Ventricular Ventricular Tachycardia Research Articles

Comparison of warfarin with direct oral anticoagulants for thromboembolic prophylaxis after catheter ablation of ventricular tachycardia.

Thromboembolic events after catheter ablation of ventricular tachycardia (VT) can result in significant morbidity. Thromboembolic prophylaxis after catheter ablation can be achieved by the use of antiplatelet agents, vitamin K antagonists, or direct oral anticoagulants (DOACs). The relative safety and efficacy of these modes of prophylaxis are uncertain. We sought to compare the outcomes of patients who received warfarin or DOACs for thromboembolic prophylaxis after catheter ablation of VT. Anticoagulation with DOACS was started after left ventricular VT ablation in a series of 42 consecutive patients with structural heart disease (67 ± 11 years, 3 women, ejection fraction 32 ± 14%). Duration of hospital stay, bleeding episodes, and thromboembolic events were compared to a historic consecutive group of patients (n = 38, 65 ± 13 years, 14 women, ejection fraction 36 ± 13%) in whom anticoagulation with a formerly described protocol of heparin and vitamin K antagonist was used after VT ablation procedures. Hospital stay was significantly shorter in the group where DOACs were used as compared to vitamin K antagonists (3.3 ± 1.8 vs. 5.0 ± 2.5 days postablation; p = 0.001) without an increase of bleeding or thromboembolic events. Anticoagulation with DOACs is safe and shortens hospital stay in patients with structural heart disease undergoing left ventricular VT ablation procedures.

B-PO02-124 NONISCHEMIC LEFT VENTRICULAR CARDIOMYOPATHY WITH PRESERVED LEFT VENTRICULAR FUNCTION: A TYPE OF ARRHYTHMOGENIC CARDIOMYOPATHY

Ventricular tachycardia (VT) may occur in nonischemic cardiomyopathy (NICM) even when left ventricular (LV) systolic function is relatively preserved. The underlying substrate and response to ablation for these subjects are not well characterized. Describe ventricular substrate and ablation outcomes in NICM patients with sustained VT and relatively preserved LV function. Consecutive NICM patients undergoing ablation of LV VTs were reviewed. Those with arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis or only right ventricular VTs were excluded. Of 82 patients (63±14 years, LV ejection fraction [LVEF] 35±14%) , 20 (24%) had LVEF >45%. Of these, pathogenic gene mutations were identified in 7 (LMNA [3], TTN [1], DSP [2], CRYAB [1]). Low bipolar or unipolar was observed in relatively small areas (median 19 cm2) with a predilection for the basal septum and inferolateral epicardial regions (Figure). Ablation was acutely successful in 80% of patients, though 6 (30%) required advanced ablation techniques (needle ablation in 4, simultaneous unipolar ablation in 2) for presumed deep intramural substrate. VT storm was eliminated in 5 of 6 patients. At a median follow-up of 7.4 months, 7 (35%) patients had VT recurrence. The VT recurrence rate was similar to NICM patients with LVEF≤45% (log-rank p = 0.70). LV VT in patients with NICM and LVEF >45% is associated with small areas of scar and can have a genetic cause. The VT substrate is often intramural and difficult to ablate, with recurrence rates comparable to patients with LVEF < 45%.

Use of Novel Electrogram "Lumipoint" Algorithm to Detect Critical Isthmus and Abnormal Potentials for Ablation in Ventricular Tachycardia.

This study reports the use of a novel "Lumipoint" algorithm in ventricular tachycardia (VT) ablation. Automatic mapping systems aid rapid acquisition of activation maps. However, they may annotate farfield rather than nearfield signal in low voltage areas, making maps difficult to interpret. The Lumipoint algorithm analyzes the complete electrogram tracing and therefore includes nearfield signals in its analysis. Twenty-two patients with ischemic cardiomyopathy and 5 with dilated cardiomyopathy underwent mapping using the ultra-high density Rhythmia system. Lumipoint algorithms were applied retrospectively. In all left ventricular substrate maps, changing the window of interest to the post-QRS phase automatically identified late potentials. In 25 of 27 left ventricular VT activation maps, a minimum spatial window of interest correctly identified the VT isthmus as seen by the manually annotated map, entrainment, and response to ablation. In 6 maps, the algorithm identified the isthmus where the standard automatically annotated map did not. The Lumipoint algorithm automatically highlights areas with electrograms having specific characteristics or timings. This can identify late and fractionated potentials and regions that exhibit discontinuous activation, as well as the isthmus of a VT circuit. These features may enhance human interpretation of the electrogram signals during a case, particularly where the circuit lies in partial scar with low amplitude nearfield signals and potentially allow a more targeted ablation strategy.

