Ventricular tachycardias mimicking those arising from the right ventricular outflow tract

INTRODUCTION: Ablation of ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) has proven highly successful, yet VTs with similar ECG features may originate outside the RVOT. METHODS AND RESULTS: We reviewed the clinical, echocardiographic, and ECG findings of 29 consecutive patients referred for ablation of monomorphic VT having a left bundle branch block pattern in lead V1 and tall monophasic R waves inferiorly. Nineteen patients (group A) had VTs ablated from the RVOT, and 10 patients (group B) had VTs that could not be ablated from the RVOT. The QRS morphology during VT or frequent ventricular premature complexes was the only variable that distinguished the two groups. During the target arrhythmia, ECGs of group B patients displayed earlier precordial transition zones (median V3 vs V5; P < 0.001), more rightward axes (90 +/- 4 vs 83 +/- 5; P = 0.002), taller R waves inferiorly (aVF: 1.9 +/- 1.0 vs 2.4 +/- 0.5; P = 0.020) and small R waves in lead V1 (10/10 vs 9/19; P = 0.011). Radiofrequency catheter ablation from the RVOT failed to eliminate VT in any group B patient, but ablation from the left ventricular outflow tract (LVOT) eliminated VT in 2 of 6 patients in whom left ventricular ablation was attempted. CONCLUSION: The absence of an R wave in lead V1 and a late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes VTs that mimic an RVOT origin. The latter VTs occasionally can be ablated from the LVOT. Recognition of these ECG features may help the physician advise patients and direct one's approach to ablation.     

Human Model Simulating Right Ventricular Outflow Tract Tachycardia by High-Frequency Stimulation in the Left Pulmonary Artery: Autonomics and Idiopathic Ventricular Arrhythmias

Introduction: Frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) in patients with structurally normal heart usually arise from the right ventricular outflow tract (RVOT). An animal model simulating RVOT tachycardia by high-frequency stimulation (HFS) of the sympathetic input to the proximal pulmonary artery (PA) has been previously described. The aim of this study was to similarly induce RVOT tachycardia in humans.
Methods: In 9 patients with no history of ventricular arrhythmias, a circumferential catheter was placed in the left, main, and proximal PA to contact the endovascular circumference of the PA. A 50-ms train of HFS (200 Hz/0.3 ms pulse duration), coupled to atrial pacing, was applied at each bipolar pair of the circumferential catheter. The coupling interval was adjusted so that the 50-ms train occurred during the ventricular refractory period.
Results: In 6 out of 9 patients, HFS in the left PA during dobutamine infusion induced monomorphic PVCs and/or VT with left bundle branch block (LBBB) morphology and inferior axis at an average stimulation level of 12.5 ± 2.7 V. HFS in the main PA and in the proximal PA did not induce any ventricular arrhythmias with the highest energy of 15 V in baseline state and during dobutamine infusion. HFS in the left PA was associated with hiccough in all patients.
Conclusion: Stimulation of the sympathetic input to the left PA during dobutamine infusion induces PVCs and/or VT exhibiting LBBB-morphology and inferior axis, closely simulating clinical RVOT tachycardia in humans.     

Left Ventricular Outflow Tract Tachycardia Including Ventricular Tachycardia from the Aortic Cusps and Epicardial Ventricular Tachycardia

Idiopathic outflow tract ventricular tachycardia (VT) can arise from the right (RVOT) or left ventricular outflow tract (LVOT). The electrocardiographic (ECG) pattern of RVOT VT is typical in most patients, showing a monomorphic left bundle branch block (LBBB) QRS morphology with an inferior axis. Radiofrequency catheter ablation can be performed with a high success rate and provides a curative therapeutic approach. However, not all VTs with LBBB and inferior axis can be ablated from the RVOT. It has become apparent that LVOT VTs including VT originating from the aortic sinus of Valsalva or epicardium represent underrecognized VT entities which are also amenable to successful catheter ablation. Twelve-lead ECG criteria can contribute to distinguish between sites of VT origin.LVOT arrhythmias represent an increasingly recognized VT entity which can be safely and successfully treated by catheter ablation. Identification of VT origin using ECG criteria and differentiation of LVOT versus RVOT origin is essential in the careful planning of the ablation strategy.     

