Myocardial injury in acute stroke: a troponin I study
Julio A Chalela1, Mustapha A Ezzeddine, Lisa Davis
1National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. chalelaj@ninds.nih.go
Insights
Elevated Troponin I (TI) occurred in 6% of acute stroke patients, associated with stroke severity. This may indicate cardiac ischemia or neurogenic injury, highlighting the complex relationship between stroke and myocardial damage.
Area of Science:
- Neurology
- Cardiology
- Biochemistry
Background:
- Acute cerebrovascular insults (strokes) can trigger cardiac abnormalities.
- Troponin I (TI) is a biomarker for myocardial damage.
- Understanding cardiac changes post-stroke is crucial for patient management.
Purpose of the Study:
- To investigate the incidence and characteristics of elevated Troponin I (TI) in patients experiencing acute stroke.
- To identify factors associated with TI elevation in this cohort.
- To explore the potential causes of TI elevation, including cardiac ischemia and neurogenic effects.
Main Methods:
- Retrospective case series analysis of 160 acute stroke patients with available TI levels.
- Data collection included demographics, stroke severity (NIHSS), stroke location, EKG, echocardiography, and cardiology evaluations.
- Logistic regression was used to identify variables linked to TI elevation.
Main Results:
- Elevated TI was observed in 6% (10/160) of patients.
- Higher National Institutes of Health Stroke Scale (NIHSS) scores were significantly associated with TI elevation (p=0.02).
- In most cases, TI elevation occurred without clear EKG or echocardiographic evidence of ischemia.
Conclusions:
- Elevated TI in acute stroke patients is relatively uncommon (6%) but linked to stroke severity.
- TI elevation may stem from coronary ischemia or, potentially, from neurogenic cardiac injury induced by the stroke.
- Further research is needed to differentiate the causes of TI elevation in stroke patients.
Introduction:
Acute cerebrovascular insults can induce a variety of cardiac changes. We sought to describe the findings in a cohort of patients who had an acute stroke in whom Troponin I (TI) was sampled to determine the presence of associated myocardial damage.
Materials And Methods:
This is a retrospective case series study. The investigators identified all patients who had an acute stroke in whom TI had been sampled. Demographics, stroke severity as determined by National Institutes of Health Stroke Scale (NIHSS), stroke location, electrocardiogram (EKG) results, echocardiography results, and cardiology evaluation were obtained from the stroke database or the medical records. Logistic regression analysis was performed to determine the clinical and paraclinical variables associated with TI elevation.
Results:
During a 14-month period, 191 patients were studied, but TI levels were available in only 160 (84%) of the 191 patients. The sample was composed of 89 (55%) men and 71 (45%) women, with a median age of 76 years. Elevated TI occurred in 10 (6%) of the 160 patients. EKG changes suggestive of cardiac ischemia occurred in 2 of the 10 patients with high TI who had a stroke. In the remainder patients' TI elevations occurred in the absence of EKG or echocardiographic abnormalities. High NIHSS but no other variable was associated with TI elevation (p=.02). Ventricular arrhythmias, congestive heart failure, post-infarct pericarditis, and sudden death did not occur.
Conclusion:
In this limited sample, elevated TI occurred in 6% of the patients with acute stroke and was associated with severe stroke. Although in some patients who have acute stroke, TI elevation may represent coronary ischemia, in others it may reflect neurogenic-induced cardiac injury.
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