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1 Krannert Institute of Cardiology, Indiana University School of Medicine, IndiIndianapolis, IN, USA
* To whom correspondence should be addressed. E-mail: olgin{at}medicine.ucsf.edu.
Chronic rapid atrial pacing (RAP) leads to changes that perpetuate atrial fibrillation (AF). Chronic atrial dilatation due to mitral regurgitation (MR) also increases AF inducibility, but it is not clear whether the underlying mechanism is similar. Therefore, we have investigated atrial electrophysiology in a canine MR model (mitral valve avulsion, 1 month) using high-resolution optical mapping and compared it to control dogs and to the canine RAP model (6-8 weeks of atrial pacing at 600 bpm, AV block and ventricular pacing at 100 bpm). At follow up, optical action potentials were recorded using a 16x16 photodiode array from 2x2 cm left atrial (LA) and right atrial (RA) areas in perfused preparations, with pacing electrodes around the field of view to study direction-dependency of conduction. Action potential duration (APD80) was not different between control and MR, but was reduced in RAP atria. Conduction velocities during normal pacing were not different between groups. However, the MR LA showed increased conduction heterogeneity during pacing at short cycle lengths and during premature extrastimuli, which frequently caused pronounced regional conduction slowing. Conduction in the MR LA during extrastimulation also displayed a marked dependence on propagation direction. These phenomena were not observed in the MR RA and in control and RAP atria. Thus, both models form distinctly different AF substrates; in RAP dogs, the decrease in APD80 may stabilize reentry. In MR dogs, regional LA conduction slowing and increased directional dependency, allowing unidirectional conduction block and preferential paths of conduction, may account for increased AF inducibility.
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