Key result
Intravenous ajmaline decreased the ventricular evoked response amplitude from 8.0 mV to 6.4 mV at 2 minutes in patients with cardiac pacemakers.
Why the study?
Does intravenous ajmaline alter the ventricular evoked response amplitude in patients with cardiac pacemakers?
Does intravenous ajmaline alter the ventricular evoked response amplitude in patients with cardiac pacemakers?
Intravenous ajmaline acutely decreases the ventricular evoked response amplitude, which can interfere with automatic capture verification algorithms in pacemakers.
Answers are grounded in this paper and cite their sources.
May interfere with pacemaker capture verification algorithms; leaves open need for periprocedural adjustments.
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.
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Schuchert et al. (2000) studied Cardiac pacemakers (n=13). Ajmaline vs. Baseline (before administration) was evaluated on Ventricular evoked response amplitude at 2 minutes. Intravenous ajmaline decreased the ventricular evoked response amplitude from 8.0 mV to 6.4 mV at 2 minutes in patients with cardiac pacemakers.
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