Slow Potential at the Entrance of the Slow Conduction Zone in the Reentry Circuit of a Verapamil‐Sensitive Atrial Tachycardia Originating From the Atrioventricular Annulus

Abstract

Background Slow conduction zone in a verapamil‐sensitive reentrant atrial tachycardia originating from atrioventricular annulus is composed of calcium channel–dependent tissue. We examined whether there was a slow potential ( SP ) at the entrance of the slow conduction zone. Methods and Results We first identified the pacing site from where manifest entrainment and orthodromic capture of the earliest atrial activation site were demonstrated in 40 atrioventricular annulus patients with atrioventricular annulus. Radiofrequency energy was then delivered 2 cm proximal to the earliest atrial activation site in the direction of entrainment pacing site and gradually advanced toward the earliest atrial activation site until atrial tachycardia termination to localize the entrance of the slow conduction zone. Electrogram characteristics were analyzed at successful and unsuccessful ablation sites. During sinus rhythm, SP was observed at all 40 successful sites, but was observed at only 12 unsuccessful sites ( P <0.0001). During sinus rhythm, there was no significant difference in electrogram amplitude nor width of atrial electrogram between successful and unsuccessful sites (0.407±0.281 versus 0.487±0.447 mV [ P =0.1989] and 37.0±9.2 versus 38.9±8.0 ms [ P =0.1773]); however, SP amplitude and width at successful sites were significantly greater than those at unsuccessful sites (0.110±0.049 versus 0.025±0.046 mV [ P <0.0001] and 38.8±13.4 versus 8.1±13.2 ms [ P <0.0001]). During atrial tachycardia, SP amplitude was significantly attenuated (0.088±0.042 versus 0.110±0.049 mV, P <0.001) and SP width was significantly prolonged (47.8±14.1 versus 38.8±13.4 ms, P <0.0001) at successful sites. Conclusions SP was observed during sinus rhythm at the entrance of the slow conduction zone; however, SP amplitude was attenuated and SP width was prolonged during atrial tachycardia, suggesting that SP reflects the characteristics of calcium channel–dependent tissue involved in atrioventricular annulus reentry circuit.