Isolated Subepicardial Right Ventricular Outflow Tract Scar in Athletes With Ventricular Tachycardia

BackgroundHigh-level endurance training has been associated with right ventricular pathological remodeling and ventricular tachycardia (VT). Although overlap with arrhythmogenic right ventricular cardiomyopathy (ARVC) has been suggested, the arrhythmogenic substrate for VTs in athletes is unknown. ObjectivesThe goal of this study was to evaluate whether electroanatomic scar patterns related to sustained VT can distinguish exercise-induced arrhythmogenic remodeling from ARVC and post-inflammatory cardiomyopathies. MethodsIn 57 consecutive patients (mean age 48 ± 16 years; 83% male) undergoing catheter ablation for scar-related right ventricular VT, 2 distinct scar distributions were identified: 1) scars involving the subtricuspid right ventricle in 46 patients (group A); and 2) scars restricted to the anterior subepicardial right ventricular outflow tract in 11 patients (group B). ResultsDefinite ARVC or post-inflammatory cardiomyopathy was diagnosed in 40 (87%) of 46 group A patients but was not diagnosed in any patients in group B. All group B patients underwent intensive endurance training for a median of 15 h/week (interquartile range [IQR]: 10 to 20 h/week) for a median of 13 years (IQR: 10 to 18 years). The cycle lengths of scar-related VTs were significantly faster in group B patients (257 ± 34 ms vs. 328 ± 72 ms in group A; p = 0.003). Catheter ablation resulted in complete procedural success in 10 (91%) of 11 group B patients compared with 26 (57%) of 46 group A patients (p = 0.034). During a median follow-up of 27 months (IQR: 6 to 62 months), 50% of group A patients but none of the group B patients had a VT recurrence. ConclusionsThis study describes a novel clinical entity of an isolated subepicardial right ventricular outflow tract scar serving as a substrate for fast VT in high-level endurance athletes that can be successfully treated by ablation. This scar pattern may allow distinguishing exercise-induced arrhythmogenic remodeling from ARVC and post-inflammatory cardiomyopathy.

Ryanodine Receptor Mutation in Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia: Clinical Implications

This is case of a 40-year-old otherwise healthy and physically active gentleman noted the onset of palpitations while running upstairs the day of admission to the emergency room. On arrival to the emergency room, his heart rate was noted to be 250 beats-per-minute (bpm) and electrocardiogram (ECG) demonstrated ventricular tachycardia (VT). Synchronized electrical cardioversion was performed to sinus bradycardia. He was stabilized and admitted to the hospital. There was demonstration of right ventricular VT with an inferior axis, T-wave inversions in the right precordial leads with a right bundle branch block (RBBB) pattern, epsilon waves, and bidirectional premature ventricular contractions (PVC).

Should you be worried?

The ECG in Fig. 1 shows a QRS tachycardia with a QRS duration of 146 ms and a frequency of 160 beats/min. There is a left axis deviation and a complete right bundle branch block. It is important to make a differentiation between ventricular tachycardia (VT) and supraventricular tachycardia (SVT). Signs suggestive of both a ventricular and supraventricular origin are present in our patient. The tachycardia was terminated by adenosine. This is (usually) suggestive of a supraventricular origin. So differential diagnostic paroxysmal SVT conducted with aberrancy is a possibility because of its relatively narrow QRS. The presence of ventriculoatrial dissociation in the electrocardiogram makes the diagnosis of VT stronger. If assuming a ventricular origin, VT originating in or near the Purkinje system (fascicular VT or idiopathic left ventricular VT) is likely. Fig. 1 Twelve-lead ECG during and after conversion to sinus rhythm In 1979, Zipes et al. were the first to identify the electrophysiological characteristics of an idiopathic VT. In 1981 Belhassen et al. described the use of verapamil in this VT, which is refractory to conventional treatment [1]. Therefore, this VT is commonly referred to as Belhassen, verapamil-sensitive or fascicular VT. It is characterised by a right bundle branch block pattern and left axis deviation (left posterior fascicle). A right axis deviation is less frequently noted. The prevalence is unknown but patients are typically young and healthy when their first episode occurs. It is more common in males than females. The mechanism of the tachycardia is postulated to be triggered activity or reentry involving the left-sided Purkinje system and abnormal Purkinje or myocardial tissue [2]. The termination of fascicular VT usually requires intravenous antiarrhythmic medication. In patients with frequent or symptomatic fascicular VT long-term medication may be required. Patients with recurrent refractory episodes of VT may be referred for radiofrequency ablation. The prognosis of fascicular VT is good, in just a few cases it can result in a tachycardia-induced cardiomyopathy. Syncope and sudden death are extremely rare [3].

