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Notes: T Wave Alternans in Brugada Syndrome and Vasospastic Angina. A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.

Notes: CHINUSHI, Y., et al.: Microdislodgment of Ventricular Pacing Lead Undetectable During Rapid Pacing One Year After Implantation. A 71-year-old woman had undergone valvular heart surgery in 1981, and implantation of a permanent ventricular pacemaker for ventricular pauses during atrial fibrillation in 2001. One year after pacemaker implantation, she complained of faintness. When pacing at 100 beats/min the pacemaker functioned properly. However, pacing and sensing failure was detected at a pacing rate of 60 beats/min. At rapid pacing rates, the lead tip was in closer contact with the endocardium, and its microdislodgment was undetectable. The symptoms have resolved since the lead was repositioned. (PACE 2003; 26:787–788)

Notes: CHINUSHI, M., et al.: Induction of Ventricular Fibrillation in Brugada Syndrome by Site-Specific Right Ventricular Premature Depolarization. This patient was a 50-year-old man. Oral pilsicainide unmasked a Brugada-type ECG abnormality and self-terminating polymorphic VT was repetitively induced. The polymorphic VT always developed following a specific ventricular premature complex showing a left bundle branch block pattern suggesting a limited origin in the right ventricle.

Notes: TAGAWA, M., et al.: Myocardium Extending from the Left Atrium onto the Pulmonary Veins: A Comparison Between Subjects with and Without Atrial Fibrillation. Rapid discharges from the myocardium extending from the left atrium onto the pulmonary vein (PV) have been shown to initiate AF, and AF may be eradicated by the catheter ablation within the PV. However, if there is any difference in the distribution patterns of the myocardial sleeve onto the PV between the subjects with and without AF is to be determined. Twenty-one autopsied hearts were examined. Eleven patients previously had AF before death and another 10 patients had normal sinus rhythm as confirmed from the medical records including ECGs before death. After exposing the heart, the distance to the peripheral end of the myocardium was measured from the PV-atrial junction in each PV. Then, the PVs were sectioned and stained and the distal end of myocardium and the distribution pattern were studied. The anteroposterior diameter of the left atrium was also measured. In 74 of 84 PVs, the myocardium extended beyond the PV-atrial junction. The myocardium was localized surrounding the vascular smooth muscle layer forming a myocardial sleeve. The peripheral end of the myocardial sleeve was irregular and the maximal and minimal distances were measured in each PV. The myocardium extended most distally in the superior PVs compared to the inferior ones and the maximal distance to the peripheral end was similar between the AF and non-AF subjects (8.4 ± 2.8 vs 8.7 ± 4.4 mm for the left superior and 6.5 ± 3.5 vs 5.1 ± 3.9 mm for the right superior PV, respectively). A significant difference was found in the maximal distance in the inferior PVs: 7.3 ± 4.6 vs 3.3 ± 2.8 mm for the left (P 〈 0.05) and 5.7 ± 2.4 vs 1.7 ± 1.9 mm for the right inferior PV (P 〈 0.001) in the subjects with and without AF, respectively. The diameter of left atrium was slightly dilated in AF patients but insignificantly (4.1 ± 0.1 vs 3.6 ± 0.1 cm, P 〉 0.07). The myocytes on the PV were less uniform and surrounded by more fibrosis in patients with AF compared to those without AF. In conclusion, the myocardium extended beyond the atrium-vein junction onto the PVs. The distribution patterns of the myocardium was almost similar between subjects with and without AF, but the histology suggested variable myocytes in size and fibrosis in patients with AF.

Notes: In nine patients who had inducible monomorphic sustained ventricular tachycardia (VT), rapid pacing was performed in 11 episodes of morphologically distinct VT at progressively shorter cycle lengths and VT was interrupted at a critical cycle length. The VT interrupting critical cycle length was defined as the block cycle length (BCL) and the effect of Class I antiarrhythmic drugs were examined. Both the VT cycle length (VTCL) and the BCL were prolonged after administration of either drug. The overall mean ratio of the BCL to the VTCL was unchanged after procainamide administration, but increased after the use of mexiletine. The ratio, however, varied in individual VTs and the BCL after treatment with Class I antiarrhythmic drugs could not be predicted from the ratio baseline value, although the ratio was always 〉 60% and the hazard of VT acceleration might be avoided if the BCL is used.

Notes: Radiofrequency catheter ablation was attempted in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). AVNRT was easily inducible but an intermittent loss of the atrial activation was observed during AVNRT suggesting the presence of a proximal common pathway. During sinus rhythm, a relatively delayed activation that was compatible with a slow potential, was recorded anterior to the ostium of coronary sinus, and radiofrequency catheter ablation application (20 watts) to the site induced junction tachycardia. After an additional radiofrequency catheter ablation application to close the site, AVNRT became noninducible without deterioration of atrioventricular conduction through a fast pathway. This is the first case in which radiofrequency catheter ablation application to the slow potential recording site has been successful, even in AVNRT having a proximal common pathway.

