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"Complex" Vasovagal Syncope: A Zebra Among Horses.

Anwer Zohaib Siddiqi1, Derrick Blackmore1, Zaeem Azfer Siddiqi1

  • 1Division of Neurology, Department of Medicine, University of Alberta, Edmonton, AB, Canada.

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|January 4, 2021
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Summary

Severe bradycardia in vasovagal syncope (VVS) predicts complex VVS, including seizures and asystole. This suggests cerebral hypoperfusion plays a key role in VVS-related seizures.

Keywords:
asystolebradycardiaseizuressyncopevasovagal syncope

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Area of Science:

  • Cardiology
  • Neurology
  • Autonomic Neuroscience

Background:

  • Vasovagal syncope (VVS) is characterized by cerebral hypoperfusion leading to blood pressure drop and often bradycardia.
  • Predicting seizures or asystole during VVS remains challenging.
  • Complex VVS is defined as VVS with associated seizures and/or asystole.

Purpose of the Study:

  • To characterize VVS presentations.
  • To identify predictive features of complex VVS.
  • To differentiate VVS-associated seizures from epileptic seizures.

Main Methods:

  • Retrospective review of medical records for patients with VVS during head-up tilt table testing (HUTT).
  • Recording of cardiovascular indices, autonomic testing results, and semiology of seizures/asystole.
  • Statistical analysis including frequency and correlation using ANOVA.

Main Results:

  • 23% of VVS cases were complex, with seizures (SySz), asystole (SyAs), or both (SySzAs).
  • Males were more prone to complex VVS.
  • Bradycardia severity correlated with complex VVS and predicted SySz; autonomic abnormalities did not differentiate subgroups.

Conclusions:

  • Complex VVS mechanisms are not fully understood.
  • Severe bradycardia-induced cerebral hypoperfusion is likely crucial for VVS-related seizure generation.
  • VVS-associated seizures exhibit distinct features compared to epileptic seizures.