Dynamics of cerebral blood flow in patients with mild non‐ischaemic heart failure

Erkelens, Christian D.; Wal, Haye H. van der; Jong, Bauke M. de; Elting, JW; Renken, Remco; Gerritsen, M; Laar, Peter Jan van; Deursen, Vincent M. van; Meer, Peter van der; Veldhuisen, Dirk J. van; Voors, Adriaan A.; Luijckx, Gert-Jan

doi:10.1002/ejhf.660

Cited by 33 publications

(36 citation statements)

References 45 publications

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“…The accumulation of such brain injury can directly contribute to pathogenesis of autonomic and other dysfunctions in HF . Mild non‐ischaemic HF patients showed significant changes in basilar inflow volume, cerebral autoregulation and vasomotor reactivity, although the small sample size precluded CBF to reach significant levels …”

Section: Discussionmentioning

confidence: 99%

Reduced regional cerebral blood flow in patients with heart failure

Roy

Woo

Wang

et al. 2017

European J of Heart Fail

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Aim Heart failure (HF) patients show significant lateralized neural injury, accompanied by autonomic, mood, and cognitive deficits. Both gray and white matter damage appears, and likely develops from altered cerebral blood flow (CBF), a consequence of impaired cardiac output. However, the distribution of regional CBF changes in HF patients is unknown, but is an issue in determining mechanisms of neural injury. Our aim was to examine regional CBF changes in HF over control subjects using non-invasive pseudo-continuous arterial spin labeling (pCASL) procedures. Methods and results We collected pCASL data from 19 HF (age, 55.5±9.1 years; body-mass-index, 27.7±5.3 kg/m2; 13 male) and 29 control subjects (51.4±5.3 years; 25.7±3.6 kg/m2; 18 male), using a 3.0-Tesla-MRI scanner. Whole-brain CBF maps were calculated, normalized to a common space, smoothed, and compared between groups using ANCOVA (covariates; age, gender, and gray matter volume). Reduced CBF appeared in multiple sites in HF over controls, with principally-lateralized lower flow in temporal, parietal, and occipital regions. Areas with decreased CBF included the bilateral pre-frontal, frontal, temporal and occipital cortex, thalamus, cerebellum, corona radiate, corpus callosum, hippocampus, and amygdala. Conclusion HF subjects showed lower, and largely lateralized, CBF in multiple autonomic, mood, and cognitive regulatory sites. The reduced CBF likely contributes to the lateralized brain injury, leading to autonomic and neuropsychological deficits found in the condition.

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Section: Discussionmentioning

confidence: 99%

Reduced regional cerebral blood flow in patients with heart failure

Roy

Woo

Wang

et al. 2017

European J of Heart Fail

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“…Mice in these models develop VCI pathology due to global brain hypoperfusion and global reduction in cerebral blood flow (CBF). In turn, in humans, before the development of advanced HF as well as in HFpEF, global CBF remains unaltered in slowly progressing heart deterioration …”

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confidence: 99%

“…In turn, in humans, before the development of advanced HF as well as in HFpEF, global CBF remains unaltered in slowly progressing heart deterioration. 21,22 In this study we assessed (1) whether slowly progressing heart pathology-before the development of LV systolic dysfunction and end-stage HF-leads to VCI, and (2) what roles the 2 previously proposed major cardiac pathomechanisms-global cerebral hypoperfusion and prothrombotic condition-play in VCI development. We employed Tgaq*44 mice in which HF develops due to slowly progressing cardiomyopathy, which mimics human HF on a molecular, morphological, phenotypic, and functional level.…”

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confidence: 99%

Vascular Cognitive Impairment Linked to Brain Endothelium Inflammation in Early Stages of Heart Failure in Mice