Radiofrequency Ablation Guided by Mechanical Termination of Idiopathic Ventricular Arrhythmias Originating in the Right Ventricular Outflow Tract

Mapping of Idiopathic Ventricular Arrhythmias. Background: Termination of ventricular tachycardia (VT) by mechanical pressure has been described for fascicular and postinfarction VT. Mechanical interruption of idiopathic ventricular arrhythmias (VT/premature ventricular complexes [PVCs]) arising in the right ventricular outflow tract (RVOT) has not been described in systematic fashion. Methods: Eighteen consecutive patients (13 females, age 49 ± 13 years, ejection fraction 0.55 ± 0.12) underwent mapping and ablation of RVOT VT or PVCs. In 7 patients, 9 distinct VTs (mean cycle length 440 ± 127 ms), and in 11 patients, 11 distinct PVCs originating in the RVOT were targeted. Mechanical termination was considered present if a reproducibly inducible VT was no longer inducible or if frequent PVCs suddenly ceased with the mapping catheter at a particular location. Endocardial activation time, electrogram characteristics, and pace‐mapping morphology were assessed at this location. Radiofrequency energy was delivered if mechanical termination was observed. Results: All targeted arrhythmias were successfully ablated. In 7 of 18 patients (39%), catheter manipulation terminated the arrhythmia with the mapping catheter located at a particular site. Local endocardial activation time was earlier at sites of mechanical termination (?31 ± 7 ms) compared with effective sites without termination (?25 ± 3 ms, P = 0.04). The 10‐ms isochronal area was smaller in patients with mechanical interruption (0.35 ± 0.2 cm²) than in patients without mechanical termination (1.33 ± 0.9 cm², P = 0.01). At all sites susceptible to mechanical trauma, the pace map displayed a match with the targeted VT/PVC. All sites where mechanical termination of VT or PVCs occurred were effective ablation sites. Conclusions: Mechanical suppression at the site of origin of idiopathic RVOT arrhythmias frequently occurs during the mapping procedure and is a reliable indicator of effective ablation sites. Mechanical termination of RVOT arrhythmias may be indicative of a more localized arrhythmogenic substrate. (J Cardiovasc Electrophysiol, Vol. 21, pp. 42–46, January 2010)     

Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism

Introduction: "Idiopathic" ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias.
Methods and Results: One hundred twenty-two consecutive patients  (61 male; 50.9 ± 15.2 years)  with outflow tract arrhythmias comprise this series, 100 (82%) with an RVOT origin, and 22 (18%) with an LVOT origin. The index arrhythmia was similar: sustained ventricular tachycardia (VT)  (RVOT = 28%, LVOT = 36%)  , nonsustained VT  (RVOT=40%, LVOT=23%)  , and premature ventricular complexes  (RVOT = 32%, LVOT = 41%) (P = 0.32)  . Cardiac magnetic resonance imaging and microvolt T-wave alternans results (normal/indeterminate) were also comparable. In addition, 41% with RVOT foci and 50% with LVOT foci were inducible for sustained VT (P = 0.48), and induction of VT was catecholamine dependent in a majority of patients in both groups (66% and 73%; RVOT and LVOT, respectively; P = 1.0). VT was sensitive to adenosine (88% and 78% in the RVOT and LVOT groups, respectively, P = 0.59) as well as blockade of the slow-inward calcium current (RVOT=70%, LVOT=80%; P = 1.00) in both groups.
Conclusions: Electrophysiologic and pharmacologic properties, including sensitivity to adenosine, are similar for RVOT and LVOT arrhythmias. Despite disparate sites of origin, these data suggest a common arrhythmogenic mechanism, consistent with cyclic AMP-mediated triggered activity. Based on these similarities, these arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias."     

