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Notes: AIBA, T., et al.: The Role of Purkinje and Pre-Purkinje Potentials in the Reentrant Circuit of Verapamil-Sensitive Idiopathic LV Tachycardia. Although the mechanism of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) is usually reentry, the actual reentrant circuit is not clearly understood. This study examined the relationship between the Purkinje potential (PP) and a dull potential preceding PP (pre-PP) during ILVT to elucidate the roles of these potentials in the reentrant circuit of ILVT. Electrophysiological studies and radiofrequency catheter ablation were performed in ten patients (7 men, 3 women, mean age 29 years) who had an ILVT with a right bundle branch block configuration and left-axis deviation. Left ventricular endocardial mapping using an octapolar catheter and entrainment and resetting studies during VT was performed by pacing from the right ventricular outflow tract (RVOT) and each site of the left ventricular mapping catheter. PP and pre-PP were recorded simultaneously during VT in all patients. The earliest PP during VT was recorded at the inferoposterior septum, and PP was activated bidirectionally toward the proximal (basal) and distal (apical) sites along the left posterior fascicle. In contrast, pre-PP was recorded at sites slightly proximal to the earliest PP recording site, and was activated toward the earliest PP site. Pacing from RVOT confirmed manifest entrainment, and the stimulus to pre-PP interval was prolonged with a shorter pacing cycle length. Concealed entrainment was demonstrated by capture of the PPs of the left ventricular mapping catheter in six patients, and the postpacing interval at each PP site was equal to the tachycardia cycle length. The pre-PP was orthodromically activated from the proximal to the distal site during pacing. More rapid pacing also produced delay in activation from PP to pre-PP, indicating slow conduction in ILVT. Catheter ablation was performed at the pre-PP recording site during VT, and was successful in all patients. The reentrant circuit of ILVT could be constructed based on the pre-PP, PP, and slow conduction between the PP and pre-PP. Catheter ablation of ILVT was successful at the pre-PP recording site.

Notes: Although chronic amiodarone has been proven to be effective to suppress ventricular tachycardia (VT) and ventricular fibrillation (VF), how we predict the recurrence of VT/VF after chronic amiodarone remains unknown. This study evaluated the predictive value of the QT interval, spatial, and transmural dispersions of repolarization (SDR and TDR) for further arrhythmic events after chronic amiodarone. Eighty-seven leads body surface ECGs were recorded before (pre) and one month after (post) chronic oral amiodarone in 50 patients with sustained monomorphic VT associated with organic heart disease. The Q-Tend (QTe), the Q-Tpeak (QTp), and the interval between Tpeak and Tend (Tp-e) as an index of TDR were measured automatically from 87-lead ECG, corrected Bazett's method (QTce, QTcp, Tcp-e), and averaged among all 87 leads. As an index of SDR, the maximum (max) minus minimum (min) QTce (max-min QTce) and standard deviation of QTce (SD-QTce) was obtained among 87 leads. All patients were prospectively followed (15 ± 10 months) after starting amiodarone, and 20 patients had arrhythmic events. The univariate analysis revealed that post max QTce, post SD-QTce, post max-min QTce, and post mean Tcp-e from 87-lead but not from 12-lead ECG were the significant predictors for further arrhythmic events. ROC analysis indicated the post max-min QTce ≥106 ms as the best predictor of events (hazard ratio = 10.4, 95%, CI 2.7 to 40.5, P = 0.0008). Excessive QT prolongation associated with increased spatial and transmural dispersions of repolarization predict the recurrence of VT/VF after amiodarone treatment. (PACE 2004; 27:901–909)

Notes: TAKAGI, M., et al.: Change in Morphology of Reentrant Atrial Arrhythmias Without Termination Following Radiofrequency Catheter Ablation. A 60-year-old woman who had previously undergone an atrial septal defect repair and had type I atrial flutter underwent electrophysiological study. After radiofrequency (RF) ablation to the isthmus between the inferior vena cava and the tricuspid annulus, type I atrial flutter was changed to atrial tachycardia following atriotomy without termination. This atrial tachycardia was eliminated by single-site RF ablation of a small lesion below the caudal end of the atriotomy scar, where continuous and fragmented potentials were recorded during tachycardia. We experienced a rare case in which RF energy changed tachycardia circuits.