Should you be worried?

The ECG in Fig. 1 shows a QRS tachycardia with a QRS duration of 146 ms and a frequency of 160 beats/min. There is a left axis deviation and a complete right bundle branch block. It is important to make a differentiation between ventricular tachycardia (VT) and supraventricular tachycardia (SVT). Signs suggestive of both a ventricular and supraventricular origin are present in our patient. The tachycardia was terminated by adenosine. This is (usually) suggestive of a supraventricular origin. So differential diagnostic paroxysmal SVT conducted with aberrancy is a possibility because of its relatively narrow QRS. The presence of ventriculoatrial dissociation in the electrocardiogram makes the diagnosis of VT stronger. If assuming a ventricular origin, VT originating in or near the Purkinje system (fascicular VT or idiopathic left ventricular VT) is likely. Fig. 1 Twelve-lead ECG during and after conversion to sinus rhythm In 1979, Zipes et al. were the first to identify the electrophysiological characteristics of an idiopathic VT. In 1981 Belhassen et al. described the use of verapamil in this VT, which is refractory to conventional treatment [1]. Therefore, this VT is commonly referred to as Belhassen, verapamil-sensitive or fascicular VT. It is characterised by a right bundle branch block pattern and left axis deviation (left posterior fascicle). A right axis deviation is less frequently noted. The prevalence is unknown but patients are typically young and healthy when their first episode occurs. It is more common in males than females. The mechanism of the tachycardia is postulated to be triggered activity or reentry involving the left-sided Purkinje system and abnormal Purkinje or myocardial tissue [2]. The termination of fascicular VT usually requires intravenous antiarrhythmic medication. In patients with frequent or symptomatic fascicular VT long-term medication may be required. Patients with recurrent refractory episodes of VT may be referred for radiofrequency ablation. The prognosis of fascicular VT is good, in just a few cases it can result in a tachycardia-induced cardiomyopathy. Syncope and sudden death are extremely rare [3].

Value of right ventricular mapping in patients with postinfarction ventricular tachycardia

Postinfarction ventricular tachycardia (VT) typically involves the left ventricular endocardium. Right ventricular involvement in the arrhythmogenic substrate of postinfarction VT is considered unusual. To assess the role of right ventricular mapping and ablation in patients with prior septal myocardial infarction. From among 37 consecutive patients with recurrent postinfarction VT, 18 patients with evidence of left ventricular septal involvement of myocardial infarction were identified; these patients were the subjects of this report. In these 18 patients, 166 VTs (cycle length 372 ± 117 ms) were induced. Right ventricular voltage mapping was performed in all 18 patients with left ventricular septal myocardial infarction. Right ventricular voltage mapping showed areas of low voltage in 11 patients; pace mapping from these areas revealed matching pace maps for 17 VTs, and radiofrequency ablation from the right ventricular endocardium but not the left ventricular endocardium eliminated 14 of 17 VTs. VTs with critical components in the right ventricle had a left bundle branch block morphology that had similar characteristics as left bundle branch block VTs with critical areas involving the left ventricular septum. Patients with right ventricular VT breakthrough sites had a lower ejection fraction than did patients without VT breaking out on the right ventricular septum (18% ± 5% vs 33% ± 15%; P = .01). Right ventricular mapping and ablation may be necessary in order to eliminate all inducible VTs in patients with postinfarction VT. More than half the patients with septal myocardial infarction have right ventricular septal areas that are critical for postinfarction VT and that cannot be eliminated by left ventricular ablation alone.