An Unusual Case Of Right Ventricular Outflow Tract Tachycardia

In this report, we describe an unusual case of right ventricular outflow tract (RVOT) tachycardia with episodes of repetitive monomorphic ventricular tachycardia (VT), paroxysmal sustained VT and incessant monomorphic VT of the same morphology. Diltiazem, adenosine, or metoprolol failed to interrupt these arrhythmias. However, administration of intravenous propafenone completely eliminated all ventricular ectopic activity. Electrophysiologic study performed off propafenone showed that the ventricular ectopic activity originated from a single locus at the anterior wall of the RVOT. Two radiofrequency applications at this site resulted in complete elimination of ventricular ectopic activity.     

Effects of Incremental Doses of Procainamide in Patients with Sustained Uniform Ventricular Tachycardia

Procainamide in Patients with Uniform VT. Introduction: Although intravenously administered procainamide has been used extensively during electropharmacologic testing for more than II) years, there is little information available on the effects of incremental dosing of procainamide in patients with inducible, monomorphic ventricular tachycardia (VT). Methods and Results: Twenty-nine patients with coronary artery disease had sustained monomorphic VT reproducibly induced in the baseline, drug-free state. Programmed stimulation was repeated 5 minutes after loading infusion (50 mg/min) of 7.5 and 15 mg/kg (all patients) and 22.5 mg/kg of procainamide (15 patients), while maintaining continuous infusion of 0.055, 0.11, and 0.165 mg/kg per minute after each increment in dose, respectively. Corresponding procainamide plasma concentrations were 5.6 ± 2, 10.5 ± 3, and 14.5 ± 3 mg/L before, and 4.7 ± 2, 9.6 ± 3, and 14.6 ± 4 4 mg/L after electrophysiologic study at each increment in dose of procainamide, respectively. Each incremental dose of procainamide resulted in significant prolongation of tachycardia cycle length and QRS duration during sinus rhythm and right ventricular pacing. Five (17%), 7 (24%), and 1 (7%) patients, respectively, had no inducible sustained VT following the incremental dosing of procainamide. Three of five patients who had no inducible VT at 7.5 mg/kg had VT induced again at a higher dose of procainamide. Four of 24 patients whose VT remained inducible at 7.5 mg/kg of procainamide had no VT induced at 15 mg/kg of procainamide. Twelve (41%), 15 (52%), and 6 (40%) patients, respectively, no longer had VT with baseline morphology induced following the incremental dosing of procainamide. VT with new morphology compared to baseline was induced in more than 40% of patients at one or more of the three different procainamide dosing regimens. The mean cycle length of VTs with new morphology was significantly shorter than the cycle length of tachycardias with baseline morphology at each particular dose of procainamide. Conclusion: Similar serum procainamide concentrations before and after programmed stimulation can be achieved at the described dosing regimen. Although 7.5 and 15 mg/kg of procainamide are both effective in suppressing induction of all VT in 20% to 25% of patients, non-inducibility at a particular dose of procainamide does not predict noninducibility at a respectively higher or lower dose. New morphologies of VT that are frequently faster than VTs with baseline morphology at a particular dose of procainamide can be induced in approximately half of the patients, and the clinical significance of these arrhythmias remains to be determined.     

Electroanatomic mapping characteristics of ventricular tachycardia in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia.

