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Blood markers of cardiac stress after generalized convulsive seizures
Robert D Nass1, Lukas J Motloch2, Vera Paar2
1Department of Epileptology, University Hospital Bonn, Bonn, Germany.
Insights
Generalized convulsive seizures (GCS) can strain the cardiovascular system, with sensitive biomarkers like high-sensitive troponin T (hsTNT) indicating cardiac stress in about 25% of patients, even without symptoms.
Area of Science:
- Cardiology
- Neurology
- Clinical Biochemistry
Background:
- Generalized convulsive seizures (GCS) place significant demands on the cardiovascular system, potentially leading to cardiac complications.
- Understanding cardiac stress markers post-GCS is crucial for patient management and risk stratification.
Purpose of the Study:
- To investigate the occurrence, influencing factors, and extent of cardiac stress or injury following GCS.
- To analyze the time course of novel cardiac blood markers after documented GCS.
Main Methods:
- Adult patients with refractory epilepsy undergoing video-EEG and ECG monitoring were included.
- Cardiac biomarkers (cTNI, hsTNT, NT-proBNP, copeptin, SST-2, GDF-15, suPAR, HFABP) and catecholamines were measured pre- and post-GCS.
- Peri-ictal cardiac parameters including heart rate (HR), HR variability (HRV), and corrected QT intervals (QTc) were assessed.
Main Results:
- Postictal catecholamine levels doubled, accompanied by increased HR, QTc, and decreased HRV.
- Elevated cardiac troponin I (cTNI) and high-sensitive troponin T (hsTNT) occurred in 10% and 26% of patients, respectively, correlating with higher dopamine levels.
- Copeptin increased significantly post-GCS, while suPAR remained unaltered; no cardiac symptoms were reported.
Conclusions:
- Sensitive biomarkers like hsTNT reveal cardiac stress in approximately 25% of GCS patients, often without overt clinical symptoms.
- suPAR may predict clinically significant troponin elevations, and copeptin warrants further investigation for GCS diagnosis specificity.
Objective:
Generalized convulsive seizures (GCS) are associated with high demands on the cardiovascular system, thereby facilitating cardiac complications. To investigate occurrence, influencing factors, and extent of cardiac stress or injury, the alterations and time course of the latest generation of cardiac blood markers were investigated after documented GCS.
Methods:
Adult patients with refractory epilepsy who underwent video-electroencephalography (EEG) monitoring along with simultaneous one-lead electrocardiography (ECG) recordings were included. Cardiac biomarkers (cardiac troponin I [cTNI]; high-sensitive troponin T [hsTNT]; N-terminal prohormone of brain natriuretic peptide [NT-proBNP]; copeptin; suppression of tumorigenicity-2 [SST-2]; growth differentiation factor 15, [GDF-15]; soluble urokinase plasminogen activator receptor [suPAR]; and heart-type fatty acid binding protein [HFABP]) and catecholamines were measured at inclusion and at different time points after GCS. Periictal cardiac properties were assessed by analyzing heart rate (HR), HR variability (HRV), and corrected QT intervals(QTc).
Results:
Thirty-six GCS (6 generalized-onset tonic-clonic seizures and 30 focal to bilateral tonic-clonic seizures) were recorded in 30 patients without a history of cardiac or renal disease. Postictal catecholamine levels were elevated more than twofold. A concomitant increase in HR and QTc, as well as a decrease in HRV, was observed. Elevations of cTNI and hsTNT were found in 3 of 30 patients (10%) and 6 of 23 patients (26%), respectively, which were associated with higher dopamine levels. Copeptin was increased considerably after most GCS, whereas SST-2, HFABP, and GDF-15 displayed only subtle variations, and suPAR was unaltered in the postictal period. Cardiac symptoms did not occur in any patient.
Significance:
The use of more sensitive biomarkers such as hsTNT suggests that signs of cardiac stress occur in about 25% of the patients with GCS without apparent clinical symptoms. SuPAR may indicate clinically relevant troponin elevations. Copeptin could help to diagnose GCS, but specificity needs to be tested.
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