Neurology -- Correspondence for Woodruff et al., 60 (10) 1690-1692

Correspondence published:

Cardiac troponin levels following monitored epileptic seizures: Claudia Stollberger, Joseph Finsterer (19 August 2003)

Cardiac troponin levels following monitored epileptic seizures 19 August 2003

Claudia Stollberger,
Krankenanstalt Rudolfstiftung
Steingasse 31/18, A-1030, Wien, Austria,
Joseph Finsterer
Send Correspondence to journal:
Re: Cardiac troponin levels following monitored epileptic seizures

claudia.stoellberger{at}chello.at Claudia Stollberger, et al.

The most probable mechanism of sudden unexplained death in epilepsy patients (SUDEP) is arrhythmia, induced by myocardial injury, vegetative imbalance, arrhythmogenic side effects of antiepileptic drugs or a combined genetic defect leading to epilepsia and arrhythmia [1]. To assess if myocardial injury occurs during seizures, Woodruff et al. measured cardiac troponin T(cTnT) and I (cTnI) levels in 11 patients before and after monitored seizures [2]. No elevations in cTnT occurred, but in two patients pre-ictal elevations of cTnI were detected. They conclude that 1) myocardial injury does not occur during uncomplicated seizures and 2) in patients with post-ictal troponin elevations a primary cardiac disease should be searched.
These findings raise several concerns: 1) The seizures were relatively short and lead only to moderate tachycardia. Perhaps myocardial injury occurs only in more severe and prolonged seizures. This assumption is substantiated by findings which show that long seizure duration increases the occurrence of electrocardiographic abnormalities [3]. 2) The mean age of the investigated patients was only 34 years. Since the prevalence of cardiovascular diseases increases with age, myocardial damage may occur only in elderly patients. Did the patients undergo a clinical cardiologic investigation? What was the prevalence of cardiovascular risk factors? 3) To explain the lack of troponin elevation it would be useful to know if the patients were under a therapy of beta-blockers. Perioperative myocardial damage may be prevented by beta-blockers [4]. Assuming that this protective effect acts also in seizures, which are associated with excess catecholamine release, beta-blockers might have prevented myocardial damage. 4) Myocardial damage does not necessarily lead to troponin elevations. It may also lead to cardiac dysfunction [5]. Did the patients undergo echocardiography? 5) Assuming SUDEP to be due to arrhythmia, it would be interesting to know whether 24-hour Holter monitoring had been performed and whether the patients showed any electrocardiographic abnormalities. 6) Which explanation do the authors have for the elevated cTnI levels in the two patients? Why was only cTnI elevated and not cTnT? Had they suffered from seizures in the days before? 7) How many patients were on antiepileptic drugs and at which dosage? To clarify the etiology of SUDEP and to answer open questions regarding cardiac implications, more extensive cardiological investigations have to be carried out in epilepsy patients with different ages and types of seizures.
References
1. Ptacek LJ. Channelopathies: ion channel disorders of muscle as a paradigm for paroxysmal disorders of the nervous system. Neuromuscul Disord 1997;7:250-255.
2. Woodruff BK, Britton JW, Tigaran S et al. Cardiac troponin levels following monitored epileptic seizures. Neurology 2003;60:1690-1692.
3. Zijlmans M, Flanagan D, Gotman J. Heart rate changes and ECG abnormalities during epileptic seizures: prevalence and definition of an objective clinical sign. Epilesia 2003;43:847-854.
4. Auerbach AD, Goldman L. Beta-Blockers and reduction of cardiac events in noncardiac surgery: scientific review. JAMA 2002;287:1435-1444.
5. Deibert E, Barzilai B, Braverman AC et al. Clinical significance of elevated troponin I levels in patients with nontraumatic subarachnoid hemorrhage. J Neurosurg 2003;98:741-746.