Demonstration of diastolic and presystolic purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia
Akihiko Nogami, MD*,
Shigeto Naito, MD ,
Hiroshi Tada, MD,
Koichi Taniguchi, MD, FACC,
Yoshihiro Okamoto, MD*,
Shigeyuki Nishimura, MD, FACC*,
Yasuteru Yamauchi, MD ,
Kazutaka Aonuma, MD,
Masahiko Goya, MD ,
Yoshito Iesaka, MD and
Michiaki Hiroe, MD||
* Division of Cardiology, Yokohama Rosai General Hospital, Yokohama, Kanagawa, Japan
Division of Cardiology, Gunma Prefectural Cardiovascular Center, Maebashi, Gunma, Japan
Division of Cardiology, Yokosuka Kyosai General Hospital, Yokosuka, Kanagawa, Japan
Cardiovascular Center, Tsuchiura Kyodo General Hospital, Tsuchiura, Ibaraki, Japan
|| Second Department of Medicine, Tokyo Medical and Dental University, Tokyo, Japan
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Figure 1 Patient 3. Representation of an octapolar electrode catheter positioned at the left ventricular septum as viewed fluoroscopically in the right oblique (RAO) and left oblique (LAO) projections. The distance between electrodes 1 and 8 of the octapolar electrode catheter was approximately 25 mm. HBE = His-bundle electrogram; LV = left ventricle; RVA = right ventricular apex; RVO = right ventricular outflow tract.
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Figure 2 Patient 3. Intracardiac recordings from octapolar electrode catheter. (A) During VT a diastolic potential (P1) and a presystolic Purkinje potential (P2) were recorded. While P1 was recorded earlier from the proximal than the distal electrodes, P2 was recorded earlier from the distal than the proximal electrodes. (B) During sinus rhythm recording at the same site demonstrated the P2, which was recorded before the onset of QRS complex.
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Figure 3 Patient 3. Concealed entrainment by pacing from VT exit site. During VT the earliest ventricular electrogram with the fused P2 was recorded from the distal two electrodes. (A) Pacing from the distal two electrodes at a cycle length and a starting coupling interval of 400 ms captured P1 orthodromically and produced QRS configurations similar to that of the VT. The postpacing interval (PPI) (S-P2) was equal to the VT cycle length. (B) Pacing from VT exit site at a cycle length of 380 ms also captured P1. Diastolic potential was simultaneously observed with pacing artifact from LV7-8. Pacing stimulus P1 interval was prolonged. (C) Pacing from VT exit at a cycle length of 400 ms but with a starting coupling interval of 300 ms terminated VT. Diastolic potential was not observed during pacing because it might be captured antidromically and masked in the ventricular electrogram. PPI = post pacing interval; P1 = diastolic potential; P2 = presystolic Purkinje potential; S = pacing stimulus; VT = ventricular tachycardia.
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Figure 4 Patient 4. Resetting and termination of VT with double ventricular extrastimuli from right ventricle. (A) The first impulse did not reset the tachycardia, but the second impulse captured a P1 orthodromically and produced the resetting manifested by a less than compensatory pause. (B) When the S1-S2 coupling interval was shortened, the conduction time from the stimulus to the orthodromically activated P1 was significantly prolonged. This resulted in the increasing return cycle. (C) When the second impulse was delivered even more prematurely, it encountered refractoriness in the orthodromic direction, and the tachycardia terminated. P1 = diastolic potential; VT = ventricular tachycardia.
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Figure 5 Patient 3. Resetting of VT by a spontaneous sinus capture. After the second complex of VT, a sinus capture occurred resulting in narrowing of the QRS width without interruption of the tachycardia. Presystolic Purkinje potential (P2) and ventricular electrogram was advanced by sinus beat, and the earliest P2 was recorded from LV3-4. The subsequent P1 and VT had been reset because pauses were less than fully compensatory. A = atrial electrogram; HBE = His bundle electrogram; LV = left ventricle; P1 = diastolic potential; P2 = presystolic Purkinje potential.
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Figure 6 Patient 4. Effect of verapamil on VT circuit. Intravenous administration of 1.5 mg verapamil significantly prolonged cycle length of VT from 305 ms (A) to 350 ms (B). Both P1-P2 and P2-P1 intervals were proportionally prolonged after verapamil. However, the interval from P2 to the onset of the QRS complex remained unchanged. HRA = high right atrium; P1 = diastolic potential; P2 = presystolic Purkinje potential; RVA = right ventricular apex; VT = ventricular tachycardia; VT CL = cycle length of ventricular tachycardia.
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Figure 7 Patient 1. Recordings at the site of successful ablation during ventricular tachycardia. Diastolic potential and P2 were recorded in the midseptal area. The proximal two electrodes of ablation catheter recorded the P1 15 ms earlier than the distal pair of electrodes. HBE = His bundle electrogram; HRA = high right atrium; LV = left ventricle; P1 = diastolic potential; P2 = presystolic Purkinje potential; RVA = right ventricular apex.
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Figure 8 Patient 7. Application of radiofrequency current delivered during ventricular tachycardia. During energy application P1-P2 interval was gradually prolonged, and ventricular tachycardia was terminated by block between P1 and P2. After ablation the P1 occurred after the QRS complex during sinus rhythm. ABL = ablation catheter; H = His bundle electrogram; HBE = His bundle electrogram; P1 = diastolic potential; P2 = presystolic Purkinje potential; RF = radiofrequency current.
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Figure 9 Patient 1. Successful ablation site during sinus rhythm. (A) Before ablation. Diastolic potential was not observed during sinus rhythm. (B) After ablation, the P1 occurred after the QRS complex. The activation sequence for P1 was identical to that observed during VT shown in Figure 7. H = His bundle electrogram; HBE = His bundle electrogram; LV = left ventricle; P1 = diastolic potential; P2 = presystolic Purkinje potential; RVA = right ventricular apex; VT = ventricular tachycardia.
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Figure 10 Patient 1. Right ventricular pacing after successful ablation. (A) The S-P1 interval was 224 ms during right ventricular pacing at a cycle length of 500 ms. (B) The S-P1 interval increased to 242 ms at a cycle length of 300 ms. CL = cycle length; HRA = high right atrium; P1 = diastolic potential; T = T-wave; VP = ventricular pacing.
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Figure 11 Patient 14. Diastolic potential before and after verapamil during atrial paced rhythm. (A) After ablation, the split P1 potentials (P1 and P1') were observed after the QRS complex. (B), (C) After intravenous administration of verapamil, the dose dependent prolongation of His-bundle (H) to P1 (H-P1) interval, H-P1' interval and P1-P1' interval occurred. AP = atrial pacing; P1 = diastolic potential.
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Figure 12 Schematic representation of the mechanism. See text for discussion. CL = cycle length; P1 = diastolic potential; P2 = presystolic Purkinje potential; VT = ventricular tachycardia.
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