Fascicular ventricular tachycardia arising from the left side His and its adjacent region: a subset of upper septal idiopathic left ventricular tachycardia.

AIMS: Fascicular ventricle tachycardia (FVT) arising from the proximal aspect of left His-Purkinje system (HPS) has not been specially addressed. Current study was to investigate its clinical, electrocardiographic, and electrophysiological characteristics. METHODS AND RESULTS: Eighteen patients who were identified as this rare FVT were consecutively enrolled, and their scalar electrocardiogram and electrophysiological data were collected and analysed. The ventricular tachycardia (VT) morphology was similar to sinus rhythm (SR) in eight patients, left bundle branch block type in one patient, right bundle branch block type in seven patients, and both narrow and wide QRS type in two patients. During VT, right-sided His potential preceded the QRS with His-ventricle (H-V) interval of 36.3 ± 12.4 ms, which was shorter than that during SR (-51.4 ± 8.6 ms) (P = 0.002). The earliest Purkinje potentials (PPs) were recorded within 7 ± 3 mm of left-side His and preceded the QRS by 49.1 ± 14.0 ms. Mapping along the left anterior fascicle and left posterior fascicle revealed an antegrade activation sequence in all with no P1 potentials recorded. In the two patients with two VT morphologies, the earliest PP was documented at the same site, and the activation sequence of HPS remained antegrade. Ablation at the earliest PP successfully eliminated the tachycardia, except one patient who developed complete atrial-ventricular block and two patients who abandoned ablations. After at least 12 months follow-up, 15 patients were free from any recurrences. CONCLUSIONS: Fascicular ventricle tachycardia arising from the proximal aspect of left HPS was featured by recording slightly shorter H-V interval and absence of P1 potentials. Termination of VT requires ablation at the left-sided His or its adjacent region.

Prevention of ventricular fibrillation through de-networking of the Purkinje system: Proof-of-Concept Paper on the Substrate Modification of the Purkinje Network.

INTRODUCTION: Sudden cardiac death from ventricular fibrillation (VF) remains a major health problem worldwide. Currently, there are limited treatment options available to patients who suffer from episodes of VF. Because Purkinje fibers have been implicated as a source of initiation of VF, we are presenting the first paper of a series highlighting the promising results of substrate modulation through "De-Networking" of the Purkinje system preventing VF in patients without an alternative ablation strategy. METHODS AND RESULTS: We studied 10 consecutive patients (two female) all but one implanted with an ICD with documented VF or fast polymorphic Ventricular tachycardia (VT) (five patients without history of structural heart disease, two with ischemic cardiomyopathy, one with hypertrophic obstructive cardiomyopathy, one with dilated cardiomyopathy, and one with aortic valve disease). After 3D electroanatomical mapping, the left bundle branch (LBB) and left ventricular Purkinje potentials were annotated creating a virtual triangle with the apex formed by the distal LBB and the base by the most distal Purkinje potentials. Linear radiofrequency catheter ablation at the base of the triangle was performed, followed by ablation within the virtual triangle sparing the LBB and both fascicles ("de-networking"). All patients were treated without complications. During 1-year follow-up, only 2/10(20%) patients experienced recurrence in form of a single episode of polymorphic VT/VF. CONCLUSION: Catheter ablation of VF through "de-networking" of the Purkinje system in patients without overt arrhythmia substrate or trigger appears safe and effective and will require further study in a larger patient cohort.

Catheter ablation of premature ventricular complexes arising from the left fascicular system.

BACKGROUND: Idiopathic premature ventricular complexes (PVCs) that originate from the left fascicular system have rarely been reported. OBJECTIVE: The present study aimed to investigate the electrophysiological characteristics and the ablation strategy for this category of PVCs. METHODS: Of 648 patients with idiopathic PVCs, 27 were enrolled in this study. All the PVCs presented with a relatively narrow QRS complex and right bundle branch block morphology. The mean QRS duration was 117.4 ± 8.6 ms. Radiofrequency catheter ablation was applied at the site recording the earliest fascicular potential (FP). RESULTS: The origin of PVCs was as follows: 15 originating from the left anterior fascicle, 7 originating from the left posterior fascicle, 2 originating from the left middle fascicle, and 3 originating from the common trunk of the left bundle branch. The earliest local FP preceded the onset of the QRS complex by 32.7 ± 6.4 ms. The immediate ablation success rate was 100%. Three patients had recurrent PVCs during follow-up. The total success rate of a single procedure was 88.9%. CONCLUSION: Ablation of PVCs originating from the left fascicular system guided by an earliest presystolic FP was found to be safe and effective.

