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  • ECG changes emerged when creating a substrate map of

    2019-06-12

    ECG changes emerged when creating a substrate map of the LV (Fig. 2A), near the inferior mitral valve. A long transseptal sheath was introduced into the LV under intracardiac echocardiography guidance without causing an air-embolism. While performing the LV substrate mapping, the long transseptal sheath and mapping catheter appeared to have pushed against the LV wall (Fig. 2A) and premature ventricular contractions were frequently observed. During the ECG change, there were no chest symptoms and his blood pressure and melanin rate remained stable. It took approximately 20s for the ECG change to appear and it lasted for approximately 2min; the change recovered spontaneously during observation. A voltage map revealed a dense scar in both the anterior and inferior regions (Fig. 2B and C), and an irrigated radiofrequency application to the inferior scar region with good pace mapping rendered the targeted VT noninducible. A pilsicainide test was negative and no coved-type ECGs have appeared since then.
    Discussion To the best of our knowledge, a Brugada-like ECG induced by catheter manipulation during ischemic VT ablation has not been previously reported. There are many reports of ST elevation in the inferior leads during ablation after the Brockenbrough technique [3]; however, this patient exhibited an ECG change mainly in leads V1 and V2 without any reciprocal changes within 5min of the Brockenbrough approach. The mechanism of the ECG change was unknown. The conus branch of the right coronary artery is well known to supply the right ventricular outflow tract. Air embolisms and vasospasms during ablation have been reported in several cases [3]. In this case, ischemia of the conus branch of the right coronary artery was considerable; however, the absence of chest symptoms and immediate recovery of ST elevation indicates that involvement of the coved-type ECG change and ischemia was impossible to verify. There are reported cases of VT/ventricular fibrillation, induced during coved-type ST-elevation by ischemia of the conus branch of the right coronary artery [4]. However, in our case, VT was sustained neither during the ST-elevation nor by electrical stimulation after the procedure; thus the clinical significance of coved-type ECG change during catheter ablation of ischemic VT was unclear.
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    Introduction Although the pulmonary veins (PVs) represent the predominant source of atrial fibrillation (AF), non-PV triggers play an important role in initiating and maintaining AF in approximately 20% of cases [1–3]. Episodes of atrial tachyarrhythmias (ATs) and AF originating from non-PV triggers are often unpredictable and difficult to identify, owing to their transient duration and diverse locations. Furthermore, the precise location may remain unknown, even with the use of a three-dimensional electroanatomic mapping system (3DEAM). Several studies have indicated that an intravenous injection of adenosine, in the form of adenosine triphosphate (ATP), can induce the transient reconnection of isolated PVs after electric isolation, consistent with unmasking dormant conduction between the PVs and the left atrium (LA) [4,5]. Furthermore, ATP, when given as an intravenous bolus, can induce AF [6]. In addition, several studies have recently described the usefulness of an ATP injection for inducing and identifying PV and/or non-PV triggers after circumferential pulmonary vein ablation (CPVI) [7,8]. Here, we describe a case of paroxysmal AF originating from a non-PV trigger, which was precisely identified using ATP infusion and successfully treated using radiofrequency catheter ablation (RFCA).
    Case report A 54-year-old woman was referred to our institution because of frequent episodes of palpitation and chest discomfort. Although she was taking several antiarrhythmic drugs, a symptomatic 12-lead electrocardiogram (ECG) revealed AF, and RFCA was indicated. After obtaining informed consent from the patient, RFCA was performed under deep sedation/analgesia using propofol and dexmedetomidine. Two circular mapping catheters (EPstar Libero, Japan Lifeline Inc., Tokyo, Japan) were placed in the superior and inferior PVs, respectively, via a transseptal puncture site, and the left and right-sided ipsilateral PVs were circumferentially and extensively ablated, using 3DEAM (CARTO, Biosense Webster, Inc., Diamond Bar, CA, USA) under electrophysiological guidance. After the initial electric isolation of all 4 PVs, a 20-mg ATP bolus was injected to provoke dormant PV conduction during coronary sinus pacing. Although no electric reconduction was observed in the left or right PVs, AF was reproducibly induced (Fig. 1). The duration of AF was very short (<20s), and no further AF episodes were observed, even during an intravenous drip infusion of isoproterenol (ISP: dosage up to 5μg/min), so no further mapping or RFCA was performed, with the exception of linear ablation at the cavotricuspid isthmus.