Masayuki Igawa

Atrioventricular Nodal Physiology After Slow Pathway Ablation

The A V nodal physiology before and 1 week after “slow pathway potential” guided catheter ablation was examined in 32 patients with AV nodal reentrant tachycardia. A mean of 4.9 applications of radiofrequency energy eliminated AV nodal reentrant tachycardia in all patients. There were no significant differences in sinus cycle length (815 ± 159 msec vs 813 ± 162 msec;P = NS) and fast pathway conduction properties before and 1 week after ablation. Slow pathway conduction was completely eliminated in 10 (31%) (group I) of 32 patients after ablation. In the remaining 22 patients residual slow pathway conduction associated with one AV node echo was observed. In 15 patients (47%) (group II), the effective refractory period of the slow pathway showed a change of < 30 msec (265 ± 51 vs 266 ± 51 msec; P = NS), and in 7 patients (22%) (group III), a prolongation of more than 80 msec (247 ± 56 vs 340 ± 42 msec; P = 0.0001) before and 1 week after ablation. Minimal and maximal A2‐H2 interval over the slow pathway in group II was not significantly changed (Min A2‐H2:241 ± 37 vs 247 ± 40 msec; P = NS, Max A2‐H2: 346 ± 79 vs 350 ± 60 msec; P = NS), while a significant prolongation was measured in group III (Min A2‐H2: 261 ± 53 VS 373 ± 107 msec; P < 0.01. Max A2‐H2: 359 ± 41 vs 427 ± 63 msec; P < 0.05) before and after ablation. Conclusion: In group II patients there was no evidence shown of impairment of the slow pathway. This suggests that disruption of the link between fast and slow pathways may be responsible for the elimination of AV nodal reentrant tachycardia, besides the elimination or impairment of the slow pathway itself, in “slow pathway potential” guided catheter ablation, and that the slow pathway potential may not necessarily represent activation of the slow pathway itself or of its atrial connection.

Prediction and mechanism of frequent ventricular premature contractions related to haemodynamic deterioration.

Frequent ventricular premature contractions (VPCs) may cause haemodynamic deterioration and reversible left ventricular (LV) dysfunction. We aimed to clarify this mechanism.

Anti-arrhythmic efficacy of nifekalant hydrochloride, a pure class III anti-arrhythmic agent, in patients with healed myocardial infarction and inducible sustained ventricular tachycardia.

In recent clinical trials, class III anti-arrhythmic drugs were found to reduce arrhythmic deaths in patients after myocardial infarction. The purpose of this study was to assess the electrophysiologic properties and anti-arrhythmic efficacy for inducible sustained ventricular tachycardias (VTs) of the pure class III agent nifekalant hydrochloride (MS-551) in comparison with those of procainamide. Programmed ventricular stimulation of up to three extra stimuli was performed for induction of VTs. Effective refractory period (ERP) of the ischemic zone and normal zone was also measured before and after nifekalant. Nifekalant and procainamide suppressed sustained VT induction in four of 15 patients and in six of 15 patients, respectively (p = NS). Sinus cycle length, PR interval, and QRS duration were not changed, but QT and QTc intervals were significantly increased with nifekalant (p < 0.01). Ventricular ERP also increased, whereas there were no significant differences in the increase of ERP between the ischemic and normal zones. The suppression of VT induction did not correlate with the changes in QT, QTc, and ERP after nifekalant administration. There were no significant differences in induced VT cycle length at baseline study between responders and nonresponders to nifekalant. Reverse use dependence was not apparent on review of electrophysiologic parameters. Neither proarrhythmic events nor hemodynamic disturbances occurred after nifekalant administration. It was concluded that nifekalant could be used safely and showed comparable effectiveness to procainamide for the suppression of VT induction.

Conversion to Purkinje-Related Monomorphic Ventricular Tachycardia After Ablation of Ventricular Fibrillation in Ischemic Heart Disease

Background—Catheter ablation is an effective therapy for ventricular fibrillation (VF) arising from the Purkinje system in ischemic heart disease. However, some patients experience newly emergent monomorphic ventricular tachycardia (VT) after the ablation of VF. We evaluated the prevalence and mechanism of monomorphic VT after VF ablation. Methods and Results—Twenty-one consecutive patients with primary VF because of ischemic heart disease who underwent catheter ablation were retrospectively analyzed. Twenty of 21 patients were in electrical storm. Ventricular premature contractions triggering VF arose from the left Purkinje system and were targeted for ablation. Before the ablation, 14 of 21 patients had only VF, and the other 7 had VF and concomitant monomorphic VT. Four of the 14 patients with only VF (29%) exhibited newly emergent monomorphic VT after VF ablation. Three of these patients had Purkinje-related VTs, which were successfully eliminated by the ablation of a Purkinje network located in the same low-voltage area as the site of prior successful VF ablation. During a median follow-up of 28 months (interquartile range, 16–68 months), VF recurred in 6 of 21 patients (29%); however, there were neither electrical storms nor monomorphic VT, and all recurring arrhythmias were controlled by medical therapy alone. Conclusions—Over one fifth of patients with primary ischemic VF experienced newly emergent Purkinje-related monomorphic VT after VF ablation. The circuit of the monomorphic VT associated with the Purkinje network was located in the same low-voltage area as the Purkinje tissue that triggered VF and could be suppressed by additional ablation.

Efficacy of Intensive Radiofrequency Energy Delivery to the Localized Dense Scar Area in Post-Infarction Ventricular Tachycardia Ablation ― A Comparative Study With Standard Strategy Targeting the Infarcted Border Zone ―

BACKGROUND Several reports have demonstrated the importance of severely low voltage areas as arrhythmogenic substrates of ventricular tachycardia (VT). However, a comparative study of dense scar-targeted and infarcted border zone-targeted strategies has not been reported.Methods and Results:We divided 109 consecutive patients with VT post-infarction from 6 centers into 2 groups according to the ablation strategy used: dense scar-targeted ablation (DS ablation, 48%) or border zone-targeted ablation (BZ ablation, 52%). During DS ablation, we attempted to identify VT isthmuses in the dense scar areas (≤0.6 mV) using detailed pace mapping, and linear ablation lesions were applied mainly to those areas. During BZ ablation, linear ablation of standard low voltage areas (0.5-1.5 mV) was performed along with good pace map sites of the clinical VT. Acute success was defined as complete success (no VTs inducible) or partial success (clinical VT was noninducible). The acute complete success rate was significantly higher for DS ablation than for BZ ablation (62% vs. 42%, P=0.043). During a median follow-up of 37 months, the VT-free survival rate was significantly higher for DS ablation than for BZ ablation (80% vs. 58% at 48 months; log-rank P=0.038). CONCLUSIONS DS ablation may be a more effective therapy for post-infarction VT than BZ ablation in terms of the acute complete success rate and long-term follow-up.