Elimination of Purkinje Fibers by Electroporation Reduces Ventricular Fibrillation Vulnerability.

Background The Purkinje network appears to play a pivotal role in the triggering as well as maintenance of ventricular fibrillation. Irreversible electroporation ( IRE ) using direct current has shown promise as a nonthermal ablation modality in the heart, but its ability to target and ablate the Purkinje tissue is undefined. Our aim was to investigate the potential for selective ablation of Purkinje/fascicular fibers using IRE . Methods and Results In an ex vivo Langendorff model of canine heart (n=8), direct current was delivered in a unipolar manner at various dosages from 750 to 2500 V, in 10 pulses with a 90-µs duration at a frequency of 1 Hz. The window of ventricular fibrillation vulnerability was assessed before and after delivery of electroporation energy using a shock on T-wave method. IRE consistently eradicated all Purkinje potentials at voltages between 750 and 2500 V (minimum field strength of 250-833 V/cm). The ventricular electrogram amplitude was only minimally reduced by ablation: 0.6±2.3 mV ( P=0.03). In 4 hearts after IRE delivery, ventricular fibrillation could not be reinduced. At baseline, the lower limit of vulnerability to ventricular fibrillation was 1.8±0.4 J, and the upper limit of vulnerability was 19.5±3.0 J. The window of vulnerability was 17.8±2.9 J. Delivery of electroporation energy significantly reduced the window of vulnerability to 5.7±2.9 J ( P=0.0003), with a postablation lower limit of vulnerability=7.3±2.63 J, and the upper limit of vulnerability=18.8±5.2 J. Conclusions Our study highlights that Purkinje tissue can be ablated with IRE without any evidence of underlying myocardial damage.

Electrophysiological Characteristics of Bundle Branch Reentry Ventricular Tachycardia in Patients Without Structural Heart Disease.

BACKGROUND: The distinct electrophysiological features of bundle branch reentry ventricular tachycardia (VT) in patients without structural heart disease have not been systemically characterized. METHODS: Nine patients (mean age, 29.6 years) with normal left ventricular function were enrolled. Bundle branch reentry VT with right and left bundle branch block (BBB) patterns was induced in 1 and 9 patients, respectively. The right bundle was attempted to record by a 6F decapolar or quadripolar catheter. Electroanatomic mapping of the left ventricle was performed in 6 patients. In all left BBB pattern VT, the mean VT cycle length was 329.3±89.1 ms, and the median HV interval during tachycardia was longer than that of baseline (78 [73-100] versus 71 [64.5-88] ms; P=0.11). RESULTS: The H-RB interval during VT was slightly shorter (P=0.14); however, the median RB-V interval was markedly longer than that during sinus rhythm (50 [29.5-83] versus 30 [8-51] ms; P=0.043]. In 6 patients with 3-dimensional mapping of the left ventricle, a slow anterograde or retrograde conduction over left HIS-Purkinje system with normal myocardial voltage was identified. In addition, Purkinje-related VTs (1.0±1.3 types) were also induced in 5 patients. Ablation was applied in distal left BB in patients with baseline left BBB and in one narrow QRS patient with sustained Purkinje-related VT, whereas right BB was targeted in other patients. During a mean follow-up of 31.4 months, frequent premature ventricular contractions occurred in one patient, and new VT developed in the other patient. CONCLUSIONS: Bundle branch reentry VT can occur in young patients with extensive conduction disturbances within HIS-Purkinje system. Ablation targeting at the distal left BB which bifurcates into left posterior and anterior fascicle can preserve the residual atrioventricular conduction, but intensive follow-up is needed.

Localized Structural Alterations Underlying a Subset of Unexplained Sudden Cardiac Death.

