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BRIEF COMMUNICATIONS: S. Tigaran, H. Mølgaard, R. McClelland, M. Dam, and A.S. Jaffe Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients Neurology 2003; 60: 492-495 [Abstract] [Full text] [PDF]

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Reply to Stollberger and Finsterer

Simona Tigaran, Allan S. Jaffe   (20 August 2003)

Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients

Claudia Stollberger, Joseph Finsterer   (20 August 2003)

Reply to Stollberger and Finsterer 20 August 2003
Simona Tigaran, Aarhus University Hospital Dept. of Neurosurgery, Aarhus University HospitalNorrebrogade 44, 8000 Aarhus C, Denmark, Allan S. Jaffe Send Correspondence to journal: Re: Reply to Stollberger and Finsterer mona{at}akhphd.au.dk Simona Tigaran, et al.	The answers to most of the questions raised by Dr. Stollberger and Finsterer are available by a close reading of the manuscript or our paper in Acta Neurologica Scandinavica Supplement : 2002; 177: 9-32, where methods that could not be included due to the word constraints imposed by the journal can be found. However, the comments question the veracity of the observations. We do not. We studied asymptomatic patients without a history of heart disease or medications for hypertension or cardiac conditions. These patients had a normal physical examination, normal EKGs at rest and negative stress tests to heart rates equivalent to or greater than those that occurred pre- and post- ictally. In cases considered equivocal, patients underwent coronary angiography. No significant coronary artery disease was found. Furthermore, the observed ST-segment changes met rigorous criteria in both Holter leads, during the ictal or post- ictal state, were not seen at other times and can be explained by reasonable pathophysiology. None of the patients complained of symptoms. No patient had more than one episode. Nonetheless, we agree that additional confirmation is needed for the observations and additional data would be helpful to explain potential mechanisms. We are pursuing such studies.
Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients 20 August 2003
Claudia Stollberger, Krankenanstalt Rudolfstiftung Steingasse 31/18 A -1030 Wien, Austria, Joseph Finsterer Send Correspondence to journal: Re: Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients claudia.stoellberger{at}chello.at Claudia Stollberger, et al.	Myocardial ischemia and arrhythmia are possible pathomechanisms for sudden unexplained death in epilepsy patients(SUDEP). To assess cardiovascular abnormalities in 23 patients with refractory epilepsy, Tigaran et al. performed noninvasive investigations (12-lead resting ECG, Holter-monitoring, echocardiography, ergometric exercise test, myocardial scintigraphy), and, if abnormalities were found, coronary angiography[1]. During video-EEG monitoring 125 seizures occurred. Holter-monitoring found that 40% (9/22) of patients had ST-segment depression during (n=1) or just after a seizure (n=8). The interpretation of the findings, that cardiac abnormalities during or after seizures potentially explain SUDEP, raises several questions: 1) ST-segment depression during Holter-monitoring with the used criterion (≥0.10 mV) is a rather unspecific finding, occurring in 11% of healthy men[2]. No details about the recording of Holter-monitoring and the number of leads are given, parameters which influence the rate of false positive findings[3]. 2) How many of the patients had cardiovascular symptoms or risk factors like arterial hypertension, diabetes or smoking? Did any of the patients take cardiovascular drugs? 3) Did the ST-segment depression occur repeatedly at each of the seizures or only once? Did ST-segment depression in these patients also occur without seizures? Were the ST-segment depressions associated with any cardiac symptoms or were they silent? Were there any patients without ST- segment depression who had a similar high heart rate like patients who developed ST-segment depression? 4) Were any other abnormalities detected during Holter-monitoring except for ST-segment depression, tachycardia and the complete heart block? 5) Since seizures associated with ST-segment depression occurred during sleep in 7/9 patients, did the authors consider decreased blood oxygen saturation as a potential mechanism for the abnormalities? Was oxygen saturation monitored? Did the authors consider other causes for ST-segment depression like changes in body posture[3]? 6) Was the heart rate during maximal exercise higher or lower than during the epileptic seizures? Was there an association between ST-segment depression at stress test or ischemic changes at scintigraphy and postictal ST-segment depression? 7)Which were the abnormal tests prompting coronary angiography in nine patients? Were these nine patients identical to the nine patients who developed ST-segment depression? Did they suffer from angina pectoris? Were tests for coronary vasospasms carried out? In view of the limited knowledge about incidence and pathogenesis of SUDEP, there is a need to evaluate all available data. Even if findings suggest some evidence for an arrhythmogenic cause of SUDEP, other causes like cerebral, respiratory or genetic factors should be considered. References 1. Tigaran S, Molgaard H, McClelland R, Dam M, Jaffe AS. Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients. Neurology 2003;60:492-495. 2. Vaage-Nilsen M, Rasmussen V, Sorum C, Jensen G. ST-segment deviation during 24-hour ambulatory electrocardiographic monitoring and exercise stress test in healthy male subjects 51 to 75 years of age. The Copenhagen City Heart Study. Am Heart J 1999;137:1070-1074. 3. Tzivoni D, Butnaru A. Diagnostic accuracy of ST changes detected by exercise testing and ambulatory electrocardiographic monitoring in apparently healthy individuals. Am Heart J 1999;137:996-999.