Ictal Asystole
2015; Lippincott Williams & Wilkins; Volume: 8; Issue: 1 Linguagem: Inglês
10.1161/circep.114.002546
ISSN1941-3149
AutoresDavid G. Benditt, Gert van Dijk, Roland D. Thijs,
Tópico(s)Sympathectomy and Hyperhidrosis Treatments
ResumoHomeCirculation: Arrhythmia and ElectrophysiologyVol. 8, No. 1Ictal Asystole Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessEditorialPDF/EPUBIctal AsystoleLife-Threatening Vagal Storm or a Benign Seizure Self-Termination Mechanism? David G. Benditt, MD, Gert van Dijk, MD, PhD and Roland D. Thijs, MD, PhD David G. BendittDavid G. Benditt From the Cardiac Arrhythmia and Syncope Center, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis (D.G.B.); Department of Neurology, Neurophysiology, Leiden University Medical Center, Leiden, The Netherlands (G.v.D., R.D.T.); and Epilepsy Institute in the Netherlands Foundation, Heemstede, The Netherlands (R.D.T.). , Gert van DijkGert van Dijk From the Cardiac Arrhythmia and Syncope Center, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis (D.G.B.); Department of Neurology, Neurophysiology, Leiden University Medical Center, Leiden, The Netherlands (G.v.D., R.D.T.); and Epilepsy Institute in the Netherlands Foundation, Heemstede, The Netherlands (R.D.T.). and Roland D. ThijsRoland D. Thijs From the Cardiac Arrhythmia and Syncope Center, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis (D.G.B.); Department of Neurology, Neurophysiology, Leiden University Medical Center, Leiden, The Netherlands (G.v.D., R.D.T.); and Epilepsy Institute in the Netherlands Foundation, Heemstede, The Netherlands (R.D.T.). Originally published1 Feb 2015https://doi.org/10.1161/CIRCEP.114.002546Circulation: Arrhythmia and Electrophysiology. 2015;8:11–14Ictal bradycardia and ictal asystole, although well known to neurologists, have received relatively little attention in the cardiology community. Consequently, in certain instances, the true pathogenesis for heart rate slowing (ie, epilepsy) may be missed, and the bradyarrhythmia incorrectly attributed to other causes.Technically, both ictal bradycardia and asystole are more precisely termed ictal-induced cardiac bradyarrhythmia or asystole. Most often the neurological trigger is a complex partial seizure, which may or may not become generalized.1 Further, if sufficiently severe, the ictal-induced bradyarrhythmia temporarily impairs both cerebral perfusion and cortical function; the result has the dual effect of terminating the seizure, while at the same time triggering syncope with consequent loss of consciousness and postural tone. In essence, a complex partial seizure patient may manifest both seizure and syncope features during the same episode.Article see p 159Symptomatic ictal-induced bradyarrhythmias seem to occur only infrequently; even in high-volume neurology centers they are typically documented in 3-second duration and a >2-fold increment over the previous R-R interval). Among these latter 10 patients, recordings revealed a latency from seizure onset to asystole ranging from 12 to 268 seconds (mean, 40 seconds) with subsequent asystole duration of 11±9 seconds. All seizures associated with asystole were complex partial seizures; in 2 instances, asystole began only after the focal seizure became secondarily generalized.The conclusion, based on video-electroencephalogram data, that ictal-induced bradycardia and ictal asystole are rare may be biased because of the highly selected population being evaluated in video-electroencephalogram laboratories. Relatively little is known about the susceptibility to ictal bradyarrhythmias in free-living seizure-prone individuals. To address this latter issue, Rugg-Gunn et al6 used insertable loop recorders to monitor cardiac rhythm in 20 ambulatory patients with refractory epilepsy. Despite the small patient population and limited insertable loop recorder memory capability, the investigators were able to monitor >220 000 hours of ECG and captured 377 seizure events. Bradyarrhythmias (defined as heart rate ≤40 beats per minute) occurred in 8 patients in this cohort and accounted for 2.1% of the 377 recorded seizure episodes; more importantly, 3 of 20 (15%) patients in the cohort exhibited 4 ictal-induced asystolic pauses of 4.6 to 18 seconds in duration. Thus, in this outpatient cohort, bradyarrhythmias occurred at a frequency that seems higher than that reported from video-electroencephalogram recording