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The Bern heart and brain interaction study (BEHABIS) - Interaction between brain and heart in acute ischemic stroke

English title The Bern heart and brain interaction study (BEHABIS) - Interaction between brain and heart in acute ischemic stroke
Applicant Jung Simon
Number 172793
Funding scheme Project funding (Div. I-III)
Research institution Universitätsklinik für Neurologie Inselspital Universität Bern
Institution of higher education University of Berne - BE
Main discipline Neurology, Psychiatry
Start/End 01.03.2018 - 31.10.2021
Approved amount 362'250.00
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All Disciplines (2)

Discipline
Neurology, Psychiatry
Clinical Cardiovascular Research

Keywords (4)

Troponin; Stroke; Myocardial Infarction; Neurogenic Stunned Myocardium

Lay Summary (German)

Lead
Schlaganfälle können durch einen Herzinfarkt (HI)entstehen, aber Schlaganfälle können auch das Herz durch die Entstehung von neurogen induzierten Veränderungen am Herzmuskel beeinträchtigen (Stresskardiomyopathie, SKM). Diese Veränderungen können sich in Form einer Enzymfreisetzung, EKG Veränderungen oder Rhythmusstörungen, Wandbewegungsstörungen oder als Herzinsuffizienz äussern. Die Differenzierung von SKM und HI bei Schlaganfallpatienten ist relevant, aber schwierig, da beide möglichen Ursachen ähnliche Veränderungen im EKG und Ultraschall bedingen können. Wir gehen davon aus, dass SKM und HI derzeit unterdiagnostiziert werden und neue Mittel zur Diagnosestellung notwendig sind.
Lay summary

INHALT UND ZIELE DES FORSCHUNGSPROJEKTS

Die Ziele des Projekts sind die Bestimmung der Häufigkeit und Schwere von SKM und HI bei 220 Schlaganfallpatienten durch Herz-MRI und Herzkatheter. Dabei sollen Hirnregionen und Blutmarkern identifiziert werden, die mit der Entstehung von SKM assoziiert sind, um schlussendlich einen Entscheidungspfad zur Unterscheidung von SKM und HI zu entwickeln.

INHALTLICHER UND GESELLSCHAFTLICHER KONTEXT DES FORSCHUNGSPROJEKTS

Diese Studie wird neue Einblicke in die Pathophysiologie und klinische Relevanz von SKM bei Schlaganfallpatienten geben. Das Projekt eröffnet die Chance, Faktoren zur Differenzierung von SKM und HI zu identifizieren und einen Entscheidungspfad zur Diagnosestellung zu entwickeln. Diese Entwicklung hätte weitreichende Konsequenzen für die Behandlung von Schlaganfallpatienten.

Direct link to Lay Summary Last update: 03.04.2017

Responsible applicant and co-applicants

Employees

Project partner

Associated projects

Number Title Start Funding scheme
170060 Stroke treatment goes personalized: Gaining added diagnostic yield by computer-assisted treatment selection (the STRAY-CATS project) 01.10.2017 Project funding (Div. I-III)

Abstract

Background: Ischemic stroke can result from thromboembolism induced by myocardial infarction (MI), but stroke can also affect the heart by inducing neurogenic stunned myocardium (NSM). NSM can be expressed as myocardial enzyme release, electrocardiographic (ECG) changes and arrhythmias, wall motion abnormalities or in its most extensive form as transient apical ballooning. High sensitive Troponin T (hsTnT) is elevated in every fifth ischemic stroke patient. Distinguishing NSM from MI in stroke patients with elevated hsTnT is clinically highly relevant but challenging because both conditions share similar ECG changes and echocardiographic abnormalities. In addition stroke with NSM is thought to be associated with worse outcome. Little is known about the mechanism leading to NSM. Stroke in some brain areas like the insular are thought to be more prone to induce NSM and sometimes MI is misdiagnosed as NSM. Working Hypothesis: We postulate that the combination of laboratory, clinical, radiological, echocardiographic and electrophysiological assessments in a predictive score can distinguish MI/myocardial ischemia and NSM in stroke patients (MI/myocardial ischemia and NSM defined by CMR and coronary angiography). Specific aims: 1) To assess the prevalence of NSM, MI, and high grade coronary stenosis in stroke patients with elevated hsTnT and the prevalence of transient wall motion abnormalities in patients with normal hsTnT values; 2) to identify cardiac morphological changes (as measured by transesophageal echocardiography), brain areas (as measured by brain MR), blood biomarkers (as measured by metabolomics, hsTnT development, CK-MB, myoglobin, NT-proBNP, D-Dimer, hsCRP), ECG changes (as measured by ECG, 7-day continuous ECG) and clinical parameters (like NIHSS, patient history) with high predictive value for MI/myocardial ischemia and NSM; 3) to develop a predictive score and diagnostic algorithm able to distinguish MI and NSM by combination of factors that have been found to be associated with NSM/MI; 4) to assess the severity of NSM and its rhythmogenic and clinical relevance (as measured by ECG, 7-day continuous ECG, CMR); 5) to gain new insights into the pathogenesis of NSM in ischemic strokeExperimental design/Methods: We will include 220 acute stroke patients (180 with and 40 without hsTnT elevations). hsTnT will be measured at admission, and after 6h, 24h, 36h and 48h and ECG will be recorded on admission, and after 24h and 48h. Brain infarct size and location will be assessed by brain MRI at baseline. All patients will undergo a short protocol CMR study at admission immediately after brain MRI and all patients except those with MI an additional standard CMR protocol including adenosine stress perfusion imaging after 36-72 hours. Transesophageal echocardiography will be performed. ECG and blood pressure will be recorded for 7 respectively 4 days. Patients with evidence of acute or subacute MI or myocardial ischemia on CMR or highly suspicious clinical or ECG signs for MI will undergo coronary angiography as early as possible. Metabolites profile of blood samples will be compared between patients with NSM and MI for known biomarkers and for potential new biomarkers using non-targeted metabolomics. Expected value of the proposed project: The project offers the chance to improve the identification of patients with MI or significant coronary sclerosis who should undergo coronary angiography and treatment. We postulate that most of these patients are not identified by current practice but an early identification of these patients is necessary for early treatment and prevention of cardiac events. In addition, the project offers the chance to improve the identification of patients with NSM and to deliver information on clinical relevance of NSM including arrhythmias and wall motion abnormalities. Given the negative association of NSM with outcome after stroke, the identification of NSM patients is the necessary condition for a treatment trial. Beta-blockers could for instance be beneficial for stroke patients with NSM and such a project could have far-reaching consequences on the management of many acute stroke patients in the near future.
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