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.

Serum reverse T3 and amiodarone efficacy.

The use of serum reverse T3 (rT3) levels in the assessment of amiodarone efficacy is controversial. We prospectively studied 10 patients with frequent ventricular ectopy and symptomatic ventricular tachycardia (VT) treated with amiodarone. Serial 24-h Holter monitor, thyroid function studies including serum rT3, and 12-lead electrocardiogram were performed on each patient at baseline, and at 1, 4, 12, and 24 weeks of oral amiodarone therapy. Serial Holter monitors on therapy were analyzed for 100% suppression of VT, 90% suppression of couplets, and 85% suppression of ventricular ectopic beats (VEBs) compared with baseline Holter, defining patient groups VT-, Co-, and VEB-, respectively. Lack of arrhythmia suppression to this degree defined groups as VT+, Co+, and VEB+. There were no statistically significant differences in rT3 levels between VT+ and VT- groups, Co+ and Co- groups, or the VEB+ and VEB- groups. VT suppression could not be predicted at any rT3 level. We conclude that serum rT3 is an insensitive means of assessing amiodarone efficacy.