Some newer cardiac pacemakers are able to control the efficacy of the ventricular pacing pulse beat by beat and to adjust the ventricular output to the actual pacing threshold. This capture verification is based on the detection of the ventricular evoked response amplitude, which has to be detected immediately after the pacing pulse. The sensitivity of the pacemaker to detect the evoked response amplitude must be adjusted individually to avoid the simultaneous detection of lead polarization. The aim of the present study was to evaluate the acute effects of a class IA antiarrhythmic drug on the evoked response amplitude and polarization in 13 pacemaker patients. The implanted pacemaker was the VVIR pacemaker Regency (St. Jude Medical), which provides the automatic capture verification algorithm Autocapture. The patients received 50 mg of ajmaline intravenously within 1 min. The evoked response amplitude and polarization were measured before and 2, 4, 6 and 8 min after ajmaline injection. The evoked response amplitude significantly decreased from 8.0 ± 4.0 mV to a minimum value of 6.4 ± 3.1 mV 2 min after drug administration. The decrease remained significant from the end of the application up to 6 min. The recommended sensitivity setting for the evoked response significantly (p < 0.05) decreased from 4.0 ± 2.3 mV before to 3.1 ± 1.3 mV 2 min after administration. No significant changes were observed for polarization. After the ajmaline application in 2 patients, the pacemaker recommended the deactivation of Autocapture for 9 min in 1 patient and 12 min in the other. The reasons were a decrease in the evoked response amplitude from 3.1 to 1.9 mV and from 9.0 to 5.7 mV, respectively, with a polarization ranging to about 3.0 mV. In conclusion, the ajmaline injection decreased the evoked response amplitude for some minutes. These findings indicate that antiarrhythmic drugs can alter the automatic capture verification function.

1.
Clarke M, Liu B, Schuller H, Binner L, Kennergren C, Guerola M, Weinmann P, Ohm OJ: Automatic adjustment of pacemaker stimulation output correlated with continuously monitored capture thresholds: A multicenter study. European Microny Study Group. Pacing Clin Electrophysiol 1998;21:1567–1575.
2.
Schuchert A, Meinertz T: Automatic measurement of the ventricular pacing threshold with a new pacemaker algorithm for pacing verification (Capturecontrol). Pacing Clin Electrophysiol 1999;22:A59.
3.
Callaghan F, Vollmann W, Livingston A, Boveja B, Abels D: The ventricular depolarization gradient: Effects of exercise, pacing rate, epinephrine, and intrinsic heart rate control on the right ventricular evoked response. Pacing Clin Electrophysiol 1989;12:1115–1130.
4.
Schuchert A, Meinertz T: Influence of exercise on the evoked response of the pacing impulse for Autocapture. Pacing Clin Electrophysiol 1998;21:977.
5.
Dhein S, Muller A, Gerwin R, Klaus W: Comparative study on the proarrhythmic effects of some antiarrhythmic agents. Circulation 1993;87:617–630.
6.
Padrini R, Piovan D, Javarnaro A, Cucchini F, Ferrari M: Pharmacokinetics and electrophysiological effects of intravenous ajmaline. Clin Pharmacokinet 1993;25:408–414.
7.
Schüller H, Kruse IB, Svennsson O, Mortensen P: Long-term benefit of autocapture – four years of follow-up. Pacing Clin Electrophysiol 1999;22:807.
8.
Huting J, Thormann J, Mitrovic V, Schlepper M: Improved diastolic LV filling after acute application of ajmaline in patients with coronary artery disease and normal systolic LV function. Clin Cardiol 1990;13:485–489.
9.
Gussak I, Antzelevitch C, Bjerregaard P, Towbin JA, Chaitman BR: The Brugada syndrome: Clinical, electrophysiologic and genetic aspects. J Am Coll Cardiol 1999;33:5–15.
10.
Englund A, Bergfeldt L, Rosenqvist M: Pharmacological stress testing of the His-Purkinje system in patients with bifascicular block. Pacing Clin Electrophysiol 1998;21:1979–1987.
11.
Rowland E, McKenna WJ, Krikler DM: Electrophysiologic and antiarrhythmic actions of bepridil. Comparison with verapamil and ajmaline for atrioventricular reentrant tachycardia. Am J Cardiol 1985;55:1513–1519.
12.
Chen X, Borggrefe M, Martinez-Rubio A, Hief C, Haverkamp W, Hindricks G, Breithardt G: Efficacy of ajmaline and propafenone in patients with accessory pathways: A prospective randomized study. J Cardiovasc Pharmacol 1994;24:664–669.
13.
Manz M, Mletzko R, Jung W, Luderitz B: Electrophysiological and haemodynamic effects of lidocaine and ajmaline in the management of sustained ventricular tachycardia. Eur Heart J 1992;13:1123–1128.
14.
Stark G, Schwarzl I, Stark U, Decrinis M, Tritthart HA: Rate-dependent effects of ajmaline and propafenone on atrioventricular conduction. Eur J Pharmacol 1996;310:29–35.
15.
Anvari A, Mast F, Schmidinger H, Schuster E, Allessie M: Effects of lidocaine, ajmaline, and diltiazem on ventricular defibrillation energy requirements in isolated rabbit heart. J Cardiovasc Pharmacol 1997;29:429–435.
16.
Mohan JC, Kaul U, Bhatia ML:Acute effects of anti-arrhythmic drugs on cardiac pacing threshold. Acta Cardiol 1984;39:191–201.
17.
Svorcik C, Bicikova L: Effect of drugs on the stimulation threshold of the human heart. Cor Vasa 1978;20:184–195.
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