Timing of syncope in ictal asystole as a guide when considering pacemaker implantation

Anouk van Westrhenen, Sharon Shmuely, Rainer Surges, Beate Diehl, Daniel Friedman, Frans S.S. Leijten, Jorien van Hoey Smith, David G. Benditt, J. Gert van Dijk, Roland D. Thijs

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Introduction: In patients with ictal asystole (IA) both cardioinhibition and vasodepression may contribute to syncopal loss of consciousness. We investigated the temporal relationship between onset of asystole and development of syncope in IA, to estimate the frequency with which pacemaker therapy, by preventing severe bradycardia, may diminish syncope risk. Methods: In this retrospective cohort study, we searched video-EEG databases for individuals with focal seizures and IA (asystole ≥ 3 s preceded by heart rate deceleration) and assessed the durations of asystole and syncope and their temporal relationship. Syncope was evaluated using both video observations (loss of muscle tone) and EEG (generalized slowing/flattening). We assumed that asystole starting ≤3 s before syncope onset, or after syncope began, could not have been the dominant cause. Results: We identified 38 seizures with IA from 29 individuals (17 males; median age: 41 years). Syncope occurred in 22/38 seizures with IA and was more frequent in those with longer IA duration (median duration: 20 [range: 5–32] vs. 5 [range: 3–9] s; p <.001) and those with the patient seated vs. supine (79% vs. 46%; p =.049). IA onset always preceded syncope. In 20/22 seizures (91%), IA preceded syncope by >3 s. Thus, in only two instances was vasodepression rather than cardioinhibition the dominant presumptive syncope triggering mechanism. Conclusions: In IA, cardioinhibition played an important role in most seizure-induced syncopal events, thereby favoring the potential utility of pacemaker implantation in patients with difficult to suppress IA.

Original languageEnglish (US)
Pages (from-to)3019-3026
Number of pages8
JournalJournal of cardiovascular electrophysiology
Volume32
Issue number11
DOIs
StatePublished - Nov 2021

Bibliographical note

Funding Information:
Rainer Surges has received fees as speaker or consultant from Bial, Desitin, Eisai, LivaNova, Novartis, and UCB Pharma. Daniel Friedman receives salary support for consulting and clinical trial‐related activities performed on behalf of the Epilepsy Study Consortium, a nonprofit organization. He receives no personal income for these activities. NYU receives a fixed amount from the Epilepsy Study Consortium toward Friedman's salary. Within the past 2 years, the Epilepsy Study Consortium received payments for research services performed by Friedman from Axcella, Biogen, Cerevel, Crossject, Engage Pharmaceuticals, Eisai, Pfizer, SK Life Science, Xenon, and Zynerba. He has also served as a paid consultant for Eisai and Neurelis Pharmaceuticals. He has received travel support from Medtronic, Eisai, and the Epilepsy Foundation. He receives research support from the centers for Disease Control and Prevention, National Institute of Neurological Disorders and Stroke, Epilepsy Foundation, Empatica, Epitel, UCB, Inc, and Neuropace. He serves on the scientific advisory board for Receptor Life Sciences. He holds equity interests in Neuroview Technology and Receptor Life Sciences. Frans Leijten receives research support from Medtronic. Roland Thijs receives research support from Medtronic and NewLife Wearables, received as speaker or consultant from Theravance Biopharma, Zogenix, Arvelle, UCB, and Novartis. Dr. Benditt is supported in part by a grant from the Dr. Earl E Bakken Family in support of Heart‐Brain research, and receives consultation funds from Medtronic Inc., and St Jude Medical Inc. Anouk van Westrhenen, Sharon Shmuely, Beate Diehl, Jorien van Hoey Smith, and Gert van Dijk: None. Disclosures:

Funding Information:
We are grateful to Catherine Scott for collecting data at the National Hospital for Neurology & Neurosurgery and to Dr. G. S. Bell and Prof. J. W. Sander for critically reviewing the manuscript.?This study was supported by the Dutch Epilepsy Foundation (15-05) and ?De Christelijke Vereniging voor de Verpleging van Lijders aan Epilepsie.? Beate Diehl receives funding from NIH-National Institute of Neurological Disorders and Stroke (U01-NS090407: Center for SUDEP Research), and Epilepsy Research, United Kingdom. This study was partly conducted at UCL Hospitals Comprehensive Biomedical Research Centre, which receives a proportion of the UK Department of Health's?National Institute for Health Research funding scheme.

Funding Information:
We are grateful to Catherine Scott for collecting data at the National Hospital for Neurology & Neurosurgery and to Dr. G. S. Bell and Prof. J. W. Sander for critically reviewing the manuscript. This study was supported by the Dutch Epilepsy Foundation (15‐05) and “De Christelijke Vereniging voor de Verpleging van Lijders aan Epilepsie.” Beate Diehl receives funding from NIH‐National Institute of Neurological Disorders and Stroke (U01‐NS090407: Center for SUDEP Research), and Epilepsy Research, United Kingdom. This study was partly conducted at UCL Hospitals Comprehensive Biomedical Research Centre, which receives a proportion of the UK Department of Health's National Institute for Health Research funding scheme.

Publisher Copyright:
© 2021 The Authors. Journal of Cardiovascular Electrophysiology published by Wiley Periodicals LLC

Keywords

  • autonomic nervous system
  • blood pressure
  • epilepsy
  • focal seizure(s)
  • transient loss of consciousness (TLOC)
  • vasodepression

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