Original articleClinicalSerum Levels of Cardiac Troponin I in Patients with Uncomplicated Epileptic Seizure
Introduction
Biochemical diagnosis of myocardial injury has been changed in the past decades, from elevation of total creatine kinase (CK) and its isoenzyme MB (CK-MB) 1, 2 towards elevation of subunits of the troponin complex in cardiac muscle including cardiac troponins I and T (cTnI, cTnT) 3, 4, 5. Cardiac troponins have been designated the preferred biomarker for the diagnosis of acute myocardial infarction (AMI) (6−8) because they have been shown to be highly sensitive and specific markers of acute myocardial injury 3, 4, 5. Moreover, total CK and CK-MB have been shown to be falsely elevated under many circumstances other than myocardial injury 2, 3. In cardiac ischemic situations, an increased cTn (I or T) above the 99th percentile of a normal reference cutoff is designated as indicative of myocardial infarction (MI) 6, 7, 8.
cTnI is a myofibrillar protein regulating the interaction of actin and myosin without calcium. Three isoforms have been isolated, slow and fast skeletal muscle and heart muscle isoforms. The cardiac form has 31 amino acids more than the skeletal forms. Blood concentrations increase 2–6 h after necrosis and only fall after 4–7 days (9) because >95% of cTnI is bound to the contractile apparatus 10, 11. The unique aspect of cTnI being 100% tissue specific for the heart makes it an excellent serum marker to serve as a biochemical tool for detecting myocardial injury and for differentiating patients who often show falsely increased CK-MB concentrations (12). CK-MB has been reported to be higher than normal in patients with chest trauma (13), cocaine-associated chest pain (14), critically ill patients in intensive care (15), muscle trauma and disease (3), renal disease (14), and electrical cardioversion (16). Presence of cTnT has been shown in patients with muscular dystrophy, polymyositis, and chronic renal disease 14, 17.
Epilepsy is one of the most common neurological disorders (18) and may present with seizures. In previous reports, cardiac troponins can be elevated in patients presenting with subacute or acute neurological disorders with or without seizures (19). On the other hand, arrhythmias and ischemic ECG changes have been reported after seizures; cardiac arrhythmia has also been proposed as a possible mechanism for sudden unexplained death in epilepsy patients (SUDEP) 20, 21, 22. Moreover, seizures can occur in the setting of cardiac arrhythmia and may even present as atypical anginal pain 3, 19, 23. Therefore, we would like to assess serum levels of cTnI in patients following uncomplicated epileptic seizures and with healthy cardiovascular systems.
Section snippets
Materials and Methods
This analytical cross-sectional study was conducted based on data gathered from epileptic patients and healthy subjects with normal cardiovascular systems referred to the emergency department and neurology clinic of Rasool-Akram Hospital of Tehran (affiliated with Iran University of Medical Sciences) in the year 2006. This study was accepted by the ethics committee of Iran University of Medical Sciences and all investigations were done in accordance with the criteria of the Declaration of
Results
In this study, 49 patients with uncomplicated seizures and normal cardiac system were evaluated. Of those, 34 cases (69.4%) were male and 15 cases (30.6%) were female. Mean age of patients was 21.18 years (standard deviation [SD] ±8.37), with a range of 15–62 years.
Demographic variables of patients are summarized in Table 1. Average time elapsed from the last epileptic seizure was 54 h (SD ±52.97) with a range of 8–216 h. Mean number of seizures was 3.45 (SD ±3.09); 17 patients (34.7%) had a
Discussion
Differentiating seizures from other conditions presenting with impairment of consciousness by clinical features alone is difficult (24). Seizures may occur in the setting of cardiac arrhythmia and may even present as atypical anginal pain (23). Therefore, elevations in cTn may be of special diagnostic value.
On the other hand, cardiac arrhythmia has been proposed as a possible mechanism for SUDEP (25). Poor seizure control, early age at seizure onset, and the presence of generalized tonic-clonic
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