Direct Transthoracic Access to the Left Ventricle for Catheter Ablation of Ventricular Tachycardia

Percutaneous approaches for radiofrequency ablation of ventricular tachycardia (VT) in the left ventricle are typically transarterial retro-aortic, antegrade transmitral via an interatrial septal puncture, or epicardial. However, all 3 approaches may be contraindicated in certain cases. We describe 2 cases of VT ablation in which aortic and mitral valve replacements did not permit utilization of any of these techniques. Direct access to the left ventricular cavity was achieved with a percutaneous puncture through the intercostal space overlying the apex in the first case and through a left minithoracotomy in the second. A sheath was then inserted via the Seldinger technique, allowing catheter access for mapping and ablation of the VT. After successful ablation, the sheaths were withdrawn and hemostasis was achieved. A large left hemothorax occurred from the left ventricular apical puncture in the first case. Direct closure with a purse-string suture in the second case achieved hemostasis. Direct percutaneous left ventricular puncture is a viable option for mapping and ablation of left ventricular VT. A minithoracotomy allows better hemostatic control. This technique has a role when other percutaneous approaches are contraindicated.

Robotic Catheter Ablation of Ventricular Tachycardia in a Patient with Congenital Heart Disease and Rastelli Repair

Robotically assisted catheter ablation has been proven feasible in patients with a variety of atrial arrhythmias. The potential to provide improved catheter tip maneuvering and stability potentially makes it ideal for complex ablation procedures. We present the case of a patient with complex congenital heart disease with previous Rastelli repair and recurrent ventricular tachycardia (VT) who underwent robotically assisted mapping and ablation for right ventricular VT, utilizing substrate mapping techniques.

Role of radiofrequency catheter ablation of ventricular tachycardia in cardiac sarcoidosis: Report from a multicenter registry

Management of ventricular tachycardia (VT) is challenging in patients with cardiac sarcoidosis. The purpose of this study was to assess the response of VT in patients with cardiac sarcoidosis to medical therapy and radiofrequency ablation. Forty-two patients with a diagnosis of cardiac sarcoidosis based on the Japanese Health Ministry criteria were followed. When VT occurred, a stepwise approach was used: implantable cardioverter-defibrillator placement, immunosuppressive agents, antiarrhythmic medications, then radiofrequency ablation. In nine patients (age 46.7 +/- 8.6 years; ejection fraction 42 +/- 14%), VT was not controlled by medical therapy, and radiofrequency ablation was performed. A total of 44 VTs (mean cycle length 348 +/- 78 ms) were induced. Endocardial radiofrequency ablation was performed in eight patients (right ventricular in 5, left ventricular in 3) and epicardial radiofrequency ablation in one patient. In 4 of 5 patients with right ventricular VTs, a peritricuspid circuit was identified. Critical areas were identified for 21 (48%) of 44 VTs, resulting in elimination of 31 (70%) of 44 VTs. The most frequent VT circuit was reentry in the peritricuspid area. This type of VT was eliminated in all patients. Arrhythmic events decreased from 271 +/- 363 episodes preablation to 4.0 +/- 9.7 postablation. All patients had either a decrease (n = 4) or complete elimination (n = 5) of VT during mean follow-up of 19.8 +/- 19.6 months. Catheter ablation of VT in patients with cardiac sarcoidosis refractory to medical therapy is effective in eliminating VT or markedly reducing the VT burden. The disease process in cardiac sarcoidosis often involves a specific area in the basal right ventricle predisposing to peritricuspid reentry.

Predictors for Successful Ablation of Right- and Left-Sided Idiopathic Ventricular Tachycardia

