Purkinje potentials have been identified in some
Purkinje potentials have been identified in some cases of successful ablation of PVCs originating in the right ventricular papillary muscles, indicating a possible involvement of the Purkinje fibers as well as the left ventricular papillary muscles [3,4]. During our first procedure, a Purkinje potential was observed at the site of successful ablation, and the PVCs were subsequently eliminated, suggesting possible involvement of the Purkinje fiber system in the arrhythmogenic substrate . However, a Purkinje potential was not recorded during the second procedure. As the first radiofrequency ablation was performed at the sites where the Purkinje potential was recorded, the Purkinje potential might have disappeared by the time the second radiofrequency ablation was performed. Moreover, since the Purkinje potential did not clearly precede the PVCs, it Sephin1 may have represented a bystander electrocardiogram. Thus, the second radiofrequency ablation was performed despite the absence of a Purkinje potential.
Because the patient\'s responsiveness to medication was not examined and continuous VT was not observed, the mechanism behind the appearance of the PVCs in this case remains unknown. However, according to Crawford et al., automaticity might cause PVCs to originate in papillary muscles . Further studies of the association between papillary muscles and Purkinje potentials are required.
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Introduction Many adenosine-sensitive focal atrial tachycardias (ATs) originating from the vicinity of the His bundle can be delineated from the earliest activation site in the right atrium around the His bundle. Recent reports have demonstrated that in some cases, these types of AT can be successfully ablated from the non-coronary cusp (NCC) [1,2].
Case report No retrograde conduction was observed during ventricular pacing. After administering isoproterenol (ISP) infusion (0.5μg/min), we detected retrograde AV nodal conduction with the earliest atrial activation recorded at the His bundle region. Under the ISP infusion, an AT (cycle length: 385ms) (Fig. 1) was easily induced by atrial extrastimulus and/or burst pacing from the right atrium without a jump-up in the atrial-His interval. The AT episodes were inducible during stimuli of basic cycle length, and spontaneous self-termination was observed without atrial premature beats. No negative correlation was observed between the coupling interval of the atrial extrastimulus that induced the tachycardia and the post-extrastimulation return cycle. The AT persisted irrespective of spontaneous AV block. An intravenous bolus of 2.5-mg adenosine-5′-triphosphate (ATP) administered during tachycardia reproducibly terminated the AT without AV block. AV dissociation was observed during ventricular overdrive pacing in AT. Tachycardia was also induced by a ventricular extrastimulus with a V-A-A-V pattern. The activation sequence during tachycardia differed from that observed during sinus rhythm and retrograde AV nodal conduction. In the right atrium, the earliest activation site was recorded at the proximal His site that preceded the onset of the P-wave on the 12 lead ECG by 22ms. RF energy delivered with a 4-mm tip catheter (30W, maximal temperature of 55°C) was applied to the earliest activation site in the right atrium, but it could not successfully terminate the AT. Therefore, we mapped the aortic NCC using the retrograde approach (Fig. 2). RF energy applications at that site transiently terminated the AT following an unstable AT cycle length, but pacing recurrently induced the AT, which then transiently terminated. The subsequent AT activation sequence and cycle length did not change significantly. Despite carefully searching the LCC, we could not find an earlier activation site. Finally, we mapped the left atrium using the transseptal approach. The earliest activation site in the left atrium was recorded in the area just behind the LCC (Fig. 3). RF energy application at this site successfully terminated the AT, and the AT could no longer be induced.