Catheter Ablation of Refractory Ventricular Fibrillation Storm After Myocardial Infarction.

BACKGROUND: Ventricular fibrillation (VF) storm after myocardial infarction (MI) is a life-threatening condition that necessitates multiple defibrillations. Catheter ablation is a potentially effective treatment strategy for VF storm refractory to optimal medical treatment. However, its impact on patient survival has not been verified in a large population. METHODS: We conducted a multicenter, retrospective observational study involving consecutive patients who underwent catheter ablation of post-MI refractory VF storm without preceding monomorphic ventricular tachycardia. The target of ablation was the Purkinje-related ventricular extrasystoles triggering VF. The primary outcome was in-hospital and long-term mortalities. Univariate logistic regression and Cox proportional-hazards analysis were used to evaluate clinical characteristics associated with in-hospital and long-term mortalities, respectively. RESULTS: One hundred ten patients were enrolled (age, 65±11years; 92 men; left ventricular ejection fraction, 31±10%). VF storm occurred at the acute phase of MI (4.5±2.5 days after the onset of MI during the index hospitalization for MI) in 43 patients (39%), the subacute phase (>1 week) in 48 (44%), and the remote phase (>6 months) in 19 (17%). The focal triggers were found to originate from the scar border zone in 88 patients (80%). During in-hospital stay after ablation, VF storm subsided in 92 patients (84%). Overall, 30 (27%) in-hospital deaths occurred. The duration from the VF occurrence to the ablation procedure was associated with in-hospital mortality (odds ratio for each 1-day increase, 1.11 [95% CI, 1.03-1.20]; P=0.008). During follow-up after discharge from hospital, only 1 patient developed recurrent VF storm. However, 29 patients (36%) died, with a median survival time of 2.2 years (interquartile range, 1.2-5.5 years). Long-term mortality was associated with left ventricular ejection fraction <30% (hazard ratio, 2.54 [95% CI, 1.21-5.32]; P=0.014), New York Heart Association class ≥III (hazard ratio, 2.68 [95% CI, 1.16-6.19]; P=0.021), a history of atrial fibrillation (hazard ratio, 3.89 [95% CI, 1.42-10.67]; P=0.008), and chronic kidney disease (hazard ratio, 2.74 [95% CI, 1.15-6.49]; P=0.023). CONCLUSIONS: In patients with MI presenting with focally triggered VF storm, catheter ablation of culprit triggers is lifesaving and appears to be associated with short- and long-term freedom from recurrent VF storm. Mortality over the long-term follow-up is associated with the severity of underlying cardiovascular disease and comorbidities in this specific patient population.

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.

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.

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

UNLABELLED: Aim Frequent ventricular premature contractions (VPCs) may cause haemodynamic deterioration and reversible left ventricular (LV) dysfunction. We aimed to clarify this mechanism. METHODS AND RESULTS: The haemodynamics, echocardiographic parameters, and plasma brain natriuretic peptide (BNP) level were assessed in 31 patients with idiopathic, frequent VPCs undergoing radiofrequency catheter ablation. The patients were classified into two groups according to the presence (n = 19) or absence (n = 12) of marked augmentation of the pulmonary capillary wedge pressure (PCWP) following VPCs (VPC-induced-PCWP augmentation; VI-PA). The VI-PA(+) group was defined as those with a peak PCWP of >15 mmHg measured after a VPC. Before the ablation, the mean PCWP, right atrial pressure (RAP), left ventricular end-diastolic pressure (LVEDP), and plasma BNP level were significantly greater in the VI-PA(+) group than in the VI-PA(-) group. In the VI-PA(+) group, the mean PCWP, RAP, LVEDP, and cardiac index all improved immediately after a successful ablation. At 7.4 ±0.9 months after the ablation, almost all the echocardiographic parameters and plasma BNP level also significantly improved in the VI-PA(+) group, and the magnitude of the improvement in those parameters measured was greater in the VI-PA(+) group than in the VI-PA(-) group. The left atrial contractions during mitral valve closure during VPCs caused a marked pulmonary venous flow regurgitation and VI-PA. VPC coupling intervals of <500 ms and the presence of a following P-wave of <300 ms predicted VI-PAs with a high accuracy. CONCLUSIONS: The VI-PA may be the main mechanism of the haemodynamic deterioration in patients with frequent VPCs. This haemodynamically deteriorating subgroup could be identified by the surface electrocardiogram and improved dramatically with catheter ablation.

Utility of short-term variability of repolarization as a marker for monitoring a safe exercise training program in patients with cardiac diseases.

In order to begin searching for new markers for safe exercise training in patients with cardiac diseases, we tested the sensitivity and reliability of the short-term variability of repolarization (STV(QT)) in comparison with QT interval, QTc, and T(peak)-T(end) interval (T(p-e)) in patients with cardiac diseases. Nine patients (8 men, 1 woman; 58 ± 10 years) were enrolled. The cardiac rehabilitation (CR) program consisted of walking, bicycling on an ergometer, and calisthenics for 30-50 minutes/session and 3-5 sessions/week for 3 months. ECGs of 31 consecutive sinus beats were obtained before and after the CR program. RR and QT intervals were measured in the aVL lead. The mean orthogonal distance from the diagonal to the points of the Poincaré plots was determined using the following equation; STV(QT) [= Σ |QT(n+1)-QT(n)/(30 × 2(1/2))], as a marker of temporal dispersion of repolarization. Also, T(p-e) of 5 consecutive beats was measured as a marker of spatial dispersion. No fatal arrhythmias were observed in the CR. No significant difference was observed in the RR or QT interval between at baseline and at the end of the CR program. Meanwhile, QTc, STV(QT) and T(p-e) decreased significantly from 429 ± 27 to 400 ± 17 (P < 0.01), from 6.8 ± 1.3 to 4.7 ± 1.4 msec (P < 0.001), and from 74.8 (61.2/79.1) to 64.8 (51.4/70.7) msec (median (25th/75th percentile), P < 0.01), respectively. STV(QT) together with T(p-e) and QTc may reflect the time-courses of safe exercise training.

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.

How to diagnose, locate, and ablate coronary cusp ventricular tachycardia.

INTRODUCTION: Although radiofrequency energy usually is applied to the most favorable endocardial site in patients with outflow tract ventricular tachycardia, there are still some patients in whom the tachycardia can be ablated only from an epicardial site. We established the characteristics and technique of catheter ablation from both the left and right coronary cusps to cure left ventricular outflow tract ventricular tachycardia. METHODS AND RESULTS: We studied 15 patients in whom VT was thought to originate from the coronary cusp by both activation and pace mapping after precise mapping of the right ventricle, left ventricle, pulmonary artery, coronary cusps, and anterior interventricular vein. Twelve-lead ECG analysis revealed an S wave on lead I, tall R wave on leads II, III, and aVF, and no S wave on either lead V5 or V6. Precordial R wave transition occurred on leads V1 and V2. The earliest ventricular electrogram at a successful ablation site was recorded 35+/-12 msec before QRS onset and 19+/-15 msec earlier than the earliest ventricular electrogram recorded from the anterior interventricular vein. Almost identical pace mappings were obtained from the coronary cusp. Catheter tip temperature was maintained at 55 degrees C during energy delivery, and the distance from the tip to the ostium of each left and right coronary artery was > 1.0 cm by coronary angiography. CONCLUSION: Left ventricular outflow tract VT that could not be ablated from an endocardial site could be safely eliminated by radiofrequency application to the left and right coronary cusps.