Hirose Masamichi, Takeishi Yasuchika, Miyamoto Takuya, Kubota Isao, Laurita Kenneth R, Chiba Shigetoshi
Department of Molecular Pharmacology, Shinshu University School of Medicine, Nagano, Japan.
J Cardiovasc Electrophysiol. 2005 Jul;16(7):760-9. doi: 10.1046/j.1540-8167.2005.40331.x.
Mechanism of chronic volume overload-induced AT.
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.
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.
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.
