Dispersion of ventricular refractoriness in experimental myocardial infarction: effect of sotalol

Dispersion of refractoriness may contribute to the propensity for reentrant arrhythmias. This study was performed to assess the effect of sotalol on the dispersion of refractoriness in experimental myocardial infarction. In 9 mongrel dogs, 14 days after induction of myocardial infarction by an occlusion reperfusion technique, programmed ventricular stimulation and epicardial mapping were performed before and during (3 mg/kg + 0.5 mg/kg per hour) sotalol administration. To assess the spatial distribution of refractoriness, ventricular fibrillation (VF) intervals were analyzed. The rationale for this method is that, during VF, when multiple reentrant wavelets are present, cells are excited as soon as they recover from previous activation. The coefficient of variation (standard deviation x 100) served as an index of spatial distribution of refractoriness.

VF was induced before sotalol in 7 dogs and in 5 of 7 during sotalol administration. The mean value of the index VF intervals decreased from 19.8 +/- 2.3 at baseline to 15.8 +/- 2.6 during sotalol (P = 0.011), indicating a more homogeneous distribution of refractoriness. Thus, the antiarrhythmic effects of sotalol may be mediated by its action on the dispersion of refractoriness.