BACKGROUND: Sudden cardiac death because of ventricular fibrillation (VF) is commonly unexplained in younger victims. Detailed electrophysiological mapping in such patients has not been reported. METHODS: We evaluated 24 patients (29±13 years) who survived idiopathic VF. First, we used multielectrode body surface recordings to identify the drivers maintaining VF. Then, we analyzed electrograms in the driver regions using endocardial and epicardial catheter mapping during sinus rhythm. Established electrogram criteria were used to identify the presence of structural alterations. RESULTS: VF occurred spontaneously in 3 patients and was induced in 16, whereas VF was noninducible in 5. VF mapping demonstrated reentrant and focal activities (87% versus 13%, respectively) in all. The activities were dominant in one ventricle in 9 patients, whereas they had biventricular distribution in others. During sinus rhythm areas of abnormal electrograms were identified in 15/24 patients (62.5%) revealing localized structural alterations: in the right ventricle in 11, the left ventricle in 1, and both in 3. They covered a limited surface (13±6 cm2) representing 5±3% of the total surface and were recorded predominantly on the epicardium. Seventy-six percent of these areas were colocated with VF drivers (P<0.001). In the 9 patients without structural alteration, we observed a high incidence of Purkinje triggers (7/9 versus 4/15, P=0.033). Catheter ablation resulted in arrhythmia-free outcome in 15/18 patients at 17±11 months follow-up. CONCLUSIONS: This study shows that localized structural alterations underlie a significant subset of previously unexplained sudden cardiac death. In the other subset, Purkinje electrical pathology seems as a dominant mechanism.

Clinical, electrocardiographic, and electrophysiological characteristics of left upper septal fascicular ventricular tachycardia.

Aims: We sought to investigate the clinical, electrocardiographic, and electrophysiological characteristics of left upper septal fascicular ventricular tachycardia (LUS-VT). Methods and results: Eleven consecutive patients with LUS-VT were identified among 196 patients with left fascicular ventricular tachycardia (VT). Clinical VTs presented as paroxysmal in 8 patients and incessant in 3 patients. Six patients had previous left posterior fascicular VT ablation history. All VTs had narrow QRS complexes with QRS duration of 101.1 ± 9.2 ms. The frontal QRS axis was normal or right deviation. Precordial morphology was either right bundle branch block type or similar to that of sinus rhythm. A retrograde His with H-V interval of 21.9 ± 7.2 ms was recorded during VT. The earliest Purkinje potential (PP) to QRS interval during VT averaged 35.7 ± 4.5 ms. Clear diastolic potentials (DPs) with high frequency and low amplitude were found in only one patient. Ten patients were managed successfully by 11 ablation sessions, and 1 patient declined ablation. Successful targets at the left upper septum were sites with the earliest PP (9 cases) or with DP (1 case) during VT. After ablation, 2 cases (10%) developed new left anterior hemiblock or incomplete left bundle branch block. No VT recurred during a median follow-up period of 3.2 (range 1.0-12.7) years. Conclusion: LUS-VT presented as narrow QRS complex tachycardia. Some LUS-VTs occurred after ablation targeting left posterior fascicular VT. The VTs can be managed successfully by focal ablation at the left upper septum with a mild risk of fascicular injury.

Catheter ablation targeting Purkinje potentials controlled ventricular fibrillation in a patient with a malignant lymphoma occurring in the ventricular septum.

Malignant lymphoma is known to cause various types of arrhythmia, including ventricular fibrillation. However, radiofrequency catheter ablation of ventricular fibrillation associated with malignant lymphoma has never been reported. We describe the case of a 53-year-old man with refractory ventricular fibrillation that was associated with malignant lymphoma. Electrophysiological testing revealed that a Purkinje potential appeared before ventricular contraction at the tumour site. We successfully treated the ventricular fibrillation with radiofrequency catheter ablation, using the Purkinje potential as an indicator. Physicians should consider this treatment if ventricular fibrillation cannot be controlled using other strategies.

Mapping and ablating ventricular premature contractions that trigger ventricular fibrillation: trigger elimination and substrate modification.

