Abstract
In paroxysmal reciprocating atrioventricular tachycardia (PRAVT), it is well established that anti-arrhythmic drugs may have an effect on one or more components of the re-entry circuit. These components depend for their depolarisation on fluxes of sodium or calcium ions [1], and agents that can specifically antagonise the transmembrane passage of these ions will have actions at specific sites. We have administered the sodium antagonist ajmaline and the calcium antagonist verapamil during intracardiac electrophysiological study. We have observed the ability of the drugs to terminate induced PRAVT, and then we examined the time-dependent changes in electrophysiological properties of the atrioventricular (AV) pathways, the accessory pathway (AP) on the one hand and the AV node on the other, in response to the drugs. As a result of these changes it is possible to comment on the effect on the mechanism of the tachycardia and more specifically on the ease of initiation.
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