Effects of Stroke on the Autonomic Nervous System

Dorrance, Anne M.; Fink, Greg D.

doi:10.1002/cphy.c140016

Cited by 89 publications

(67 citation statements)

References 214 publications

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“…Beta‐blocker has been part of the antihypertension treatment arsenal for many years, but meta‐analyses have shown they are less effective than other agents in primary and secondary stroke prevention. Yet, BB may confer a benefit in stroke by mitigating the acute hyper activation of the sympathetic nervous system, which has been associated with adverse cardiovascular and immune effects …”

Section: Discussionmentioning

confidence: 99%

“…Yet, BB may confer a benefit in stroke by mitigating the acute hyper activation of the sympathetic nervous system, which has been associated with adverse cardiovascular and immune effects. 22 Previous works addressed the relationship between survival and pre-stroke BB use, most of them using shorter follow-up periods. Two studies with a similar follow-up period showed results consistent with ours: Sykora and colleagues analyzed individual patient data from approximately 5200 ischemic stroke patients and found no difference in 3-month mortality by pre-stroke BB use.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pre admission treatment with Beta‐blockers in hypertensive patients with acute stroke and 3‐month outcome—Data from a national stroke registry

Eizenberg

Grossman

Tanné

et al. 2018

J of Clinical Hypertension

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Cerebrovascular disease is a leading cause of morbidity and mortality worldwide, 1 with hypertension being its most important modifiable risk factor. Landmark studies have shown that lowering blood pressure decreased rates of stroke incidence and mortality. 2 However, not all anti-hypertensive agents were found to be equally effective in preventing stroke. Comparative studies and meta-analyses have demonstrated that beta-blockers (BB) provide less protection against stroke compared with other anti-hypertensive agents. 3 On the other hand, stroke is associated with dysregulation of the autonomous nervous system with subsequent derangements of the cardiovascular, endocrine, and immune systems. Several studies have shown that pre-and on-stroke use of BB was associated with less severe stroke 4 and reduced mortality, 5-7 but results have been inconsistent. [8][9][10][11][12][13] In 2006 published data on the effect of pre-stroke treatment with BB on ischemic stroke severity, disability or death at discharge, and 1 month mortality. 16 The present study is aimed at exploring the effect of prestroke treatment with BB on ischemic stroke and intracerebral hemorrhage (ICH) outcomes 3 months after stroke. | METHODS | Study setting and participantsThe National Acute Stroke Israeli Survey (NASIS) registry is an ongo- The impact of beta-blockers (BB) treatment on stroke outcome is unclear. We used data from a prospective national stroke registry to assess the associations between use of BB and poor outcome 3 months after stroke. Using the National Acute StrokeIsraeli (NASIS) registry, we identified 1126 patients with ischemic stroke and intracerebral hemorrhage with pre-stroke hypertension treatment, who were followed for 3-months. Functional outcome and mortality at 3-month were compared by use of BB, adjusting for demographics and clinical factors. Pre-stroke use of BB was reported by 615 (54.6%) patients. Users of BB showed higher rates of atrial fibrillation, heart disease, statin use, cancer, and severe stroke. Adjusted odds-ratios (ORs, 95% CI) for BB users compared with non-users 3 months after stroke were 0.86 (0.49-1.52) for mortality and 1.07 (0.76-1.50) for Barthel Index ≤60. In conclusion, treatment with BB is not associated with 3-month poor outcome in hypertensive patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pre admission treatment with Beta‐blockers in hypertensive patients with acute stroke and 3‐month outcome—Data from a national stroke registry

Eizenberg

Grossman

Tanné

et al. 2018

J of Clinical Hypertension

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“…The mechanisms underlying the crosstalk between the acutely injured brain and the heart are not well understood at present. Current thinking is that cerebral ischaemia triggers an acute stress response that is mediated by the overactive sympathetic nervous system . However, the signalling pathways between the brain and the heart as well as the molecular downstream processes in the heart remain to be characterized.…”

