Cardiac dysfunction and high-sensitive C-reactive protein are associated with troponin T elevation in ischemic
Felipe A Montellano1,2,3,4, Elisabeth J Kluter5, Viktoria Rücker5
1Institute of Clinical Epidemiology and Biometry, University of Würzburg, Würzburg, Germany. Montellano_f@ukw.de.
Insights
Troponin elevation in ischemic stroke patients is linked to cardiac dysfunction and inflammation, not autonomic dysfunction indicated by heart rate variability. These findings help understand cardiac injury mechanisms in stroke survivors.
Area of Science:
- Cardiology
- Neurology
- Biochemistry
Background:
- Troponin elevation is frequent in ischemic stroke (IS) patients, with unclear causes.
- Potential mechanisms include coronary and non-coronary factors like autonomic dysfunction.
- Heart rate variability (HRV) is used to assess autonomic function.
Purpose of the Study:
- To investigate determinants of troponin elevation in acute IS patients.
- To explore the role of autonomic dysfunction markers (HRV) in troponin elevation.
- To identify factors associated with elevated high-sensitive troponin T (hs-TnT) levels.
Main Methods:
- The study analyzed data from 543 IS patients in the Stroke Induced Cardiac FAILure (SICFAIL) cohort.
- hs-TnT levels were measured, and HRV variables were calculated from Holter monitoring.
- Multivariable logistic regression identified independent determinants of hs-TnT ≥14 ng/L.
Main Results:
- 37% of IS patients had elevated hs-TnT (≥14 ng/L).
- Independent predictors included older age, male sex, reduced kidney function, systolic/diastolic dysfunction, atrial fibrillation, and elevated C-reactive protein.
- No independent association was found between troponin elevation and HRV variables.
Conclusions:
- Cardiac dysfunction and elevated C-reactive protein are associated with increased hs-TnT in IS patients.
- Reduced HRV, as a marker of autonomic dysfunction, was not independently associated with troponin elevation.
- Findings highlight cardiac and inflammatory factors over autonomic dysfunction in IS-related troponin elevation.
Background:
Troponin elevation is common in ischemic stroke (IS) patients. The pathomechanisms involved are incompletely understood and comprise coronary and non-coronary causes, e.g. autonomic dysfunction. We investigated determinants of troponin elevation in acute IS patients including markers of autonomic dysfunction, assessed by heart rate variability (HRV) time domain variables.
Methods:
Data were collected within the Stroke Induced Cardiac FAILure (SICFAIL) cohort study. IS patients admitted to the Department of Neurology, Würzburg University Hospital, underwent baseline investigation including cardiac history, physical examination, echocardiography, and blood sampling. Four HRV time domain variables were calculated in patients undergoing electrocardiographic Holter monitoring. Multivariable logistic regression with corresponding odds ratios (OR) and 95% confidence intervals (CI) was used to investigate the determinants of high-sensitive troponin T (hs-TnT) levels ≥14 ng/L.
Results:
We report results from 543 IS patients recruited between 01/2014-02/2017. Of those, 203 (37%) had hs-TnT ≥14 ng/L, which was independently associated with older age (OR per year 1.05; 95% CI 1.02-1.08), male sex (OR 2.65; 95% CI 1.54-4.58), decreasing estimated glomerular filtration rate (OR per 10 mL/min/1.73 m2 0.71; 95% CI 0.61-0.84), systolic dysfunction (OR 2.79; 95% CI 1.22-6.37), diastolic dysfunction (OR 2.29; 95% CI 1.29-4.02), atrial fibrillation (OR 2.30; 95% CI 1.25-4.23), and increasing levels of C-reactive protein (OR 1.48 per log unit; 95% CI 1.22-1.79). We did not identify an independent association of troponin elevation with the investigated HRV variables.
Conclusion:
Cardiac dysfunction and elevated C-reactive protein, but not a reduced HRV as surrogate of autonomic dysfunction, were associated with increased hs-TnT levels in IS patients independent of established cardiovascular risk factors. Registration-URL: https://www.drks.de/drks_web/; Unique identifier: DRKS00011615.
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