OBJECTIVE: Cerebral hypoperfusion is common in heart failure (HF) and believed to underlie poor neurocognitive outcomes in this population. Up to 42% of HF patients also exhibit depressive symptomatology that may stem from reduced cerebral blood flow. However, no study has examined this possibility or whether reduced brain perfusion increases risk for future cognitive dysfunction in older adults with HF. METHODS: One hundred HF patients underwent transcranial Doppler ultrasonagraphy to quantify global cerebral blood flow velocity (CBF-V) and were administered a cognitive test battery to assess global cognition, attention/executive function, and memory abilities. All participants then completed the Beck Depression Inventory-II to assess depressive symptomatology. These procedures were performed at baseline and at 12-month follow-up. RESULTS: Repeated measures revealed that CBF-V declined over the 12-month period. Regression analyses showed that reduced baseline CBF-V predicted worse performances in attention/executive function (p < 0.05 for all) and a trend for memory (p = 0.09) in addition to greater depressive symptomatology (p < 0.05) at the 12-month follow-up, even after controlling for baseline factors and medical and demographic variables. CONCLUSIONS: Cerebral perfusion declined over time and was associated with poorer cognitive function and greater depressive symptoms at a 1-year follow-up in HF. Prospective studies with long-term follow-ups that employ neuroimaging are needed to examine whether cognitive dysfunction and depression in HF stem from the adverse effects of cerebral hypoperfusion on the cerebral structure.
OBJECTIVE:Cerebral hypoperfusion is common in heart failure (HF) and believed to underlie poor neurocognitive outcomes in this population. Up to 42% of HF patients also exhibit depressive symptomatology that may stem from reduced cerebral blood flow. However, no study has examined this possibility or whether reduced brain perfusion increases risk for future cognitive dysfunction in older adults with HF. METHODS: One hundred HF patients underwent transcranial Doppler ultrasonagraphy to quantify global cerebral blood flow velocity (CBF-V) and were administered a cognitive test battery to assess global cognition, attention/executive function, and memory abilities. All participants then completed the Beck Depression Inventory-II to assess depressive symptomatology. These procedures were performed at baseline and at 12-month follow-up. RESULTS: Repeated measures revealed that CBF-V declined over the 12-month period. Regression analyses showed that reduced baseline CBF-V predicted worse performances in attention/executive function (p < 0.05 for all) and a trend for memory (p = 0.09) in addition to greater depressive symptomatology (p < 0.05) at the 12-month follow-up, even after controlling for baseline factors and medical and demographic variables. CONCLUSIONS: Cerebral perfusion declined over time and was associated with poorer cognitive function and greater depressive symptoms at a 1-year follow-up in HF. Prospective studies with long-term follow-ups that employ neuroimaging are needed to examine whether cognitive dysfunction and depression in HF stem from the adverse effects of cerebral hypoperfusion on the cerebral structure.
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