Adamski

Sternak

Mohaissen

et al. 2018

JAHA

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BackgroundAlthough advanced heart failure (HF) is a clinically documented risk factor for vascular cognitive impairment, the occurrence and pathomechanisms of vascular cognitive impairment in early stages of HF are equivocal. Here, we characterize vascular cognitive impairment in the early stages of HF development and assess whether cerebral hypoperfusion or prothrombotic conditions are involved.Methods and ResultsTgαq*44 mice with slowly developing isolated HF triggered by cardiomyocyte‐specific overexpression of G‐αq*44 protein were studied before the end‐stage HF, at the ages of 3, 6, and 10 months: before left ventricle dysfunction; at the stage of early left ventricle diastolic dysfunction (with preserved ejection fraction); and left ventricle diastolic/systolic dysfunction, respectively. In 6‐ to 10‐month‐old but not in 3‐month‐old Tgαq*44 mice, behavioral and cognitive impairment was identified with compromised blood‐brain barrier permeability, most significantly in brain cortex, that was associated with myelin sheet loss and changes in astrocytes and microglia. Brain endothelial cells displayed increased E‐selectin immunoreactivity, which was accompanied by increased amyloid‐β1‐42 accumulation in piriform cortex and increased cortical oxidative stress (8‐OHdG immunoreactivity). Resting cerebral blood flow measured by magnetic resonance imaging in vivo was preserved, but ex vivo NO‐dependent cortical arteriole flow regulation was impaired. Platelet hyperreactivity was present in 3‐ to 10‐month‐old Tgαq*44 mice, but it was not associated with increased platelet‐dependent thrombogenicity.ConclusionsWe report for the first time that vascular cognitive impairment is already present in the early stage of HF development, even before left ventricle systolic dysfunction. The underlying pathomechanism, independent of brain hypoperfusion, involves preceding platelet hyperreactivity and brain endothelium inflammatory activation.

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“…The other notable finding of Erkelens et al's study was a reduced cerebral vasomotor reactivity when challenged by raised pCO 2 . While average arterial CO 2 is normal (or even reduced in CHF) the frequent Cheyne–Stokes pattern and very low frequency oscillations seen in CHF as described above, mean that the altered cerebral vasculature and brain tissue may be subject to regular oscillating low and high CO 2 and O 2 levels that may stress an already deficient cerebral autoregulatory system and worsen subtle brain changes in the longer term.…”

mentioning

confidence: 75%

“…Any attempt to understand disease interactions at the patient level and especially if involving different specialities and methodologies is to be welcomed. Thus, the paper by Erkelens and colleagues in this issue is particularly valuable. What does it show?…”

mentioning

confidence: 99%

Early abnormalities of cerebral blood flow in mild non‐ischaemic heart failure: part of a whole‐body response?

Coats

2017

European J of Heart Fail

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This article refers to 'Dynamics of cerebral blood flow in patients with mild non-ischaemic heart failure', by C.D. Erkelens et al., published in this issue on pages 261-268.Chronic heart failure (CHF) is a syndrome consisting of alterations of cardiac function associated with an array of abnormalities of haemodynamic, neuroendocrine, autonomic, and vascular function and frequently co-existing with abnormalities with other major organ systems. 1 It is common in the elderly and its risk factors are frequently the risk factors for other organ pathologies, including the kidneys, liver, lungs, and brain. For both these reasons, and because of the compensatory changes in the body in response to early cardiac dysfunction, clinically evident co-morbidities are common and are frequently clinically important in CHF. 2 -4 Some of the least well studied co-morbidities are those affecting the brain. A wide range of neurological and neuropsychological co-morbidities are associated with CHF, including autonomic, cerebral, cerebrovascular, cognitive, psychiatric, psychological, and neuromuscular. The scale and complexity of the potential interactions at disease and treatment levels are daunting, complicated sadly by the medical profession's tendency to micro-specialize and lose effective communication with other specialities in the management of our mutual patients. Any attempt to understand disease interactions at the patient level and especially if involving different specialities and methodologies is to be welcomed. Thus, the paper by Erkelens and colleagues in this issue 5 is particularly valuable. What does it show? The authors studied 15 relatively young patients with mild CHF of non-ischaemic aetiology matched to 15 healthy controls of a similar age. They found that global cerebral blood flow was normal at rest in their CHF population but with some regional reduction in basilar artery flow. They also showed evidence of altered cerebrovascular autoregulation and vasomotor reactivity in the cerebral vascular bed in the CHF patients. The strengths of the study were that the patients were carefully selected, excludingThe opinions expressed in this article are not necessarily those of the

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Dynamics of cerebral blood flow in patients with mild non‐ischaemic heart failure

Cited by 33 publications

References 45 publications

Reduced regional cerebral blood flow in patients with heart failure

Reduced regional cerebral blood flow in patients with heart failure

Vascular Cognitive Impairment Linked to Brain Endothelium Inflammation in Early Stages of Heart Failure in Mice

Early abnormalities of cerebral blood flow in mild non‐ischaemic heart failure: part of a whole‐body response?

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