926-29 Mechanisms for Pacing-induced Slowing in Conduction within the Reentrant Ventricular Tachycardia Circuit. Importance of True Fatigue in Conduction

Abstract

It has been demonstrated experimentally and suggested clinically that post-repolarization refractoriness can produce pacing-induced conduction delays in ventricular tachycardia (VT) circuits. To evaluate the contribution of true fatigue in conduction to such phenomena during burst pacing, we compared the response to single extrastimuli entering the reentrant circuit with a known coupling interval (CI) to the response to synchronized 15 to 21 beat bursts with repetitive fast penetration of the VT circuit. Each extrastimulus was preceded by a 15 to 21-beat “slow” pacing train producing entrainment of the VT to ensure that the extrastimuli entered the VT circuit with an interval similar to the CI at the pacing site. The degree of fatigue was quantitated by subtracting the first post-pacing interval (FPPI) after each extrastimulus from the FPPI after a pacing burst of a cycle length (CL) identical to the CI of that extrastimulus. We evaluated the degree of fatigue during 44 CL in 11 VT (mean VT CL 340 ± 47 ms). FPPI was shorter after extrastimuli (465 ± 79 ms) than after their correspondent bursts (486 ± 93 ms, p < 0.001 by paired t-test). The degree of fatigue was related to the pacing CL (29 ± 42 ms for bursts CL <85% of VT CL vs 11 ± 21 for bursts CL = 85% of VT CL, p < 0.05). There was a trend towards a higher degree of fatigue in VT while on antiarrhythmic drugs (25 ± 41 ms vs 11 ± 9 ms, p<0.1). True fatigue in conduction adds to the possible conduction delays related to refractoriness within clinical reentrant VT circuits. This may explain why, not only rate but duration of pacing, can be critical for VT termination, particularly with fast pacing rates.