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  • Title: Repetitive electrical remodeling by paroxysms of atrial fibrillation in the goat: no cumulative effect on inducibility or stability of atrial fibrillation.
    Author: Garratt CJ, Duytschaever M, Killian M, Dorland R, Mast F, Allessie MA.
    Journal: J Cardiovasc Electrophysiol; 1999 Aug; 10(8):1101-8. PubMed ID: 10466491.
    Abstract:
    INTRODUCTION: Episodes of atrial fibrillation (AF) are known to cause both a rapid reduction in atrial refractoriness (atrial electrical remodeling) and a more delayed increase in AF stability in the chronic goat model. The aims of this study were to examine (1) the hypothesis that an AF-induced increase in AF stability might be due to a mechanism with a longer onset and offset than that of changes in refractoriness and (2) the possibility that repeated paroxysms of maintained AF might cause a cumulative increase in AF stability independent of changes in atrial refractoriness. METHODS AND RESULTS: AF was maintained by rapid atrial pacing in seven goats for three consecutive 5-day periods, each separated from each other by 48 hours of sinus rhythm. Assessments of atrial refractory periods, conduction velocity, AF inducibility, and duration of individual episodes of AF were attempted at intervals throughout the protocol. Forty-eight hours of sinus rhythm was just sufficient for refractoriness changes to fully reverse in all goats, with no evidence of any "residual" increase in AF inducibility. There was no significant difference among any of the three periods of pacing-maintained AF with regard to time to develop episodes of AF of 60-second duration (22.1+/-13, 23.8+/-16, and 30.3+/-29 hours), 1-hour duration (56.6+/-28, 61.3+/-31, and 60.1+/-32 hours), or 24-hour duration (84.0+/-31, 87.0+/-33, and 83.5+/-32 hours). CONCLUSION: There is no evidence for a cumulative effect of AF paroxysms on AF inducibility or stability independent of changes in refractoriness. These findings highlight the importance of atrial refractoriness as a potential target for antiarrhythmic strategies aimed at inhibiting the self-perpetuation of AF.
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