Ventricular fibrillation (VF) is a malignant arrhythmia, usually initiated by a ventricular premature contraction (VPC) during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPC preceded Purkinje potentials or the right ventricular outflow tract (RVOT) in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. The most important issue before the ablation session is the recording of the 12-lead electrocardiogram (ECG) of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pacemapping. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, a modification of the Purkinje network might be applied when the earliest site cannot be determined or is located close to the His-bundle. Furthermore, the electrical isolation of the pulmonary artery (PA) can suppress RVOT type polymorphic ventricular tachycardia in some patients with rapid triggers from the PA. Suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.

Focal Purkinje ventricular tachycardia ablation in structurally normal heart.

A 21-year-old man presented with recurrent palpitations and giddiness. Clinical examination, echocardiography, and magnetic resonance imaging revealed a structurally normal heart. Electrocardiography showed broad-complex tachycardia with 250 beats per minute, which required cardioversion. An electrophysiological study could not induce tachycardia by programmed electrical stimulation. On isoprenaline infusion, frequent ventricular ectopics, bigeminy, nonsustained ventricular tachycardia, and broad-complex tachycardia similar to clinical tachycardia were readily inducible. This was considered to be ventricular tachycardia due to enhanced automaticity. Using 3-dimensional electroanatomical mapping, successful ablation was undertaken. The patient was asymptomatic on follow-up after 12 and 18 months.

First case of left posterior fascicle in a bystander circuit of idiopathic left ventricular tachycardia.

We describe a case of idiopathic left ventricular tachycardia in which the left posterior fascicle was clearly delineated to be a bystander in a re-entry circuit, with participation of the left interventricular myocardium as the retrograde limb instead. To the best of our knowledge, this is the first case report that has directly proven the left posterior fascicle to be a bystander during idiopathic left ventricular tachycardia.

Multiform premature ventricular contractions and polymorphic ventricular tachycardia caused by Purkinje activity with slow conduction in idiopathic ventricular fibrillation.

In several cases with idiopathic ventricular fibrillation (VF), VF was initiated by premature ventricular contractions (PVCs) from the Purkinje system. However, the precise characteristics of the Purkinje activity in patients with idiopathic VF remain unclear. We performed an electrophysiological study in a patient with idiopathic VF and examined the correlation between the Purkinje potential and the incidence of PVCs/polymorphic ventricular tachycardia (PMVT). In this case of idiopathic VF, the Purkinje activity caused multiform PVCs and PMVT. The The Purkinje activity and slow conduction of Purkinje fibers are associated with the occurrence of multiform PVCs and PMVT.

Mapping and ablation of ventricular fibrillation-how and for whom?

The involvement of the Purkinje system in a subset of patients with idiopathic ventricular fibrillation or polymorphic VT/VF related to structural heart disease was first demonstrated in the pioneering work of Michel Haissaguerre and co-workers (Circulation 106:962-967, 2002 and Lancet 359:677-678, 2002). It is very important to identify these patients with recurrent episodes of ventricular fibrillation and/or ICD shocks with regard to the presence of triggering premature ventricular contractions (PVC), which may be amenable to mapping and catheter ablation by screening Holter and ICD recordings. The practical problem, which is frequently encountered, is the absence of these PVCs when the patients are brought to the EP lab. However, catheter ablation is an important adjunctive tool to antiarrhythmic drug treatment, beta blocker therapy, and general anesthesia in this setting. Local electrogram criteria related to this phenomenon have been identified guiding mapping and ablation (e.g., low amplitude, high-frequency Purkinje potentials preceding a closely coupled ventricular signal (Fig. 1a)). The favorable long-term follow-up after catheter ablation has been demonstrated in the setting of right and left ventricular Purkinje-related PVCs leading to polymorphic VT/VF (Leenhardt et al., Circulation 89:206-215, 1994) and also following myocardial infarction (Baensch et al., Circulation 108:3011-3016, 2003) and right ventricular outflow tract-associated VF (Noda et al., Journal of the American College of Cardiology 46:1288-1294, 2005). Most recently, epicardial ablation strategies leading to suppression of polymorphic VT/VF episodes related to the Brugada syndrome have been described irrespective to the presence of premature ventricular beats (Nademanee et al., Circulation 123:1270-1279, 2011).