Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke
Sung-Ho Ahn1, Young-Hak Kim2, Chol-Ho Shin3
1Department of Neurology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, Korea.
Insights
Troponin elevation in acute ischemic stroke patients is linked to specific cardiac and neurological factors. Understanding these predictors, like left ventricular hypertrophy and insular cortical lesions, is key for better patient management.
Area of Science:
- Cardiology
- Neurology
- Biomarkers
Background:
- Troponin elevation and ECG changes are common in acute ischemic stroke.
- The cause is debated: cardiac issues or neurally mediated myocytic damage.
- Predictors of troponin elevation require investigation.
Purpose of the Study:
- To identify cardiac and neurological predictors of troponin elevation in acute ischemic stroke patients.
- To differentiate between cardiac and neurological mechanisms of troponin elevation.
- To explore the relationship between stroke severity and cardiac biomarkers.
Main Methods:
- Retrospective analysis of prospectively registered ischemic stroke patients.
- Inclusion criteria: serum troponin I and ECG within 24 hours of symptom onset.
- Exclusion criteria: patients with known troponin-elevating comorbidities.
Main Results:
- 121 out of 1404 patients (8.7%) had elevated troponin I (>0.04 mg/mL).
- Cardiac predictors included QTc-prolongation, left ventricular hypertrophy, Q-waves, and ST elevation.
- Neurological predictors included higher NIH Stroke Scale score and insular cortical lesions.
Conclusions:
- Cardiac and neurological conditions contribute to troponin elevation in acute ischemic stroke.
- Cerebrogenic stress may induce cardiac vulnerability, explaining troponin elevation and ECG abnormalities.
- Combined cardiac and neurological factors increase troponin elevation and QTc-prolongation incidence.
Background:
Troponin elevation with electrocardiography changes is not uncommon in patients with acute ischemic stroke; however, it is still unclear whether the mechanism of these changes is due to cardiac problems or neurally mediated myocytic damage. Thus, we investigated cardiac and neurological predictors of troponin elevation in those patients.
Methods And Results:
We retrospectively analyzed medical data of the prospectively registered ischemic stroke patients on stroke registry who were admitted and underwent a serum cardiac troponin I and 12-lead electrocardiography within 24 hours of symptom onset. However, patients with well-known troponin-elevating comorbidities were excluded from the analysis. Among 1404 ischemic stroke patients, 121 (8.7%) had elevated troponin, which was defined as more than 0.04 mg/mL. Multivariable analysis identified electrocardiography abnormalities such as QTc-prolongation (odds ratio [OR]: 1.52, 95% CI: 1.02-2.28), left ventricular hypertrophy (OR: 2.14, 95% CI 1.43-3.19), Q-wave (OR: 2.53, 95% CI: 1.48-4.32), and ST elevation (OR: 2.74, 95% CI: 1.12-6.72) as cardiac variables associated with troponin elevation, and higher National Institutes of Health Stroke Scale score (OR: 1.04, 95% CI: 1.01-1.07) and insular cortical lesions (OR: 2.78, 95% CI: 1.85-4.19) as neurological variables associated with troponin elevation. Incidence of troponin elevation as well as QTc-prolongation was increased further in combination with cardiac and neurological factors.
Conclusions:
Certain cardiac and neurological conditions in acute ischemic stroke may contribute to troponin elevation. The proposed concept of cardiac vulnerability to cerebrogenic stress can be a practical interpretation of troponin elevation and electrocardiography abnormalities in stroke patients.
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