INTRODUCTION: Although decreased vagal tone, as measured by heart rate variability is a risk factor for ventricular fibrillation (VF) and sudden cardiac death, it is unknown whether increasing vagal tone has an antiarrhythmic effect. The purpose of this study was to determine whether edrophonium hydrochloride (HCI), a vagomimetic agent, increases VF threshold. METHODS AND RESULTS:Twenty-eight consecutive patients with previouslyimplanted defibrillators had two inductions of VF by monophasic direct-current shocks delivered at 10 to 30 msec after the T wave peak, escalating energies (0.4, 1, then 3 J) until VF was induced. If VF was not induced, this protocol was repeated at the T wave peak and then at 10 to 30 msec before the T wave until VF was induced. Patients were randomized to receive edrophonium HCl (12 to 18 mg) or no drug before repeating the protocol for the second VF induction. The mean sinus cycle length increased from 782 to 872 msec in the group receiving edrophonium HCI (P = 0.006 ). In the control group, the mean sinus cycle length remained unchanged (838 vs 858 msec). The mean energy to induce VF, coupling interval relative to the T wave, and the number of attempts to induce VF were not different between VF induction attempts 1 and 2, and they were not different between the group receiving edrophonium HCl and the control group. CONCLUSION: In a sedated patient population with implantable defibrillators, edrophonium HCI infusion prolongs sinus cycle length but does not change inducibility of VF using T wave shocks.
RCT Entities:
INTRODUCTION: Although decreased vagal tone, as measured by heart rate variability is a risk factor for ventricular fibrillation (VF) and sudden cardiac death, it is unknown whether increasing vagal tone has an antiarrhythmic effect. The purpose of this study was to determine whether edrophonium hydrochloride (HCI), a vagomimetic agent, increases VF threshold. METHODS AND RESULTS: Twenty-eight consecutive patients with previously implanted defibrillators had two inductions of VF by monophasic direct-current shocks delivered at 10 to 30 msec after the T wave peak, escalating energies (0.4, 1, then 3 J) until VF was induced. If VF was not induced, this protocol was repeated at the T wave peak and then at 10 to 30 msec before the T wave until VF was induced. Patients were randomized to receive edrophonium HCl (12 to 18 mg) or no drug before repeating the protocol for the second VF induction. The mean sinus cycle length increased from 782 to 872 msec in the group receiving edrophonium HCI (P = 0.006 ). In the control group, the mean sinus cycle length remained unchanged (838 vs 858 msec). The mean energy to induce VF, coupling interval relative to the T wave, and the number of attempts to induce VF were not different between VF induction attempts 1 and 2, and they were not different between the group receiving edrophonium HCl and the control group. CONCLUSION: In a sedated patient population with implantable defibrillators, edrophonium HCI infusion prolongs sinus cycle length but does not change inducibility of VF using T wave shocks.