Document Detail


Electrophysiologic basis for T wave alternans as an index of vulnerability to ventricular fibrillation.
MedLine Citation:
PMID:  8055149     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Substantial evidence indicates that T wave alternans is an intrinsic property of ischemic myocardium. The electrophysiologic basis appears to be spatial and temporal heterogeneity of repolarization resulting from changes in action potential morphology rather than in activation sequence. Ischemia-induced changes in postrepolarization refractoriness and depressed electrical restitution of action potential duration have also been implicated. The main underlying ionic basis for T wave alternans during coronary occlusion appears to be derangements in intracellular cycling of calcium. Accumulation of potassium in the extracellular space adjoining ischemic cells and disruption in electrogenic sodium-calcium exchange may also be involved. In humans, T wave alternans has been observed in Prinzmetal's and classical angina, angioplasty, and bypass graft occlusion. Under these conditions associated with acute myocardial ischemia, alternans is restricted to the ischemic zone, and alternation in action potential morphology is an underlying factor. Recently, repolarization alternans has been shown to be a statistically significant predictor of the results of electrophysiologic testing and arrhythmia-free survival in individuals with and without organic heart disease. Collectively, these observations provide a rationale for quantitation of T wave alternans magnitude for assessment of vulnerability to life-threatening ventricular arrhythmias both in response to and independent of the effects of myocardial ischemia.
Authors:
R L Verrier; B D Nearing
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Journal of cardiovascular electrophysiology     Volume:  5     ISSN:  1045-3873     ISO Abbreviation:  J. Cardiovasc. Electrophysiol.     Publication Date:  1994 May 
Date Detail:
Created Date:  1994-09-13     Completed Date:  1994-09-13     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9010756     Medline TA:  J Cardiovasc Electrophysiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  445-61     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Georgetown University School of Medicine, Washington, D.C. 20007.
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MeSH Terms
Descriptor/Qualifier:
Angina Pectoris, Variant / physiopathology
Angioplasty / adverse effects
Animals
Arrhythmias, Cardiac / etiology
Autonomic Nervous System / physiopathology
Coronary Artery Bypass
Coronary Disease / complications,  etiology
Disease Susceptibility
Electrocardiography, Ambulatory
Humans
Myocardial Ischemia / physiopathology
Myocardial Reperfusion
Postoperative Complications
Ventricular Fibrillation / etiology*
Grant Support
ID/Acronym/Agency:
HL-33567/HL/NHLBI NIH HHS

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


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