Document Detail


Local depolarization abnormalities are the dominant pathophysiologic mechanism for type 1 electrocardiogram in brugada syndrome a study of electrocardiograms, vectorcardiograms, and body surface potential maps during ajmaline provocation.
MedLine Citation:
PMID:  20170818     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing. BACKGROUND: BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization. METHODS: Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps. RESULTS: A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 +/- 23 ms vs. 125 +/- 14 ms, p < 0.01) and right terminal conduction delay (60 +/- 11 ms vs. 53 +/- 9 ms, p < 0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 +/- 8% vs. 8 +/- 4%, p = NS), lower spatial QRS-T integrals (33 +/- 12 mV.ms vs. 40 +/- 16 mV.ms, p < 0.05), similar spatial QRS-T angles (92 +/- 39 degrees vs. 87 +/- 31 degrees , p = NS), similar T(peak)-T(end) interval (143 +/- 36 ms vs. 138 +/- 25 ms, p = NS), and similar T(peak)-T(end) dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS). CONCLUSIONS: The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities.
Authors:
Pieter G Postema; Pascal F H M van Dessel; Jan A Kors; Andre C Linnenbank; Gerard van Herpen; Henk J Ritsema van Eck; Nan van Geloven; Jacques M T de Bakker; Arthur A M Wilde; Hanno L Tan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  55     ISSN:  1558-3597     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-22     Completed Date:  2010-03-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  789-97     Citation Subset:  AIM; IM    
Copyright Information:
Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Affiliation:
Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Adult
Ajmaline / diagnostic use
Anti-Arrhythmia Agents / diagnostic use
Body Surface Potential Mapping*
Brugada Syndrome / diagnosis*,  physiopathology*
Female
Humans
Male
Middle Aged
Chemical
Reg. No./Substance:
0/Anti-Arrhythmia Agents; 4360-12-7/Ajmaline
Comments/Corrections
Comment In:
J Am Coll Cardiol. 2010 Feb 23;55(8):798-800   [PMID:  20170819 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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