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Peri-ictal QTc changes are not associated with hypoxemia.
MedLine Citation:
PMID:  24721200     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
It has previously been suggested that abnormalities in cardiac repolarization (QTc lengthening and shortening) are more likely to accompany seizures with hypoxemia and may be involved in sudden unexpected death in epilepsy (SUDEP). Accordingly, we evaluated for associations between peri-ictal QTc changes and hypoxemia. We performed a reanalysis of cardiac and respiratory data gathered prospectively in our epilepsy monitoring units. The Bazett, Fridericia, Framingham, and Hodges heart rate correction formulas were utilized to calculate QTc in the pre-ictal, ictal, and post-ictal periods. Hypoxemia (defined as a drop in oxygen saturation below 90% for at least four contiguous seconds) was also examined during identical periods. Fifty-eight seizures from 29 patients were analyzed. Peri-ictal hypoxemia was not rare, occurring in 18/58 (31%) seizures. QTc lengthening was more commonly observed than shortening, with 11/58 (19%) seizures demonstrating peri-ictal QTc values≥500 using the Bazett formula. There was no significant difference between the minimum and maximum QTc values in seizures with and without peri-ictal hypoxemia, regardless of the correction formula utilized. All examined parameters of QTc lengthening and shortening were not associated with peri-ictal hypoxemia. This suggests that factors other than hypoxia result in peri-ictal cardiac repolarization abnormalities.
Authors:
Brian D Moseley; Jeffrey W Britton
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-3-27
Journal Detail:
Title:  Epilepsy research     Volume:  -     ISSN:  1872-6844     ISO Abbreviation:  Epilepsy Res.     Publication Date:  2014 Mar 
Date Detail:
Created Date:  2014-4-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8703089     Medline TA:  Epilepsy Res     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 Elsevier B.V. All rights reserved.
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