Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study

BackgroundElevated cardiac troponin, which indicates cardiomyocyte injury, is common after acute ischemic stroke and is associated with poor functional outcome. Myocardial injury is part of a broad spectrum of cardiac complications that may occur after acute ischemic stroke....

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Main Authors: Stengl, Helena, Ganeshan, Ramanan, Hellwig, Simon, Blaszczyk, Edyta, Fiebach, Jochen B, Nolte, Christian H, Bauer, Axel, Schulz-Menger, Jeanette, Endres, Matthias, Scheitz, Jan F
Format: Article
Language:English
Published: JMIR Publications 2021-02-01
Series:JMIR Research Protocols
Online Access:http://www.researchprotocols.org/2021/2/e24186/
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spelling doaj-f560e2ba5f3747a8a306f81c1c5d2e7e2021-05-03T02:52:32ZengJMIR PublicationsJMIR Research Protocols1929-07482021-02-01102e2418610.2196/24186Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort StudyStengl, HelenaGaneshan, RamananHellwig, SimonBlaszczyk, EdytaFiebach, Jochen BNolte, Christian HBauer, AxelSchulz-Menger, JeanetteEndres, MatthiasScheitz, Jan F BackgroundElevated cardiac troponin, which indicates cardiomyocyte injury, is common after acute ischemic stroke and is associated with poor functional outcome. Myocardial injury is part of a broad spectrum of cardiac complications that may occur after acute ischemic stroke. Previous studies have shown that in most patients, the underlying mechanism of stroke-associated myocardial injury may not be a concomitant acute coronary syndrome. Evidence from animal research and clinical and neuroimaging studies suggest that functional and structural alterations in the central autonomic network leading to stress-mediated neurocardiogenic injury may be a key underlying mechanism (ie, stroke-heart syndrome). However, the exact pathophysiological cascade remains unclear, and the diagnostic and therapeutic implications are unknown. ObjectiveThe aim of this CORONA-IS (Cardiomyocyte injury following Acute Ischemic Stroke) study is to quantify autonomic dysfunction and to decipher downstream cardiac mechanisms leading to myocardial injury after acute ischemic stroke. MethodsIn this prospective, observational, single-center cohort study, 300 patients with acute ischemic stroke, confirmed via cerebral magnetic resonance imaging (MRI) and presenting within 48 hours of symptom onset, will be recruited during in-hospital stay. On the basis of high-sensitivity cardiac troponin levels and corresponding to the fourth universal definition of myocardial infarction, 3 groups are defined (ie, no myocardial injury [no cardiac troponin elevation], chronic myocardial injury [stable elevation], and acute myocardial injury [dynamic rise/fall pattern]). Each group will include approximately 100 patients. Study patients will receive routine diagnostic care. In addition, they will receive 3 Tesla cardiovascular MRI and transthoracic echocardiography within 5 days of symptom onset to provide myocardial tissue characterization and assess cardiac function, 20-min high-resolution electrocardiogram for analysis of cardiac autonomic function, and extensive biobanking. A follow-up for cardiovascular events will be conducted 3 and 12 months after inclusion. ResultsAfter a 4-month pilot phase, recruitment began in April 2019. We estimate a recruitment period of approximately 3 years to include 300 patients with a complete cardiovascular MRI protocol. ConclusionsStroke-associated myocardial injury is a common and relevant complication. Our study has the potential to provide a better mechanistic understanding of heart and brain interactions in the setting of acute stroke. Thus, it is essential to develop algorithms for recognizing patients at risk and to refine diagnostic and therapeutic procedures. Trial RegistrationClinicaltrials.gov NCT03892226; https://www.clinicaltrials.gov/ct2/show/NCT03892226. International Registered Report Identifier (IRRID)DERR1-10.2196/24186http://www.researchprotocols.org/2021/2/e24186/
collection DOAJ
language English
format Article
sources DOAJ
author Stengl, Helena
Ganeshan, Ramanan
Hellwig, Simon
Blaszczyk, Edyta
Fiebach, Jochen B
Nolte, Christian H
Bauer, Axel
Schulz-Menger, Jeanette
Endres, Matthias
Scheitz, Jan F
spellingShingle Stengl, Helena
Ganeshan, Ramanan
Hellwig, Simon
Blaszczyk, Edyta
Fiebach, Jochen B
Nolte, Christian H
Bauer, Axel
Schulz-Menger, Jeanette
Endres, Matthias
Scheitz, Jan F
Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
JMIR Research Protocols
author_facet Stengl, Helena
Ganeshan, Ramanan
Hellwig, Simon
Blaszczyk, Edyta
Fiebach, Jochen B
Nolte, Christian H
Bauer, Axel
Schulz-Menger, Jeanette
Endres, Matthias
Scheitz, Jan F
author_sort Stengl, Helena
title Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
title_short Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
title_full Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
title_fullStr Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
title_full_unstemmed Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
title_sort cardiomyocyte injury following acute ischemic stroke: protocol for a prospective observational cohort study
publisher JMIR Publications
series JMIR Research Protocols
issn 1929-0748
publishDate 2021-02-01
description BackgroundElevated cardiac troponin, which indicates cardiomyocyte injury, is common after acute ischemic stroke and is associated with poor functional outcome. Myocardial injury is part of a broad spectrum of cardiac complications that may occur after acute ischemic stroke. Previous studies have shown that in most patients, the underlying mechanism of stroke-associated myocardial injury may not be a concomitant acute coronary syndrome. Evidence from animal research and clinical and neuroimaging studies suggest that functional and structural alterations in the central autonomic network leading to stress-mediated neurocardiogenic injury may be a key underlying mechanism (ie, stroke-heart syndrome). However, the exact pathophysiological cascade remains unclear, and the diagnostic and therapeutic implications are unknown. ObjectiveThe aim of this CORONA-IS (Cardiomyocyte injury following Acute Ischemic Stroke) study is to quantify autonomic dysfunction and to decipher downstream cardiac mechanisms leading to myocardial injury after acute ischemic stroke. MethodsIn this prospective, observational, single-center cohort study, 300 patients with acute ischemic stroke, confirmed via cerebral magnetic resonance imaging (MRI) and presenting within 48 hours of symptom onset, will be recruited during in-hospital stay. On the basis of high-sensitivity cardiac troponin levels and corresponding to the fourth universal definition of myocardial infarction, 3 groups are defined (ie, no myocardial injury [no cardiac troponin elevation], chronic myocardial injury [stable elevation], and acute myocardial injury [dynamic rise/fall pattern]). Each group will include approximately 100 patients. Study patients will receive routine diagnostic care. In addition, they will receive 3 Tesla cardiovascular MRI and transthoracic echocardiography within 5 days of symptom onset to provide myocardial tissue characterization and assess cardiac function, 20-min high-resolution electrocardiogram for analysis of cardiac autonomic function, and extensive biobanking. A follow-up for cardiovascular events will be conducted 3 and 12 months after inclusion. ResultsAfter a 4-month pilot phase, recruitment began in April 2019. We estimate a recruitment period of approximately 3 years to include 300 patients with a complete cardiovascular MRI protocol. ConclusionsStroke-associated myocardial injury is a common and relevant complication. Our study has the potential to provide a better mechanistic understanding of heart and brain interactions in the setting of acute stroke. Thus, it is essential to develop algorithms for recognizing patients at risk and to refine diagnostic and therapeutic procedures. Trial RegistrationClinicaltrials.gov NCT03892226; https://www.clinicaltrials.gov/ct2/show/NCT03892226. International Registered Report Identifier (IRRID)DERR1-10.2196/24186
url http://www.researchprotocols.org/2021/2/e24186/
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