centers.Basis of BradyarrhythmiasThe cause of ictal-induced bradyarrhythmia is not clearly established.1 However, underlying heart or conduction system disease does not seem to be a predisposing factor. Furthermore, the reported time-delays between seizure onset and development of asystole suggest that the prime mover is most likely activation of certain key regions of the brain, with secondary impact on cardiac function via efferent neural pathways.Areas in the brain that seem to be of particular importance with regard to triggering bradyarrhythmias are those within and surrounding the central autonomic network including the insular cortex and amygdalae. Furthermore, although previous reports often suggested that the left cerebral hemisphere was the more important in this regard, more recent findings have undermined that concept; when cases are pooled, both left and right hemispheres seem to be equally important.1,7 In any event, several reports suggest that stimulation of regions within the central autonomic network may trigger efferent parasympathetic pathways and favor development of bradyarrhythmias.1,8–11 By way of example, Catenoix et al11 reported the impact of stimulation of the left hippocampus, amygdale, and insula in humans. Stimulation resulted in high-frequency discharges in a portion of the insula 7 seconds after stimulus termination, followed by asystole 2 seconds later; furthermore, asystole was then accompanied within ≈30 seconds by generalized electroencephalogram slowing and subsequent suppression of the abnormal activity (ie, an unanticipated therapeutic effect).It is thought that seizure-induced central nervous system activation may have a direct postganglionic effect on the heart, with a tendency to synchronize cardiac autonomic input to the epileptic activity.12 Various arrhythmias may ensue, but in animal models microstimulation of the insular cortex synchronized to the ECG T-wave has been reported to induce severe bradyarrhythmias that by virtue of their duration could become life threatening.8Based on available data, it seems that an event along the lines of a vagal storm is the most likely basis for ictal-induced bradycardia. However, not all seizure patients are susceptible; in fact, sinus tachycardia and other tachyarrhythmias are much more frequently observed in this setting.1,6 The factors that may predispose certain individuals to ictal bradyarrhythmia events are unclear; furthermore, they may not be fixed risk factors, as many patients manifest both bradycardias and tachycardias at various times in conjunction with their seizures.Does Ictal-Induced Bradyarrhythmia Contribute to Sudden Death in Epilepsy?Epilepsy is associated with a 2- to 3-fold increased mortality rate.13–15 Sudden death in epilepsy (SUDEP) refers to the unexpected death of an epilepsy patient in the absence of status epilepticus, evident trauma, or other identified cause at postmortem examination; an association with a concomitant seizure is often assumed but is almost impossible to prove conclusively.14SUDEP frequency increases with severity of epilepsy, ranging from 0.4 to 9 deaths per 1000 patient-years. Unfortunately, the cause of SUDEP remains elusive, with events tending to be nocturnal and unwitnessed.15 The most important risk factor is treatment-refractory tonic-clonic seizures.Eyewitness accounts are uncommon but suggest that SUDEP is most often preceded by a generalized tonic-clonic seizure. Complex partial seizures are rarely associated with SUDEP. In this regard, Ryvlin et al14 evaluated data from 147 epilepsy monitoring units. These centers reported findings in 16 SUDEP and 9 near-SUDEP cases. Among the 20 evaluable cases, only 2 of 20 had complex partial seizures (the remainder were generalized tonic-clonic seizures), and only 1 of 20 (albeit in this study a patient with a complex partial seizure) had documented ictal-induced asystole. Deaths were associated with postictal cardiorespiratory arrest; bradyarrhythmia seems to be a secondary factor.Consequently, although a connection between ictal-bradycardia and SUDEP has often been suggested, available evidence suggests that any such relationship is weak for several reasons. First, as noted above, most SUDEP cases are associated with generalized seizures, which are rarely accompanied by bradyarrhythmias, whereas most ictal-induced bradycardia occurs in the setting of focal complex partial seizures. Second, among the