Document Detail

Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure.
MedLine Citation:
PMID:  12776867     Owner:  NLM     Status:  MEDLINE    
INTRODUCTION: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. METHODS AND RESULTS: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. CONCLUSIONS: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.
Bruce S Stambler; Guilherme Fenelon; Richard K Shepard; Henry F Clemo; Colette M Guiraudon
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cardiovascular electrophysiology     Volume:  14     ISSN:  1045-3873     ISO Abbreviation:  J. Cardiovasc. Electrophysiol.     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-06-02     Completed Date:  2003-10-09     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:  499-507     Citation Subset:  IM    
Department of Medicine/Cardiology, West Roxbury Veterans Affairs Medical Center, Harvard Medical School, West Roxbury, Massachusetts, USA.
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MeSH Terms
Action Potentials / physiology
Adrenergic beta-Antagonists / pharmacology
Anti-Arrhythmia Agents / pharmacology
Atrial Natriuretic Factor / blood
Blood Pressure / physiology
Cardiac Pacing, Artificial / adverse effects*
Disease Models, Animal
Electrophysiologic Techniques, Cardiac
Heart Atria / drug effects,  physiopathology,  ultrasonography
Heart Failure / etiology*,  mortality,  physiopathology
Heart Ventricles / drug effects,  physiopathology,  ultrasonography
Models, Cardiovascular
Recovery of Function / physiology
Stroke Volume / physiology
Survival Analysis
Tachycardia, Ectopic Atrial / classification*,  etiology*,  physiopathology
Ventricular Dysfunction, Left / etiology,  physiopathology
Grant Support
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Anti-Arrhythmia Agents; 85637-73-6/Atrial Natriuretic Factor
Comment In:
J Cardiovasc Electrophysiol. 2003 May;14(5):508-9   [PMID:  12776868 ]

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

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