Cardiac Troponin I elevation after epileptic seizure

Abstract

Background Cardiac troponin-I (cTNI) is highly specific biomarker to prove myocardial damage, e.g. in acute coronary syndrome (ACS). However, it occurs in other conditions as well. We therefore analysed cTNI increase in patients after generalized convulsive seizure. Methods Consecutive patients admitted with acute generalized convulsive seizure were included in case of cTNI measurement on admission. Among 898 selected cases, 53 patients were referred secondary to our department; in 845 cases cTNI measurements on admission were available. In case of multiple admissions (81 cases), only the first admission entered our analysis. In 17 patients elevated cTNI was determined due to ACS; in one patient a myocarditis was found. 5 patients suffered of relevant renal insufficiency. Finally 741 patients were included in the analysis. A cTNI cut-off level of ≥ 0.1 ng/ml was considered. Factors associated with a cTNI increase were analysed subsequently. Results The mean age of the study population (n = 741) was 47.8 years (SD ± 18.6), 40.9% were female. In 50 patients (6.7%) a cTNI elevation of unknown origin was found; no obvious cardiac involvement could be detected in these patients who all remained asymptomatic. A vascular risk profile (including at least hypertension, hypercholesterolemia or diabetes) (OR = 3.62; CI: 1.59 to 8.21; p = 0.001) and elevated creatine kinase on admission (OR = 2.36; CI: 1.26 to 4.39; p = 0.002) were independent factors associated with cTNI release. Conclusion cTNI release occurs in patients with generalized convulsive seizure with predominance in patients with vascular risk profile.

Who to target in sudden unexpected death in epilepsy prevention and how? Risk factors, biomarkers, and intervention study designs

“…Whereas the onset of transitory periictal repolarization abnormalities is most likely due to differential activation of specific brain regions and seizure‐related complications (including hypoxemia, hypercapnia, hyperkalemia, acidosis, and massive catecholamine‐release), the origin of interictal repolarization abnormalities remains to be elucidated. Because frequent GTCS is an established risk factor for SUDEP, it is tempting to speculate that a critical number of recurrent GTCS induce multiple subtle cardiac microinjuries with subsequent multifocal fibrotic changes over time, which, in turn, persistently disturb cardiac repolarization properties . Gene mutations or genetic variants linked to cardiac arrhythmias, such as long or short QT syndrome and catecholaminergic polymorphic ventricular tachycardia, may also perturb cardiac repolarization in a subgroup of patients …”

The role of cardiac troponin I in prognostication of patients with isolated severe traumatic brain injury

“…Neurocardiac axis has been well-defined in various non-traumatic head injuries including subarachnoid hemorrhage (SAH), (11–15) acute stroke, (16,17) intracerebral hemorrhage, (18,19) seizure, (20) and Guillain-Barre syndrome. (21) Increased risks of complications and mortality are found to be associated with a classic triad of transient left ventricular wall motion abnormality, electrocardiography changes, and elevation in cardiac enzymes in the absence of coronary artery disease.…”

Diagnostic Performance of High-Sensitive Troponin T in Patients With Renal Insufficiency

“…Several conditions, such as acute pulmonary embolism, peri-or myocarditis, acute heart failure, strenuous exercise, cardioverter-defibrillator shocks, cardiac amyloidosis, blunt chest trauma, epileptic seizures, and rhabdomyolysis, have been described to be associated with increased levels of troponins without the presence of ACS. 1,2 Additionally, increased cardiac troponin levels have been described in patients with renal insufficiency. 3,4 These findings led to a discussion in the medical community about how to interpret elevated high-sensitive troponin levels in patients with impaired renal function.…”