BACKGROUND: Ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) has been previously explored using entrainment mapping techniques but little is know about VT mechanisms and the characteristics of their circuits using an electroanatomical mapping system. METHODS AND RESULTS: Three-dimensional electroanatomical mapping was performed in 11 patients with well tolerated sustained VT and ARVD. Sinus rhythm mapping of the right ventricle was performed in eight patients showing areas of low bipolar electrogram voltage (<1.2 mV). In total 12 tachycardias (mean cycle length 382+/-62 ms) were induced and mapped. Complete maps demonstrated a reentry mechanism in eight VTs and a focal activation pattern in four VTs. The reentrant circuits were localized around the tricuspid annulus (five VTs), around the right ventricular outflow tract (one VT) and on the RV free lateral wall (two VTs). The critical isthmus of each peritricuspid circuit was bounded by the tricuspid annulus with a low voltage area close to it. The isthmus of tachycardia originating from the right ventricular outflow tract (RVOT) was delineated by the tricuspid annulus with a low voltage area localized on the posterior wall of the RVOT. Each right ventricular free wall circuit showed an isthmus delineated by two parallel lines of block. Focal tachycardias originated on the right ventricular free wall. Linear radiofrequency ablation performed across the critical isthmus was successful in seven of eight reentrant tachycardias. The focal VTs were successfully ablated in 50% of cases. During a follow-up of 9-50 months VT recurred in four of eight initially successfully ablated VTs. CONCLUSIONS: Peritricuspid ventricular reentry is a frequent mechanism of VT in patients with ARVD which can be identified by detailed 3D electroanatomical mapping. This novel form of mapping is valuable in identifying VT mechanisms and in guiding RF ablation in patients with ARVD.     

Mechanisms Underlying Different Surface ECG Morphologies of Recurrent Monomorphic Ventricular Tachycardia and Their Modification by Procainamide

ECG Pleomorphism of Ventricular Tachycardia. Introduction: Distinct surface ECG morphologies (ECGMs), from one episode to the next, of recurrent monomorphic ventricular tachycardia (VT) in the same patient complicate endocardial catheter mapping and the success of ablative therapy. This study investigates the incidence and mechanisms of multiple ECGMs during recurrent monomorphic VTs in a canine model of experimental myocardial infarction (MI). Methods and Results: Computerized ECG analysis and simultaneous endocardial and epicardial activation mapping with a 64 bipolar electrode array were used to analyze the relation between site of VT origin, local activation sequence, and surface ECGM in 72 VT episodes induced in 9 of 17 dogs with experimental MI. Pairwise comparisons of all VTs induced in the same animal were done in drug-free state (47 VTs) and after intravenous procainamide (25 VTs). In drug-free state, VT pairs with similar surface ECGMs manifested endocardial hreak-through sites (BSs) within a distance < 10 mm in 46 (100%) of 46 VT pairs compared to 43 (45%) of 95 VT pairs with different surface ECGMs (P < 0.0001). Of all 89 VT pairs with endocardial BSs within < 10 mm, similar endocardial activation patterns were found in 34 (74%) of 46 pairs with similar ECGMs in contrast to 6 (14%) of 43 pairs with different ECGMs (P < 0.001). Similar comparisons of VT pairs induced after intravenous procainamide administration showed that the endocardial BSs were located within < 10 mm in 9 (75%) of 12 VT pairs with similar and in 17 (49%) of 95 with different surface ECGMs, respectively (P = NS). Conclusions: In the same heart, similar surface ECGMs of recurrent VT are highly predictive of closely spaced endocardial BSs in drug-free state, hut not after procainamide administration. Nearly half of the VTs with different surface ECGMs still originate from closely spaced endocardial BSs but commonly manifest a change in the endocardial activation spread from this site. Thus, assumptions about different mechanisms and sites of VT origin based on dilTerent surface ECGMs should be made with caution.     

非接触球囊标测指导血流动力学不稳定性或非持续性室性心动过速的射频消融

目的探讨非接触球囊标测在指导血流动力学不稳定性或非持续性室性心动过速(室速)射频消融中的作用。方法17例室速患者,年龄50岁±9岁,经心室刺激诱发血流动力学不稳定性或非持续性室速后,使用非接触标测系统ENSITE3000标测室速的出口和(或)慢传导区,然后使用温控大头导管在室速出口作环形消融或横跨慢传导区进行线性消融。结果17例患者共诱发18次室速,周长为336MS±58MS。15例患者可确定室速的出口,为QRS波前10MS±16MS;其中5例是心肌梗死后室速,9例为右室流出道室速。5例心肌梗死后室速均可确定舒张期慢传导区,最早的心内膜舒张期电活动在QRS波前60·1MS±42·6MS。3例非持续性室速均可确定最早的心室激动点。18次室速中15次消融成功,1例没有进行消融,2例消融失败。结论非接触球囊心内膜标测能成功指导血流动力学不稳定性或非持续性室速的射频消融。     

