Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure

Autor: Richard K. Shepard, Colette M. Guiraudon, Bruce S. Stambler, Guilherme Fenelon, Henry F. Clemo
Rok vydání: 2003
Předmět:
Tachycardia
Tachycardia
Ectopic Atrial
medicine.medical_specialty
Atrial enlargement
Heart Ventricles
Adrenergic beta-Antagonists
Action Potentials
Blood Pressure
Electrocardiography
Ventricular Dysfunction
Left
Dogs
Physiology (medical)
Internal medicine
medicine
Animals
cardiovascular diseases
Heart Atria
Atrium (heart)
Atrial tachycardia
Coronary sinus
Heart Failure
business.industry
Cardiac Pacing
Artificial
Models
Cardiovascular
Stroke Volume
Recovery of Function
medicine.disease
Survival Analysis
Disease Models
Animal
medicine.anatomical_structure
Ventricle
Echocardiography
Anesthesia
Heart failure
cardiovascular system
Cardiology
Verapamil
medicine.symptom
Cardiology and Cardiovascular Medicine
business
Electrophysiologic Techniques
Cardiac
Anti-Arrhythmia Agents
Atrial Natriuretic Factor
medicine.drug
Zdroj: Journal of cardiovascular electrophysiology. 14(5)
ISSN: 1045-3873
Popis: 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. After20 ± 7 daysof rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length120 ± 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (≤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.(J Cardiovasc Electrophysiol, Vol. 14, pp. 499-507, May 2003)
Databáze: OpenAIRE
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