Notes: In 23 consecutive patients, radiofrequency (RF) ablation was used as treatment for idiopathic ventricular tachycardia (VT) originating from the outflow tract of the right ventricle. In this study, we focused on the repetitive ventricular response (〉 5 consecutive QRS beats during RF application). The incidence and clinical implications of the repetitive ventricular response were examined through the results of endocardial mapping and RF ablation. VT origin was mapped as the earliest activation site during VT, and it was determined within 0.5 × 0.5 cm (narrow site) in 13 patients and wider than 0.5 × 0.5 cm (wide origin) in the other 10 patients. The repetitive ventricular response was induced during application of RF current in 14 of 23 patients (61%), and it was more frequently observed in VT from a wide origin (100%) than in the VT from a narrow site (31%). The QRS morphology of the repetitive ventricular response was identical to that of clinical VT. As RF application was continued and/or repeated, the RR interval of the repetitive ventricular response was gradually prolonged, the number of consecutive QRS complexes was decreased, and clinical VT was finally eliminated. The overall success rate of RF ablation was 96% (22/23 patients), and no complications were observed. In conclusion, a repetitive ventricular response was frequently observed in idiopathic right VT. The changing pattern of repetitive ventricular response, slowing, and/or disappearing was consistent with successful RF ablation.

Notes: RF catheter ablation was performed in 16 patients with nonreentrant idiopathic VT originating from the RVOT. All documented VT was monomorphic, but subtle morphological variation in the VT-QRS complex was observed in 10 (63%) of 16 patients. Through endocardial mapping, VT origin was determined within a narrow site (〈 0.5 ± 0.5 cm) in 4 of the 10 patients with the morphological variation. In the other 6 of 10 patients, the origin extended to an area of 〉 0.5 ± 0.5 cm. In VT with morphological variation, the local electrogram at the site of VT origin also showed variation in morphology and activation sequence. For VT of narrow origin, RF application to the site eliminated the VT. However, in VT from a wide arrhythmogenic area, RF current had to be delivered to 3–7 distinct sites to cover the possible origin, and specific QRS configuration of VT and/or PVC was ablated at each of the earliest activation site. All but one VT were successfully ablated by RF current. Subtle morphological variation was frequent in this type of VT, and about half were associated with a wide arrhythmogenic area. Precise mapping and analysis of the efficacy of each BF application might be helpful to better understand the relationship between subtle changes of VT-QRS morphology and their origins.

Notes: T Wave Alternans in Brugada Syndrome. A 71-year-old man who experienced aborted sudden death was referred to our hospital. Coronary artery disease and cerebral accident were ruled out by conventional tests. The 12-lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V1 to V3. Double ventricular extrastimuli at coupling intervals 〉 180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V1 to V3, and visible T wave alternans was induced in leads V2 and V3 at a dose of 450 mg. Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V2 and V3. Class I antiarrhythmic drug-related T wave alternans has been reported rarely in Brugada syndrome, but it may represent enhanced arrhythmogenicity of VF. We need to monitor closely and study the clinical implications of T wave alternans in Brugada syndrome.

Notes: Intramural TWA and Its Arrhythmogenesis. Introduction: T wave alternans (TWA) is characterized by cycle-to-cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin-A model of long QT syndrome. Methods and Results: The cardiac cycle length was gradually shortened by interruption of vagal stimulation, and TWA was induced in six canine hearts. Transmural unipolar electrograms were recorded with plunge needle electrodes from endocardial (Endo), mid-myocardial (Mid), and epicardial (Epi) sites, along with the surface ECG and BP. The activation-recovery interval (ARI) was measured to estimate local refractoriness. During TWA, ARI alternans was greater at the Mid than the Epi/Endo sites, and it was associated with the development of marked spatial dispersion of ventricular repolarization. As TWA increased, ventricular activation of the cycles associated with shorter QT intervals displayed delayed conduction at the Mid sites as a result of a critically longer ARI of the preceding cycle and longer QT interval, while normal conduction was preserved at the Epi site. Delayed conduction at the Mid sites manifested as surface ECG QRS and BP waveform alternans, and spontaneous ventricular tachyarrhythmias developed in absence of ventricular prematurity. In other instances, in absence of delayed conduction during TWA, ventricular premature complexes infringed on a prominent spatial dispersion of ventricular repolarization of cycles with long QT intervals and initiated ventricular tachyarrhythmia. Conclusion: TWA accompanied by QRS alternans may signal a greater ventricular electrical instability, since it is associated with intramural delayed conduction, which can initiate ventricular tachyarrhythmia without ventricular premature complexes.