Relationship between successful ablation sites and the scar border zone defined by substrate mapping for ventricular tachycardia post-myocardial infarction

INTRODUCTION: It is unknown if identification of scar border zones by electroanatomical mapping correlates with successful ablation sites determined from mapping during ventricular tachycardia (VT) post-myocardial infarction (MI). We sought to assess the relationship between successful ablation sites of hemodynamically stable post-MI VTs determined by mapping during VT with the scar border zone defined in sinus rhythm. METHODS AND RESULTS: Forty-six patients presenting with hemodynamically stable, mappable monomorphic VT post-MI and who had at least one such VT successfully ablated were prospectively included in the study. In each patient, VT was ablated by targeting regions during VT that exhibited early activation, +/- isolated mid-diastolic potentials, and concealed entrainment suggesting a critical isthmus site. Prior to ablation, a detailed sinus-rhythm CARTO voltage map of the left ventricle was obtained. A voltage <0.5 mV defined dense scar. Successful VT ablation sites were registered on the sinus voltage map to assess their relationship to the scar border zone. Of the 86 VTs, 68% were successfully ablated at sites in the endocardial border zone. The remaining VTs had ablation sites within the scar in (18%), in normal myocardium (4%), and on the epicardial surface (10%). There were no significant differences in VT recurrence amongst the different groups. CONCLUSION: Successful ablation sites of hemodynamically stable, monomorphic VTs post-MI are often located in the scar border zone as defined by substrate voltage mapping. However, in a sizable minority, ablation sites are located within endocardial scar, epicardially, and even in normal myocardium.     

Intracoronary infusion of catecholamines causes focal arrhythmias in pigs

Background: Acute ischemia causes myriad changes including increased catecholamines. We tested the hypothesis that elevated catecholamines alone are arrhythmogenic. Methods and Results: A 504 electrode sock was placed over both ventricles in six open‐chest pigs. During control infusion of saline through a catheter in the left anterior descending coronary artery (LAD), no sustained arrhythmias occurred, and the refractory period estimated by the activation recovery interval (ARI) was 175 ± 14 ms in the LAD bed below the catheter. After infusion of isoproterenol at 0.1 μg/kg/min through the catheter, the ARI in this bed was significantly reduced to 109 ± 10 ms. A sharp gradient of refractoriness of 43 ± 10 ms was at the border of the perfused bed. Sustained monomorphic ventricular tachycardia occurred after drug infusion in the perfused bed or near its boundary in all animals with a cycle length of 329 ± 26 ms and a focal origin. The maximum slope of the ARI restitution curve at the focal origins of the tachyarrhythmias was always <1 (0.62 ± 0.15). Similar results with a focal arrhythmia origin occurred in two additional pigs in which intramural mapping was performed with 36 plunge needle electrodes in the left ventricular perfused bed. Conclusion: Regional elevation of a catecholamine, which is one of the alterations produced by acute ischemia, can by itself cause tachyarrhythmias. These arrhythmias are closely associated with a shortened refractory period and a large gradient of the spatial distribution of refractoriness but not with a steep restitution curve.     

Clinical usefulness of a multielectrode basket catheter for idiopathic ventricular tachycardia originating from right ventricular outflow tract

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.     

Short-Long Sequences Prior to Ventricular Tachycardia Onset: Analysis of VAST Trial Electrograms

Background: The recently published Ventricular Arrhythmia Suppression Trial (VAST) found no effect of rate-smoothing (RS) algorithm on frequency of ventricular tachycardia (VT) episodes in patients with implantable defibrillator. A similar recent trial reported an opposite result. In order to determine possible reasons for the discrepancy between the trials and achieve better understanding of events preceding VT onset, we analyzed stored device electrograms preceding 162 VT episodes from 50 VAST trial patients with dual-chamber devices.
Results: In this analysis, short-long sequences were more common prior to polymorphic VTs than before monomorphic VTs. The proportion of VT episodes preceded by short-long sequences was lower during randomization to RS ON (5.3% vs 31.3%, P < 0.001). For patients with multiple episodes of monomorphic VT, there was higher interpatient than intrapatient variability in preceding RR intervals. When adjusting for this similarity of RR interval sequences preceding VT onset in individual patients, the difference in proportion short-long sequences between RS ON and RS OFF programming was no longer significant.
Conclusion: Episodes of VT were preceded by stereotypic, patient-specific sequences of RR intervals in several VAST trial patients. RS reduced the percentage of VTs preceded by short-long sequences, but did not change overall VT incidence.     