Notes: Ogawa, M., et al.: Acute Effects of Different Atrial Pacing Sites in Patients with Atrial Fibrillation: Comparison of Single site and Biabrial Pacing. It has been reported that atrial single site or biatrial pacing can suppress the occurrence of AF. However, its mechanism remains unclear. The study population included 32 patients with AF (n = 20: AF group), or without paroxysmal AF (n = 12: control group). The mechanism and efficacy of atrial pacing were investigated by electrophysiological studies to determine which was more effective for suppressing AF induction; single site pacing of the right atrial appendage (RAA) or distal coronary sinus (CS–d), or biatrial (simultaneous RAA and CS–d) pacing. In the AF group, AF inducibility was significantly higher with RAA extrastimulus during RAA (12/20; P 〈 0.0001) or biatrial paced drive (7/20; P 〈 0.01) than during CS–d paced drive (0/20). In the control group, AF was not induced at any site paced. In the AF group, the conduction delay and other parameters of atrial vulnerability significantly improved during CS–d paced drive. The atrial recovery time (ART) at RAA and CS–d was measured during each basic pacing mode. ART was defined as the sum of the activation time and refractory period, and the difference between ARTs at RAA and CS–d was calculated as the ART difference (ARTD). The ARTD was significantly longer during RAA pacing in the AF group than in control group (155.0 ± 32.8 vs 128.8 ± 32.9 ms, P 〈 0.05). In the AF group, ARTDs during biatrial (52.0 ± 24.2 ms) and CS–d pacing (51.7 ± 26.0 ms) were significantly shorter than ARTD during RAA pacing. The CS–d paced drive was more effective for suppressing AF induction than biatrial or RAA paced drive by alleviating conduction delay. CS–d and biatrial pacing significantly reduced ARTD compared with RAA pacing.

Notes: The retrograde atrial potential at a successful ablation site is usually obscured by the wide and large ventricular potential during atrioventricular reentrant tachycardia or ventricular pacing, which makes it difficult to determine the appropriate ablation site for concealed accessory pathway. A pacing maneuver named the “simultaneous pacing method” is proposed herein to differentiate the retrograde atrial potential from the ventricular potential for a successful ablation of the concealed accessory pathway. Catheter ablation was performed in 12 patients with a single left free-wall concealed accessory pathway. The atrial insertion site was determined by the simultaneous pacing method in six patients (group I) and by ventricular pacing in six patients (group II), In the simultaneous pacing method, electrograms recorded during ventricular pacing in the earliest retrograde atrial activation site are a fusion of the ventricular potential and the following retrograde atrial potential. When atrial and ventricular pacings are performed simultaneously (simultaneous pacing), the end portion of the electrograms recorded at the same site is solely the ventricular component, because atrial is activated earlier. The atrial potential can be confirmed during ventricular pacing in comparison with the electrograms during the “simultaneous pacing.” Radiofrequency catheter ablation was successful in eliminating conduction through the accessory pathway in all 12 patients. The radiofrequency applications in group I were significantly fewer than those in group II (1.7 ± 1.0 in group I, 5.3 ± 3.2 in group II, P 〈 0.05). The total procedure time in group I was significantly shorter than in group II (57.8± 15.7 vs 106.7 ± 41.6 mins in group II. respectively, P 〈 0.05). The fluoroscopy time in group I was significantly shorter than in group II (54.0 ± 7.9 vs 81.3± 26.3 mins, respectively, P 〈 O.05). We were able to determine the atrial insertion site of accessory pathways by the simultaneous pacing method. The simultaneous pacing method was useful in eliminating concealed left free-wall accessory pathways.

