Neuroimaging and Correlates of Cognitive Function among Patients with Heart Failure

Vogels, Raymond L.C.; Oosterman, Joukje M.; Harten, Barbera van; Gouw, Alida A.; Schroeder‐Tanka, Jutta M.; Scheltens, Philip; Flier, Wiesje M. van der; Weinstein, Henry C.

doi:10.1159/000109811

Cited by 91 publications

(92 citation statements)

References 62 publications

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“…131,132 Energy depletion is associated with decreased brain size, 133 and in patients with cardiac failure medial temporal lobe atrophy, but not T2 white matter hyperintensities, it is associated with hypotension 134 and impaired cognitive functioning. 135 Furthermore, in a large prospective study in patients with chronic obstructive pulmonary disease, hypoxemia was the only parameter associated with the occurrence of cognitive failure after multivariable regression analysis and treatment with supplemental oxygen decreased the risk 136 matching functional damage without structural lesions.…”

Section: Discussionmentioning

confidence: 99%

Ischemic Cerebral Damage

Hofmeijer¹,

Putten²

2012

Stroke

223

128

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Abstract-In the human brain, Ϸ30% of the energy is spent on synaptic transmission. Disappearance of synaptic activity is the earliest consequence of cerebral ischemia. The changes of synaptic function are generally assumed to be reversible and persistent damage is associated with membrane failure and neuronal death. However, there is overwhelming experimental evidence of isolated, but persistent, synaptic failure resulting from mild or moderate cerebral ischemia. Early failure results from presynaptic damage with impaired transmitter release. Proposed mechanisms include dysfunction of adenosine triphosphate-dependent calcium channels and a disturbed docking of glutamate-containing vesicles resulting from impaired phosphorylation. We review energy distribution among neuronal functions, focusing on energy usage of synaptic transmission. We summarize the effect of ischemia on neurotransmission and the evidence of long-lasting synaptic failure as a cause of persistent symptoms in patients with cerebral ischemia. Finally, we discuss the implications of synaptic failure in the diagnosis of cerebral ischemia, including the limited sensitivity of diffusion-weighted MRI in those cases in which damage is presumably limited to the synapses. (Stroke. 2012;43:607-615.)Key Words: brain metabolism Ⅲ cerebral ischemia Ⅲ synaptic failure T he human brain is metabolically expensive. Although it represents only 2% of the body weight, it accounts for 20% of oxygen consumption and 25% of glucose utilization. 1,2 Cerebral ischemia is a pathological condition in which blood flow to the brain is insufficient to meet these metabolic demands, causing a loss of neuronal function and viability. Ischemia may be focal if a brain artery is occluded or global, for example, after cardiac arrest.In the 1950s, the concept of perfusion thresholds was introduced. 3 It was shown that functional activity became impaired with moderately reduced perfusion (14 -35 mL/100 g/min), along with electroencephalographic and evoked potential disturbances, whereas loss of ion gradients across the plasma membrane and subsequent cell swelling occur at lower perfusion levels Ϸ4.8 to 8.4 mL/100 g/min (Figure 1). [3][4][5] In focal brain ischemia, the brain tissue that is perfused in the flow range between these 2 levels is now called the penumbra. 6 The penumbra is considered structurally intact and viable, but functionally silent. The dysfunction is, in principle, reversible by restoration of blood flow. However, if oxygen and glucose are not resupplied in time, irreversible damage occurs.Knowledge on the distribution of energy usage among different neuronal activities may contribute to understanding the successive loss of cell function and cell damage in cerebral ischemia. In the human brain, Ϸ30% of the energy is spent on synaptic transmission. 7 Disappearance of synaptic activity is the earliest consequence of cerebral ischemia 8 and failure of synaptic transmission has been proposed to account for electric silence in the penumbra. 3,6,8 -10 The changes of syna...

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Section: Discussionmentioning

confidence: 99%

Ischemic Cerebral Damage

Hofmeijer¹,

Putten²

2012

Stroke

223

128

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“…39 Cerebral abnormalities detected on magnetic resonance imaging and cognitive performance in HF patients have been reported. 40 For instance, medial temporal lobe atrophy was related to cognitive dysfunction, involving memory impairment and executive dysfunction, whereas total white matter hyperintensities were related to depression resulting in insomnia. 40 To date, there are no data on effective treatment for insomnia in HF patients.…”

Section: Discussionmentioning

confidence: 99%

“…40 For instance, medial temporal lobe atrophy was related to cognitive dysfunction, involving memory impairment and executive dysfunction, whereas total white matter hyperintensities were related to depression resulting in insomnia. 40 To date, there are no data on effective treatment for insomnia in HF patients. General behavioral measures for improved sleep hygiene, such as minimal use of caffeine, cigarettes and alcohol, maintaining a regular sleep schedule, going to bed only when sleepy, regular exercise, and avoiding daytime naps, should be explained to the patients.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Significance of Insomnia in Heart Failure

Kanno

Yoshihisa

Watanabe

et al. 2016

Circ J

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“…Pooled analysis of 22 case-control studies investigating cognitive function in CHF patients demonstrated an odds ratio of 1.62 (P < 0.0001) for cognitive impairment in patients with CHF [139]. Neuroimaging studies have shown evidence of structural alteration of brain associated with heart failure.…”

Section: Cognitive Dysfunctionmentioning

confidence: 99%

Management of Noncardiac Comorbidities in Chronic Heart Failure

Chong

Singh

Parry

et al. 2015

Cardiovascular Therapeutics

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SummaryPrevalence of heart failure is increasing, especially in the elderly population. Noncardiac comorbidities complicate heart failure care and are increasingly common in elderly patients with reduced or preserved ejection fraction heart failure, owing to prolongation of patient's lives by advances in chronic heart failure (CHF) management. Common comorbidities include respiratory disease, renal dysfunction, anemia, arthritis, obesity, diabetes mellitus, cognitive dysfunction, and depression. These conditions contribute to the progression of the disease and may alter the response to treatment, partly as polypharmacy is inevitable in these patients. Cardiologists and other physicians caring for patients with CHF need to be vigilant to comorbid conditions that complicate the care of these patients. There is now more guidance on management of noncardiac comorbidities in heart failure, and this article contains a comprehensive review of the most recent updates on management of noncardiac comorbidities in CHF.

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Neuroimaging and Correlates of Cognitive Function among Patients with Heart Failure

Cited by 91 publications

References 62 publications

Ischemic Cerebral Damage

Ischemic Cerebral Damage

Prognostic Significance of Insomnia in Heart Failure

Management of Noncardiac Comorbidities in Chronic Heart Failure

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