Section: Introductionmentioning

confidence: 99%

Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction

Veltkamp

Uhlmann

Marinescu

et al. 2018

J cachexia sarcopenia muscle

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Background Stroke can lead to cardiac dysfunction in patients, but the mechanisms underlying the interaction between the injured brain and the heart are poorly understood. The objective of the study is to investigate the effects of experimental murine stroke on cardiac function and molecular signalling in the heart. Methods and results Mice were subjected to filament‐induced left middle cerebral artery occlusion for 30 or 60 min or sham surgery and underwent repetitive micro‐echocardiography. Left ventricular contractility was reduced early (24–72 h) but not late (2 months) after brain ischaemia. Cardiac dysfunction was accompanied by a release of high‐sensitive cardiac troponin (hsTNT (ng/ml): d1: 7.0 ± 1.0 vs. 25.0 ± 3.2*; d3: 7.3 ± 1.1 vs. 52.2 ± 16.7*; d14: 5.7 ± 0.8 vs. 5.2 ± 0.3; sham vs. 60 min. MCAO; mean ± SEM; * p < 0.05); reduced heart weight (heart weight/tibia length ratio: d1: 6.9 ± 0.2 vs. 6.4 ± 0.1*; d3: 6.7 ± 0.2 vs. 5.8 ± 0.1*; d14: 6.7 ± 0.2 vs. 6.4 ± 03; sham vs. 60 min. MCAO; mean ± SEM; * p < 0.05); resulting from cardiomyocyte atrophy (cardiomyocyte size: d1: 12.8% ± 0.002**; d3: 13.5% ± 0.002**; 14d: 6.3% ± 0.003*; 60 min. MCAO vs. sham; mean ± SEM; ** p < 0.01; * p < 0.05), accompanied by increased atrogin‐1 and the E3 ubiquitin ligase murf‐1. Net norepinephrine but not synthesis was increased, suggesting a reduced norepinephrine release or an increase of norepinephrine re‐uptake, resulting in a functional denervation. Transcriptome analysis in cardiac tissue identified the transcription factor peroxisome proliferator‐activated receptor gamma as a potential mediator of stroke‐induced transcriptional dysregulation involved in cardiac atrophy. Conclusions Stroke induces a complex molecular response in the heart muscle with immediate but transient cardiac atrophy and dysfunction.

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“…[20] The ischemic brain can act through the autonomic nervous system to have suppressive effect that can induce intercurrent infections and contribute to the morbidity and mortality after stroke. [21][22][23] Therefore, immune system-mediated inflammation is critically involved in determining the fate of the brain following ischemic stroke. [24][25][26] Understanding the mechanisms underlying role of neuroinflammation in ischemic stroke would provide important targets for the development of therapy in ischemic stroke.…”

Section: Introductionmentioning

confidence: 99%

Role of neuroinflammation in ischemic stroke

Li¹,

Pan²,

Tang³

et al. 2017

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Ischemic stroke causes the depletion of energy and induce excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Neuroinflammation occurs initially depending on activated resident microglia that has the same function as the macrophage. Activated microglia participates in the neuroinflammatory process by phagocytosing the injured brain cells and producing the pro-and anti-inflammatory mediators. In this review, the authors present an overview of the role of microglia in mediating neuroinflammation in ischemic stroke. Key words:Microglia, ischemic stroke, neuroinflammation ABSTRACT Topic: StrokeThis is an open access article distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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Effects of Stroke on the Autonomic Nervous System

Cited by 89 publications

References 214 publications

Pre admission treatment with Beta‐blockers in hypertensive patients with acute stroke and 3‐month outcome—Data from a national stroke registry

Pre admission treatment with Beta‐blockers in hypertensive patients with acute stroke and 3‐month outcome—Data from a national stroke registry

Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction

Role of neuroinflammation in ischemic stroke

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