Notes: Mid-Diastolic Potential in Idiopathic VT. We report a case of verapamil-sensitive idiopathic ventricular tachycardia in which a mid-diastolic potential (MDP) 45 msec preceding the Purkinje potential (P potential) was recorded. Pacing during the tachycardia caused concealed entrainment, and the stimulus–QRS interval was equal to the P potential–QRS interval. The interval between the last pacing stimulus and the next P potential (postpacing interval) was longer than the ventricular tachycardia cycle length, but the MDP was orthodromically activated. These findings suggest that the MDP was on the reentrant circuit and the P potential was not on the reentrant circuit, but a bystander.

Notes: Ventricular Fibrillation with J Wave in Inferior Leads. Introduction: The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described. Methods and Results: All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation. Conclusion: These characteristics were very similar to those of patients with Brugada syndrome. These three patients with these specific features might have a variant of Brugada syndrome.

Notes: Basket Catheter in Idiopathic VT. Introduction: It often is difficult to determine the optimal ablation site for idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) when the VT or premature ventricular complex (PVC) does not occur frequently. The aim of our study was to evaluate the usefulness of a multielectrode basket catheter for ablation of idiopathic VT originating from the RVOT. Methods and Results: Radiofrequency (RF) catheter ablation was performed using a 4-mm tip, quadripolar catheter in 50 consecutive patients with 81 VTs originating from the RVOT with (basket group = 25 patients with 45 VTs) or without (control group = 25 patients with 36 VTs) predeployment of a multielectrode basket catheter composed of 64 electrodes. Deployment of the multielectrode basket catheter was possible and safe in all 25 patients in the basket group. Ablation was successful in 25 (100%) of 25 patients in the basket group and in 22 (88%) of 25 patients in the control group. The total number of RF applications and the number of RF applications per PVC morphology did not differ between the two groups. However, both the fluoroscopic and ablation procedure times per PVC morphology were shorter in the basket group than in the control group (36.8 ± 14.1 min vs 52.0 ± 32.5 min, P = 0.04; 60.0 ± 14.6 vs 81.5 ± 51.2 min, P = 0.05). This difference was more pronounced in the 29 patients in whom VT or PVC was not frequently observed. Conclusion: The multielectrode basket catheter is safe and useful for determining the optimal ablation site in patients with idiopathic VT originating from the RVOT, especially in those without frequent VT or PVC.

Notes: ST Elevation in Brugada Syndrome. Introduction: Body surface distribution and magnitude of ST segment elevation and their reflection in 12-lead ECGs have not been clarified in Brugada syndrome. Methods and Results: Eighty-seven-lead body surface potential mapping and 12-lead ECGs were recorded simultaneously in 25 patients with Brugada syndrome and 40 control patients. The amplitude of the ST segment 20 msec after the end of QRS (ST20) was measured from all 87 leads, and an ST isopotential map was constructed. The maximum ST elevation (maxST20) was distributed in an area of the right ventricular outflow tract in all Brugada patients, and it was larger than that in control patients (0.37 ± 0.13 vs 0.12 ± 0.04 mV; P 〈 0.0005). The maximum was observed on the level of the parasternal fourth intercostal space, on which the VI and V2 leads of the standard 12-lead ECG were located, in 18 of the 25 Brugada patients in whom typical coved- or saddleback type ST elevation was seen in leads VI and V2. The maximum was located on the second intercostals space in the remaining seven Brugada patients in whom only a mild saddleback-type ST elevation was seen in leads V1 and V2 of the 12-lead ECG. Typical ST segment elevation was recognized in leads V1 and V2, which were recorded on the second or third intercostal space. ST elevation in Brugada patients was dramatically normalized by isoproterenol, a β-adrenergic agonist (maxST20 = 0.17 ± 0.08 mV; P 〈 0.0005 vs control conditions), and accentuated by disopyramide, an Na+ channel blocker (maxST20 = 0.50 ± 0.15 mV; P 〈 0.0005 vs control conditions), without any change in the location of the maxST20. Conclusion: Our data indicate that recordings of leads V1-V3 of the 12-lead ECG on the parasternal second or third intercostal space would be helpful in diagnosing suspected patients with Brugada syndrome. The data suggest that Na+ channel blockers are capable of accentuating ST elevation in leads V1-V3.