In the acquired long QT syndrome, torsades de pointes (TP) is invariably preceded by pauses or bradycardia. Thus, it has been proposed that out-of-hospital initiation of drugs that prolong repolarization should be safe in patients with permanent pacemakers. However, a minimal protective pacing rate has not been identified. The authors reviewed published reports of acquired TP in patients with permanent pacing. Those providing documentation of tachycardia onset and pacemaker programming were included in the analysis. Events occurring < or = 1 month after AV nodal ablation were excluded. Eighteen cases were identified (age 74 +/- 5; 10 women). QT prolonging drugs were present in 15 patients (quinidine 5, sotalol 3, disopyramide 3, amytriptiline, chloroquine, cisapride + haloperidol, and monopride + flecainide 1 each). Hypokalemia was present in eight patients. At the time of TP, the programmed lower rate was 63 +/- 13 beats/min. However, the effective pacing rate was lower (55 +/- 11 beats/min) due to invocation of pause-promoting features (hysteresis [4 patients]; + PVARP extension on PVC [1 patient]) or ventricular oversensing (2 patients). No patient developed TP with an effective pacing rate > 70 beats/min. TP is possible in the presence of a functional permanent pacemaker. Programmed lower rates < or = 70 beats/min are not protective. At programmed lower rates > 70 beats/min, TP may occur only when facilitated by programmable pause-promoting features or oversensing. It remains to be seen if rate smoothing algorithms can prevent TP when the baseline rate is programmed < or = 70 beats/min.

A patient with a dual chamber implantable defibrillator and pause dependent VT in whom a rate smoothing algorithm failed to operate during automatic mode switching due to device idiosyncrasy is reported. Preventive measures are discussed.

EGUÍA, L.E., ET AL.: Which is the Optimal Testing Method for Identifying an AV Delay that Allows In trinsic Conduction? It is desirable to maintain normal, conducted ventricular activation in patients with dual-chamber pacemakers and preserved atrioventricular (A V) conduction. The shortest A V delay result ing in consistent ventricular inhibition (avoiding ventricular pseudofusion) was determined by a conven tional incremental (inside-out) technique vs the alternate décrémentai (outside-in) technique in 20 such patients. Determinations were made in VDD mode in 20 patients and DDD mode (-10 beats/min faster than the intrinsic rate) in 19. In VDD mode, the shortest AV delay avoiding ventricular pseudofusion was never found during inside-out testing. It was identical with both methods in 10 patients (50%o), and shorter by 10-80 ms (mean 20 ± 20 ms) with the outside-in method in the remaining 10 (P = 0.004). In DDD mode, the shortest A V delay resulting in consistent ventricular inhibition was found only once during inside-out testing. It was the same with both methods in 13 patients (68%), and shorter by 10-20 ms (mean 14 ± 5 ms) with the outside-in method in the remaining 5 (26%, P = 0.18; Fisher's exact test). The shortest sensed A V delay preventing ventricular pseudofusion is most likely to be found with a décrémentai method (out side-in). In rare patients, it identifies AV delays resulting in inhibition, while ventricular pacing persists at longer programmable AV delays with the conventional inside-out approach. (PACE 2000; 23[Pt. II]:1758-1761 pacemaker, AV delay, sinus node dysfunction, PR interval