Background-We sought to determine the potential of right ventricular VVI backup pacing to induce ventricular tachyarrhythmias in patients with implanted cardioverter-defibrillators. Methods and Results-All consecutive patients presenting exclusively with pacemaker-induced tachycardias (PITs) were included in a prospective study using a crossover protocol. Patients were randomized to either group 1 (augmentation of the baseline frequency of the pacemaker to 60 bpm) or group 2 (pacemaker turned off) and were followed up for 1 year and then crossed over to the other programming, looking for reoccurrence of PIT. Of 150 consecutive patients, 39 (26%) had PIT, 13 of them exclusively (8.6%). Forty of 1063 analyzed tachyarrhythmias of all the patients were PIT (3%). Before inclusion in the study, the patients had 2.7Ϯ0.9 PITs in 11Ϯ6.5 months with their pacemakers programmed empirically at 42.3 bpm. During the study phase, no PIT occurred while the pacemaker was turned off, whereas programming to 60 bpm led to the recurrence of PIT in 5 of 6 patients (1.4Ϯ0.6 per patient). At the end of the study, 9 patients underwent a prolonged follow-up with their pacemakers turned off, resulting in spontaneous episodes of ventricular tachycardia/fibrillation in 5 patients, but PITs were no longer observed. Conclusions-This crossover protocol proves the potential proarrhythmic effect of pacemaker stimulation in implantable cardioverter-defibrillator patients. Resulting PITs led to clinical symptoms and antitachycardia therapy by the implantable cardioverter-defibrillator. Thus, in patients presenting with PIT but without a pacemaker indication, the pacemaker feature should be turned off, or, alternatively, the longest possible escape interval should be programmed.

, and was insensitive to dihydropyridines (up to 30 mM). It was signi®cantly blocked by o-CTx-GVIA (1 mM), o-Aga-IVA (30 nM) and was con®rmed to be abolished by o-CTx-MVIIC (3 mM), indicating involvement of N-, P-and Q-type channel subtypes. , suggesting that Na + rather than Q-type Ca 2+ channels are involved. 5 Taken together, our results suggest that verapamil can block P-and at higher concentrations possibly N-and Q-type Ca 2+ channels linked to [ 3 H]-DA release, whereas diltiazem appears to block P-type Ca 2+ channels only.

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