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Cardiomyocyte Injury Following Acute Ischemic Stroke: Protocol for a Prospective Observational Cohort Study
Helena Stengl1,2,3, Ramanan Ganeshan1,2, Simon Hellwig1,2
1Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Insights
Elevated cardiac troponin after ischemic stroke indicates heart injury, often due to autonomic dysfunction, not coronary syndrome. This study investigates the stroke-heart connection to improve patient risk recognition and care.
Area of Science:
- Cardiology
- Neurology
- Biomedical Engineering
Background:
- Elevated cardiac troponin is common after acute ischemic stroke, indicating cardiomyocyte injury and poor outcomes.
- The mechanism is often neurogenic (stroke-heart syndrome) rather than acute coronary syndrome.
- Understanding the central autonomic network's role in stroke-associated myocardial injury is crucial.
Purpose of the Study:
- To quantify autonomic dysfunction in acute ischemic stroke patients.
- To identify downstream cardiac mechanisms causing myocardial injury post-stroke.
- To explore the stroke-heart syndrome pathophysiology.
Main Methods:
- Prospective, observational cohort study of 300 acute ischemic stroke patients.
- Classification into no, chronic, or acute myocardial injury groups based on troponin levels.
- Utilized cardiovascular MRI, echocardiography, and electrocardiogram for cardiac assessment; biobanking and 12-month follow-up for cardiovascular events.
Main Results:
- Pilot phase completed; recruitment of 300 patients with full cardiovascular MRI protocol estimated over 3 years.
- Study aims to provide detailed mechanistic insights into stroke-associated myocardial injury.
- Data collection ongoing to analyze autonomic dysfunction and cardiac mechanisms.
Conclusions:
- Stroke-associated myocardial injury is a significant complication requiring further investigation.
- This research aims to enhance understanding of heart-brain interactions post-stroke.
- Findings may inform risk stratification algorithms and refine diagnostic/therapeutic strategies.
Background:
Elevated 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.
Objective:
The 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.
Methods:
In 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.
Results:
After 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.
Conclusions:
Stroke-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 Registration:
Clinicaltrials.gov NCT03892226; https://www.clinicaltrials.gov/ct2/show/NCT03892226.
International Registered Report Identifier (Irrid):
DERR1-10.2196/24186.