射频消融治疗室性早搏触发特发性室性心动过速／心室颤动的病例分析

目的探讨射频消融治疗在室性早搏（室早）触发特发性室性心动过速／心室颤动（室速／室颤）中的作用。方法总结3例由室早触发室速／室颤的治疗经验,1例对室早进行射频消融（RF—CA）并植入心律转复除颤器（ICD）,另1例经射频消融未完全消除室早而选择植入ICD,第3例经射频消融成功消除室早,未再发室颤。结果随访2年,3例患者均存活,ICD未再记录到室速／室颤。结论在室早触发室速／室颤病例中,应分析室早与室速／室颤的相关性,给予个体化治疗,射频消融室早可以消除／减少晕厥和室颤的发作。     

Electrocardiographic determinants of the polymorphic QRS morphology in idiopathic right ventricular outflow tract tachycardia

Coupling Intervals and Polymorphic QRS Morphologies . Introduction: Premature ventricular contractions (PVCs) arising from the right ventricular outflow tract (RVOT) can trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) in patients with no structural heart disease. We aimed to clarify the ECG determinants of the polymorphic QRS morphology in idiopathic RVOT PVT/VF. Methods and Results: The ECG parameters were compared between 18 patients with idiopathic PVT/VF (PVT‐group) and 21 with monomorphic VT arising from the RVOT (MVT‐group). The coupling interval (CI) of the first VT beat was comparable between the 2 groups. However, the prematurity index (PI) of the first VT beat was smaller in the PVT‐group than in the MVT‐group (P < 0.001). Furthermore, the QT index, defined as the ratio of the CI to the QT interval of the preceding sinus complex, was also smaller for the PVT/VF in the PVT‐group than that for the VT in the MVT‐group (P < 0.01). In the PVT‐group, the CI of the first VT beat was comparable between that of VT and isolated PVCs, but the PI of the first VT beat was shorter for VT than isolated PVCs (P < 0.05). The PI was the only independent determinant of the polymorphic QRS morphology (odd ratio = 2.198; 95% confidence interval = 1.321–3.659; P = 0.002). Conclusion: The smaller PIs of the first VT beat may result in a polymorphic QRS morphology. (Cardiovasc Electrophysiol, Vol. 23, pp. 521‐526, May 2012)     

Acute coronary artery occlusion and ischemia-related ventricular tachycardia during catheter ablation in the right ventricular outflow tract

Coronary artery injury is a rare complication of catheter ablation in the right ventricular outflow tract (RVOT). Furthermore, acute myocardial ischemia usually causes polymorphic ventricular tachycardia (VT) or ventricular fibrillation. We herein describe a case in which catheter ablation for VT originating from the RVOT provoked ischemia-related VTs due to acute occlusion of the left anterior descending artery.     

Ventricular Arrhythmias in the North American Multidisciplinary Study of ARVC : Predictors,Characteristics, and Treatment

Background

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is associated with sudden cardiac death. However, the selection of patients for implanted cardioverter-defibrillators (ICDs), as well as programming of the ICD, is unclear.

Objectives

The objective of this study was to identify predictors, characteristics, and treatment of ventricular arrhythmias in patients with ARVC.

Methods

The Multidisciplinary Study of Right Ventricular Cardiomyopathy established the North American ARVC Registry and enrolled patients with a diagnosis of ARVC. Patients were followed prospectively.

