Key result
Chronic volume overload in rabbits caused atrial dilatation, conduction slowing, and induced atrial tachyarrhythmia in 87.5% of hearts compared to 0% of controls.
Absolute Event Rate: 87.5% vs 0%
Chronic volume overload induces atrial dilatation and conduction slowing, leading to reentrant and focal atrial tachyarrhythmias originating primarily from the posterior left atrium.
Animal data link volume overload to atrial remodeling and tachyarrhythmias; leaves open relevance to clinical AF.
UNLABELLED: Mechanism of chronic volume overload-induced AT. INTRODUCTION: Atrial dilatation associated with chronic volume overload (CVO) plays an important role in the development of atrial fibrillation (AF). However, the underlying mechanisms are unknown. METHODS AND RESULTS: CVO-induced atrial dilatation was created in Japanese white rabbits using arteriovenous shunt formation for 6 weeks. Epicardial action potentials were measured from both atria in Langendorff-perfused sham-operated control hearts (n=8) and in CVO hearts (n=8) using high-resolution optical mapping techniques. The left atrial diameter was greater in CVO hearts (16.0+/-0.4 mm) compared to control hearts (11.0+/-0.8 mm). During steady-state pacing, right and left atrial conduction velocities were significantly lower in CVO hearts compared to control hearts (P<0.01). Rapid atrial pacing did not induce atrial tachyarrhythmia (AT) in any control hearts. However, in seven of eight CVO hearts 16 episodes of AT were induced, of which 9 exhibited a single reentrant circuit. The remaining 7 episodes exhibited a focal pattern of excitation without evidence of reentry. Interestingly, the activation rate was higher during reentry (16.1+/-1.5 Hz) compared to focal AT (9.8+/-1.0 Hz). In addition, 15 of 16 episodes occurred in the posterior left atrium (PLA). In all seven CVO hearts, AT was self-sustained for more than 10 minutes. CONCLUSION: CVO caused atrial dilatation, conduction slowing, and AT associated with reentrant and focal excitation originating from the PLA. These results suggest that the PLA may play an important role in AT induction associated with CVO-induced atrial dilation.
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Hirose et al. (2005) studied Chronic volume overload-induced atrial dilatation (n=16). Chronic volume overload (CVO) via arteriovenous shunt formation vs. Sham-operated control was evaluated on Induction of atrial tachyarrhythmia (AT) by rapid atrial pacing. Chronic volume overload in rabbits caused atrial dilatation, conduction slowing, and induced atrial tachyarrhythmia in 87.5% of hearts compared to 0% of controls.
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