This study reports on predictors for successful radiofrequency (RF) ablation of idiopathic ventricular tachycardia (VT) in 48 patients—35 with right ventricular (RV) outflow tract and 13 with left ventricular VT. In RV outflow tract idiopathic VT, RF ablation was successful in 29 of 35 patients (83%). The following information allowed differentiation between patients with and without a successful RF ablation: >1 induced VT morphology (0 vs 3); presence of delta wave-like beginning of the QRS (2 vs 3) and ≥11 of 12 leads showing a “match” between the clinical VT and the pacemap (28 vs 1). Endocardial activation times were not different between both groups (−15 ± 18 vs −4 ± 5 ms). In left ventricle idiopathic VT, RF ablation was successful in 12 of 13 patients (92%). In patients who underwent successful ablation, 1 VT morphology was induced and no delta wave-like beginning of the QRS was present; a correlation between clinical VT and the pacemap ≥11 of 12 leads was found and the endocardial activation time preceded the QRS (range of −5 to −58 ms [mean −30 ± 14]). Purkinje activity was observed in 5 of 7 patients with an idiopathic VT originating from the inferoposterior region but not from the inferoapical region of the left ventricle. Four patients (14%) with RV outflow tract idiopathic VT had recurrence during a mean follow-up of 2 to 50 months (mean 30 ± 12). Thus, (1) in RV outflow tract idiopathic VT a good pacemap was more important than an early endocardial activation time; (2) an optimal pacemap as well as an early endocardial activation time were important predictors for successful ablation of the left ventricle idiopathic VT; (3) Purkinje activity was recorded in VTs arising in the inferoposterior region of the left ventricle; and (4) factors for unsuccessful ablation for idiopathic VT were >1 induced VT morphology, a delta wave-like beginning of the QRS, and a VT/pacemap correlation <11 of 12 leads. Idiopathic VT can be successfully ablated with both immediate and long-term success.

Catheter ablation of ventricular tachycardia with radiofrequency currents, with special reference to the termination and minor morphologic change of reinduced ventricular tachycardia

During catheter ablation with radiofrequency (RF) currents, the incidence of the termination or reentrant ventricular tachycardia (VT) during application of RF energy and the morphologic change of the reinduced VT were analyzed. Twenty-five patients (20 men and 5 women, aged 44 ± 17 years) were studied. After induction of monomorphic sustained VT, the ablation site was determined by endocardial activation mapping, identification of isolated mid-diastolic potential, and pacing during tachycardia. Thirty-six monomorphic VTs were induced in 25 patients and terminated with programmed stimulation. The cycle length was 323 ± 55 ms and all VTs were entrained with rapid ventricular pacing. The target site was the earliest site of activation of VT in 26 VTs in 16 patients, and the area of slow conduction in 10 VTs in 9 patients. VT was terminated soon after the application of RF currents in 33 VTs in 22 patients at 6.0 ± 3.1 seconds, and VT was induced immediately after the cessation of RF currents in 11 patients. Of these, 4 patients with idiopathic left ventricular VT had an alternation in the QRS configuration before catheter ablation and required repeat ablation of the other VT morphology. In the other 7 patients, such morphology was not observed before ablation, but was observed in VT induced when the original VT was terminated. Repeated attempts of catheter ablation 2 to 9 times at the remapped site was, however, successful in 7 of 8 VTs. In the remaining 3 patients, ablation was attempted within the area of slow conduction, but VT was not terminated during RF and only minor morphologic change was observed in 1 patient. With the inclusion of these 3 patients, catheter ablation was unsuccessful only during 4 VTs in 4 patients.

Fulguration of Ventricular Tachycardia Using High Cumulative Energy: Results in Thirty‐one Patients with a Mean Follow‐Up of Twenty‐seven Months

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 31 patients (57 +/- 15 years) who had refractory recurrent VT. Fifteen patients had coronary artery disease, seven had arrhythmogenic right ventricular dysplasia, four had cardiomyopathy and five had no structural heart disease. Ten patients were NYHA class III-IV. Ten patients experienced cardiac arrest or syncope during VT. Twenty-two patients had only one documented morphologic type of spontaneous VT. Whereas nine patients had more than one: the VT was incessant or daily in 17 patients. One to 16 shocks (mean 5.6) of 160 to 240 joules each (1162 +/- 1060 joules) were delivered to the endocardial exit site of VT--as identified by endocardial activation mapping (29 patients) and pacemapping (31 patients)--during one (22 patients) or more than one session (nine patients). Cumulative delivered energy was 840 +/- 558 joules for right ventricular VT (11 patients) and 1362 +/- 1240 joules for left ventricular VT (20 patients). Reversible side effects occurring immediately after shocks included: nonclinical VT (two patients), ventricular fibrillation (two patients), AV block (three patients). Mean CK-MB fraction 6 hours after shocks was 91 +/- 46 IU/1. An electrophysiology study performed 7 to 10 days later demonstrated that the original clinical VT was inducible in seven patients, nonclinical monomorphic VT was inducible in eight patients and no VT was inducible in 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)