many available published reports assessing ictal-induced bradycardia, the severity of the heart rate slowing has largely been modest. Third, when SUDEP has been documented, it seems to be triggered most often by a postictal cardiorespiratory failure.14 Finally, depending on its duration, cardiac asystole tends to induce cerebral ischemia that affects cortical function before other brain areas as evidenced by slowing and then flattening of the electroencephalogram.16,17 The loss of cortical function not only stops the seizure but also eliminates the efferent neural signals (primarily parasympathetic) deemed responsible for the bradycardia.Distinguishing Ictal-Induced Bradyarrhythmias With Loss of Consciousness From Reflex SyncopeFor the non-neurologist clinician, particularly the emergency room practitioner, the difficulty in differentiating seizure disorders from syncope is a considerable burden. The problem is exaggerated when one attempts to distinguish ictal-induced bradyarrhythmias with transient loss of consciousness from neurally mediated reflex faints.As noted earlier, the cortical centers thought to be primarily responsible for triggering the presumed vagal storm in ictal-induced bradycardia/asystole are those comprising the central autonomic network. The course of events is typically initial sinus tachycardia followed by progressive heart rate slowing and thereafter, in a minority of cases, by asystolic pauses of various durations. However, this course of events is not unique to ictal-induced bradyarrhythmic events. The same progression is observed in vasovagal and situational reflex faints,18 with the insula having been implicated as the central origin of bradyarrhythmia in these conditions as well.Apart from the temporal arrhythmia progression, there is indirect evidence to suggest that the onset of ictal-induced bradycardia may also be accompanied by a vasodepressor (ie, vasodilator) component. If this is substantiated, then the parallel between ictal bradycardia and neurally mediated reflex syncope may be even closer than ECG findings alone would suggest. Consequently it may be challenging to establish an unequivocal clinical distinction by either hemodynamic assessment or ECG alone; a concomitant electroencephalogram record would almost certainly be necessary in the absence of an experienced neurologist witnessing the event.In the end, as is generally true for the assessment of all other forms of complete or near transient loss of consciousness spells, having both a carefully documented medical history and if possible a detailed eye-witness account of the episode in the hands of an experienced clinician is the crucial diagnostic step. In particular, historical findings of automatisms, visual, olfactory, auditory or gustatory hallucinations, or the déjà vu or jamais vu sensations are suggestive of a seizure origin. These symptoms are not observed with reflex faints.Prevention and TreatmentPrevention of ictal bradycardia and asystole relies primarily on conventional antiepileptic medications and epilepsy surgery when needed.1,10,19–24 In terms of cardiac pacing, there is no official guidance on indications for prevention of ictal-induced bradycardia. In any case, the role of pacing is subsidiary to treatment of seizure susceptibility. However, if as is suggested by Bestawros et al5 in this issue, pauses of ≥6 seconds contribute to transient loss of consciousness in complex partial seizure patients, and then 6 seconds may be a reasonable threshold for considering pacing. The goal would be to reduce risk of falls and injury if antiepileptic medications and epilepsy surgery fail to prevent symptomatic bradycardia.The proposed 6-second threshold duration for considering pacemaker therapy is plausible from both biological (ie, the residual energy storage of nervous system cells is commonly thought to be in the 6- to 9-second range) and clinical perspectives (ie, preventing an abrupt fall with injury). However, apart from uncontrolled case reports, there is currently no other supportive evidence for cardiac pacing. Furthermore, it must be recognized that prevention of asystole and associated cerebral ischemia may paradoxically prolong the seizure duration for reasons alluded to earlier.As noted above, ictal-induced bradycardia is likely driven by an abrupt vagal storm. To the extent that the vagal mechanism predominates, cardiac pacing should be highly effective. However, in