Results

Of 137 patients enrolled, 108 received ICDs. Forty-eight patients had 502 sustained episodes of ventricular arrhythmias, including 489 that were monomorphic and 13 that were polymorphic. In the patients with ICDs, independent predictors of ventricular arrhythmias in follow-up included spontaneous sustained ventricular arrhythmias before ICD implantation and T-wave inversions inferiorly. The only independent predictor for life-threatening arrhythmias, defined as sustained ventricular tachycardia (VT) ≥240 beats/min or ventricular fibrillation, was a younger age at enrollment. Anti-tachycardia pacing (ATP), independent of the cycle length of the VT, was successful in terminating 92% of VT episodes.

Conclusions

In the North American ARVC Registry, the majority of ventricular arrhythmias in follow-up are monomorphic. Risk factors for ventricular arrhythmias were spontaneous ventricular arrhythmias before enrollment and a younger age at ICD implantation. ATP is highly successful in terminating VT, and all ICDs should be programmed for ATP, even for rapid VT.     

Role of Purkinje fibers in post-infarction ventricular tachycardia.

OBJECTIVES: The objective of this study was to assess the role of Purkinje fibers in monomorphic, post-infarction ventricular tachycardia (VT). BACKGROUND: Ventricular fibrillation and polymorphic VT in the setting of acute myocardial infarction (MI) may be triggered by ectopy arising from Purkinje fibers. METHODS: From among a group of 81 consecutive patients with post-infarction monomorphic VT referred for catheter ablation, 9 patients were identified in whom the clinical VT had a QRS duration < or =145 ms. Mapping was performed focusing on areas with Purkinje potentials. RESULTS: A total of 11 VTs with a QRS duration < or =145 ms were induced and mapped in the 9 patients; 9 of the 11 VTs had a right bundle branch block/left-axis morphology that mimicked left posterior fascicular VT. The mean VT cycle length was 402 +/- 82 ms. Eight of 9 patients had a history of inferior MI involving the left ventricular septum. One patient had an anterior wall MI with septal involvement. Mapping during VT demonstrated re-entry involving the inferior left ventricular wall. In each of the VTs, a Purkinje potential was present at the exit site of the VT re-entry circuit. Single radiofrequency catheter ablation lesions were successful in eliminating these VTs in all patients. CONCLUSIONS: The Purkinje system may be part of the re-entry circuit in patients with post-infarction monomorphic VT, resulting in a type of VT with a relatively narrow QRS complex that mimics fascicular VT.     

Evaluation of Saline-Enhanced Radiofrequency Needle-Tip Ablation for Ventricular Tachycardia (SERF VT CANADA Trial)

BackgroundEndocardial catheter ablation for ventricular tachycardia (VT) may fail owing to the inability to deliver transmural lesions. Saline-enhanced radiofrequency (SERF) ablation uses a needle-tip catheter that is placed at varying depths into the myocardial tissue and heated saline solution is injected along with radiofrequency power (RF), creating fully transmural lesions. We report the first in-human SERF ablation for VT in Canada.MethodsTwenty-five patients with ischemic and nonischemic cardiomyopathy, with recurrent monomorphic drug-refractory VT who had failed a prior catheter ablation underwent SERF ablation in 3 different centres in Canada. After a voltage map, the mapping catheter was replaced with the needle-tipped ablation catheter, which was located perpendicular to the myocardium and extended either 6 or 8 mm into the tissue. Sterile saline solution was infused at a flow rate of 10 mL/min and at 60 °C, and 20-50 W RF was used.ResultsBaseline left ventricular ejection fraction was 33.3 ± 8.6%, mean age was 69.5 ± 6.4 years; 92% were male. From 43 clinical VTs induced, 42 were ablated and 266 SERF lesions were delivered (10.6 ± 4.9 per patient). Of the 42 treated clinical VTs, 41 VTs (98%) were noninducible and 24 patients (96%) had their VT eliminated. At 6 months’ follow-up, 42% of patients were free from VT and there was a 73% reduction in shocks.ConclusionsSERF ablation is feasible and permits control of symptomatic monomorphic VT in drug-refractory patients with a prior failed ablation.