Evidence for a reexcitability gap in man after treatment with type I antiarrhythmic drugs

The intention of this study was to determine whether type IA antiarrhythmic drugs cause a disparity between refractoriness and repolarization, and if so, its magnitude. We simultaneously measured monophasic action potential duration (MAPD) and effective refractory period (ERP) at a right ventricular site in 11 patients without overt right ventricular disease. The pacing protocol, which included sinus rhythm and a 600 and 400 msec cycle length of ventricular drive, was performed at baseline and after the intravenous administration of 15 mg/kg of procainamide in nine patients, and of 10 mg/kg of quinidine in two patients. Despite trivial changes in sinus rates, drug therapy caused a 10% to 17% increase in MAPD and ERP that shortened with decreasing drive cycle lengths. At baseline there was a small gap (10 to 13 msec) between MAPD and ERP in sinus rhythm and with a 600 or 400 msec drive. However, the type IA drug caused a significant widening of this gap that was most profound in sinus rhythm (45 msec) and that shortened but was not abolished with a 600 and 400 msec drive (28 and 29 msec, respectively). The disparity was caused in one third of cases by postrepolarization refractoriness. Type I drugs increase the difference between repolarization and refractoriness, and this effect is partially reversed with increases in heart rate. The clinical implications of these findings are discussed.