Blood markers of cardiac stress after generalized convulsive seizures

Abstract

Summary 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.

Blood Pressure in Seizures and Epilepsy

“…Sympathetic outflow is commonly enhanced during seizures, as shown by elevated levels of circulating catecholamines (49, 50), increased HR, QT-shortening, elevated electrodermal activity or reduced HR variability (51, 52). About 80% of focal seizures go along with ictal sinus tachycardia (which increases CO), whilst cardiac arrhythmias such as atrial fibrillation or ventricular tachycardias are very rare (53).…”

“…For example, electrical stimulation of insular and thalamic areas as well as basal ganglia in humans can increase both BP and HR (27, 73). In addition, FS may also increase HR and BP through a release of catecholamines via stimulation of adrenergic receptors in heart and blood vessels (49, 50, 71). Surprisingly, a seizure-related decrease of BP was accompanied by an increase in HR in a subgroup of patients (Figure 2D) (70).…”

Plötzlicher, unerwarteter Tod bei Epilepsie

“…Ein geringerer Anteil ist jedoch auch pos-tiktual auftretenden, z. T. primären ventrikulären Arrhythmien zuzuschreiben, wie kleinere Fallserien belegen, teils auch im Kontext einer Takotsubo-Kardiomyopathie [33][34][35][36]. Klassischerweise führen epileptische Anfälle zu Sinustachykardien, was auf die vermehrte katecholaminerge Ausschüttung und Hypoxämie im Kontext vermehrter Muskelaktivität zurückzuführen ist [37,38]. Häufig finden sich hierbei auch potenziell arrhythmogene EKG-Veränderungen [39][40][41][42][43].…”

“…Diese können zu Synkopen mit Stürzen führen und per Herzschrittmacher behandelt werden [44,45]. In bis zu 25 % der GTKA/FBTKA und in bis zu 40 % der Status epileptici finden sich Troponinerhöhungen [38].…”

Directed Connectivity Analysis of the Neuro-Cardio- and Respiratory Systems Reveals Novel Biomarkers of Susceptibility to SUDEP

“…Seizures can impact the electrochemical coupling through the vagus and glossopharyngeal nerves, as well as metabolic and hormonal coupling linked by the vasculature [13]. In a study of cardiac stress biomarkers in epilepsy patients, significant increases (up to two-fold) in the levels of cardiac stress proteins (cardiac troponin I [cTNI]; high-sensitive troponin T [hsTNT]) were identified within 30 minutes following seizures [14]. Despite advances in identifying potential SUDEP mechanisms, validated and Technology quantitative risk factors and biomarkers of SUDEP susceptibility remain undetermined.…”