AD risk via widespread structural brain changes, including many of the same regions affected by AD. Case-controlled prospective neuroimaging studies with long-term follow-ups are needed to clarify the risk of AD in HF and elucidate the neural underpinnings of AD risk in HF.