reflex syncope syndromes (eg, vasovagal syncope and carotid sinus syndrome, among others), which are analogous to ictal-induced bradycardia in terms of the vagal storm concept, concomitant vasodilatation is an almost universal accompaniment and is largely unresponsive to pacing. In regard to ictal-induced bradycardia, additional study is needed to ascertain whether a vasodilatory component is also present; however, the report from Nguyen-Michel et al20 provides suggestive evidence that this may be the case. These investigators noted that among their group of video-electroencephalogram patients who exhibited ictal-asystole, the bradycardia began to evolve at 32±18 seconds after onset of the seizure, and the heart rate progressively decreased over approximately the subsequent 11 seconds ultimately resulting in a pause of 13±7 seconds. Pallor and atonia were observed during the episodes, and these seem to be similar to the symptoms expected with reflex faints. Furthermore, in 1 case the collapse was unassociated with asystole and was attributed to vasoplegia (ie, vasodepressor or vasodilatation response). Similarly, Tinuper et al7 managed to perform beat-to-beat blood pressure recordings in 2 cases with ictal asystole demonstrating that the asystole may be followed as well as preceded by a blood pressure drop.If vasodepression is a major ancillary feature in ictal-induced bradyarrhythmias, pacing may be only partially effective for preventing falls. In any case, more needs to be learned about blood pressure responses during seizures, how blood pressure changes alone affect clinical manifestations of seizure episodes, and whether pacing predictably ameliorates the resulting clinical picture.SummaryIctal-induced bradyarrhythmias are an uncommon manifestation of epilepsy, and any proposed relationship between ictal-induced bradyarrhythmias and SUDEP is unconvincing at this time. The majority of documented ictal-induced bradyarrhythmias accompany complex partial seizures of temporal lobe origin, whereas SUDEP is more commonly associated with generalized tonic-clonic seizures. The ECG evolution during an ictal-bradyarrhythmia episode is essentially indistinguishable from that of a vasovagal faint or near-faint, with sinus tachycardia being followed by progressive heart rate slowing which at times progresses to an asystolic pause. Most documented pauses are of non–life-threatening duration (range, 3–20 seconds), but longer pauses have been observed. In any event, it seems likely that the accompanying loss of brain blood flow because of the bradycardia may actually be paradoxically beneficial, by facilitating termination of the epileptic event.Antiepileptic medications and occasionally epilepsy surgery are the mainstays of treatment. Cardiac pacing may help to reduce falls risk, but in the absence of official practice guidelines, pacing should only be considered for patients in whom conventional antiepileptic therapy has failed to prevent ictal asystole (the proposed threshold for asystole duration being >6 seconds). However, the possibility that a separate vasodepressor mechanism may coexist with ictal-induced bradycardia (as it does with reflex syncope syndromes) should be kept in mind; hypotension and falls risk may persist in these patients despite pacing.Sources of FundingDr Benditt was supported in part by a philanthropic grant from the Dr Earl E. Bakken Family to the University of Minnesota Foundation for heart-brain research. Dr Thijs receives research support from the Dutch Epilepsy Foundation (Project No. 15-10), Christelijke Vereniging voor de Verpleging van Lijders aan Epilepsie (Nederland), Nuts Ohra Fund, Medtronic and AC Thomson Foundation.DisclosuresDr Benditt reports consultantship and equity interests in Medtronic Inc., and St Jude Medical Inc, and equity interest in Advanced Circulatory Inc. Dr Thijs has received fees for lectures from Medtronic, Union Chimique Belge (UCB) Pharma and Glaxo Smith Klein Pharmaceuticals. He is the principal investigator of a prospective registry on cardiac arrhythmias in epilepsy (ClinicalTrials.gov Identifier: NCT01946776). The other author reports no conflicts.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Correspondence to David G. Benditt, MD, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical Center, Mail Code 508, 420 Delaware St SE, Minneapolis, MN 55455. 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