Evidence map›Paper›PMID 29023958›Full record

ArticleAnnals of neurology2017

Stroke-induced chronic systolic dysfunction driven by sympathetic overactivity.

Michael Bieber, Rudolf A Werner, Edit Tanai, Ulrich Hofmann, Takahiro Higuchi, Kai Schuh, Peter U Heuschmann, Stefan Frantz, Oliver Ritter, Peter Kraft and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
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  5. Role of beta-blocker therapy on the sympathetic effects in stroke heart syndrome.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
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  8. Can Acute Neurological Disease Cause Cardiomyopathy in Horses?Animals : an open access journal from MDPI · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 3 countries.

Michael BieberDepartment of Neurology, University Hospital Würzburg, Würzburg, Germany.
Rudolf A WernerComprehensive Heart Failure Center Würzburg, Würzburg, Germany.
Edit TanaiComprehensive Heart Failure Center Würzburg, Würzburg, Germany.
Ulrich HofmannMedical Clinic and Policlinic III, University Hospital of Halle (Saale), Halle (Saale), Germany.
Takahiro HiguchiComprehensive Heart Failure Center Würzburg, Würzburg, Germany.
Kai SchuhInstitute of Physiology, University of Würzburg, Würzburg, Germany.
Peter U HeuschmannComprehensive Heart Failure Center Würzburg, Würzburg, Germany.
Stefan FrantzComprehensive Heart Failure Center Würzburg, Würzburg, Germany.
Oliver RitterComprehensive Heart Failure Center Würzburg, Würzburg, Germany.
Peter KraftDepartment of Neurology, University Hospital Würzburg, Würzburg, Germany.
Christoph KleinschnitzDepartment of Neurology, University Hospital Würzburg, Würzburg, Germany.
Comprehensive Cancer Center Mainfranken · DEUniversitätsklinikum Würzburg · DEUniversity Hospital in Halle · DEUniversity of Würzburg · DEEssen University Hospital · DENational Cerebral and Cardiovascular Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveCardiac diseases are established risk factors for ischemic stroke incidence and severity. Conversely, there is increasing evidence that brain ischemia can cause cardiac dysfunction. The mechanisms underlying this neurogenic heart disease are incompletely understood. Although it is established that ischemic stroke is associated with cardiac arrhythmias, myocardial damage, elevated cardiac enzymes, and plasma catecholamines in the acute phase, nothing is known about the delayed consequences of ischemic stroke on cardiovascular function.

methodsTo determine the long-term cardiac consequences of a focal cerebral ischemia, we subjected young and aged mice to a 30-minute transient middle cerebral artery occlusion and analyzed cardiac function by serial transthoracic echocardiography and hemodynamic measurements up to week 8 after surgery. Finally, animals were treated with metoprolol to evaluate a pharmacologic treatment option to prevent the development of heart failure.

resultsFocal cerebral ischemia induced a long-term cardiac dysfunction with a reduction in left ventricular ejection fraction and an increase in left ventricular volumes; this development was associated with higher peripheral sympathetic activity. Metoprolol treatment prevented the development of chronic cardiac dysfunction by decelerating extracellular cardiac remodeling and inhibiting sympathetic signaling relevant to chronic autonomic dysfunction.

interpretationFocal cerebral ischemia in mice leads to the development of chronic systolic dysfunction driven by increased sympathetic activity. If these results can be confirmed in a clinical setting, treating physicians should be attentive to clinical signs of heart failure in every patient after ischemic stroke. Therapeutically, the successful β-blockade with metoprolol in mice could also have future clinical implications. Ann Neurol 2017;82:729-743.

Indexed as

Adrenergic beta-1 Receptor AntagonistsAnimalsBrain IschemiaEchocardiographyEpinephrineHeart FailureHemodynamicsHydrocortisoneInfarction, Middle Cerebral ArteryMaleMetoprololMiceNatriuretic Peptide, BrainNorepinephrineStrokeSympathetic Nervous SystemAdrenergic beta-1 Receptor AntagonistsEpinephrineHydrocortisoneMetoprololNatriuretic Peptide, BrainNorepinephrine

Identifiers

PMID29023958
PMCPMC5765487
OpenAlexW2762882182

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.