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Cardiovascular Research 2004 61(4):764-770; doi:10.1016/j.cardiores.2003.12.013
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Pathophysiological findings in a model of persistent atrial fibrillation and severe congestive heart failure

Alexander Bauer1, Amy D. McDonald and J.Kevin Donahue*

Institute of Molecular Cardiobiology, Johns Hopkins University School of Medicine, Ross 844, 720 N. Rutland Avenue, Baltimore, MD 21205, USA

* Corresponding author. Tel.: +1-410-955-2775; fax: +1-410-955-7953. kdonahue{at}jhmi.edu

1 Current address: Universitäet Heidelberg, Innere Medizin III Rhythmusgruppe, Bergheimerstr. 58, Heidelberg D-69115, Germany.

Objective: Develop and evaluate a model of persistent atrial fibrillation (AF) and severe congestive heart failure (CHF). Methods: A single-chamber atrial pacemaker was implanted in pigs (20–30 kg). Burst atrial pacing at 42 Hz led to development of persistent AF. Immediately and 20 days after activation of the burst pacing protocol, animals underwent echocardiography. Heart rate, rhythm and general condition were monitored on a daily basis. After 20 days of atrial fibrillation, the animals were sacrificed. Conventional histological methods were used to evaluate microscopic structural changes. Results: In the pig model, persistent atrial fibrillation developed 5±0.7 days after initiation of the burst protocol. Ventricular response rate was 274±5 bpm during atrial fibrillation, leading to a tachycardiomyopathy. Heart failure symptoms occurred approximately 15 days after initiation of burst pacing. Increases in QT interval on electrocardiogram, heart weight-to-body weight ratio, and laboratory values suggestive of a hypercatecholaminergic state, as well as liver and kidney dysfunction occurred during the 20-day duration of the study. Microstructural changes consistent with cellular hypertrophy, variable fibrosis, myolysis and apoptosis were found in the atria and ventricles of the study animals. Conclusions: The combined entity of atrial fibrillation and severe congestive heart failure leads to multiple organ dysfunction, ultrastructural and microscopic cardiac changes. Cellular hypertrophy, fibrosis and apoptosis are more prominent in this combined entity than previously reported models of lone atrial fibrillation or heart failure. This model can be used for further investigation into the pathophysiology and treatment of atrial fibrillation and advanced heart failure.

KEYWORDS Atrial fibrillation; Congestive heart failure; Cardiac hypertrophy; Cardiac dilation; Apoptosis

Time for primary review 25 days


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