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 antiarrhy thmic drugs cause a disparity between refractoriness and repolarizatio n, and if so, its magnitude. We simultaneously measured monophasic act ion potential duration (MAPD) and effective refractory period (ERP) at a right ventricular site in 11 patients without overt right ventricul ar disease. The pacing protocol, which included sinus rhythm and a 600 and 400 msec cycle length of ventricular drive, was performed at base line and after the intravenous administration of 15 mg/kg of procainam ide in nine patients, and of 10 mg/kg of quinidine in two patients. De spite trivial changes in sinus rates, drug therapy caused a 10% to 17% increase in MAPD and ERP that shortened with decreasing drive cycle l engths. 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, th e 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 abo lished with a 600 and 400 msec drive (28 and 29 msec, respectively). T he disparity was caused in one third of cases by postrepolarization re fractoriness. Type I drugs increase the difference between repolarizat ion and refractoriness, and this effect is partially reversed with inc reases in heart rate. The clinical implications of these findings are discussed.