Left Ventricular Tachycardia Research Articles

Abstract Tu049: Stabilization of RyR2 with dantrolene treatment ameliorates left ventricular remodeling and ventricular tachycardia after myocardial infarction

Background: Dantrolene has been reported to suppress diastolic Ca 2+ leakage through the cardiac ryanodine receptor (RyR2) by restoring defective inter-subunit interactions within RyR2 and enhancing the binding affinity of calmodulin (CaM) to RyR2. Here, we investigated whether chronic administration of dantrolene which was started after myocardial infarction (MI) inhibits ventricular tachycardia (VT) and alleviates left ventricular remodeling. Methods: We developed MI model by left anterior descending coronary artery (LAD) ligation in mice. Wild type mice were divided into 4 groups; sham-operated mice (WT-Sham), sham-operated mice treated with dantrolene (WT-Sham-DAN, 20mg/kg/day, i.p.), MI mice (WT-MI) and MI mice treated with dantrolene (WT-MI-DAN). Then, they were followed up for 12 weeks. Results: The 12-week survival rate was significantly higher in MI-DAN group (71 %) than in WT-MI (40%). Serial echocardiography showed that adverse LV remodeling was ameliorated in WT-MI-DAN group compared to WT-MI group (WT-MI 6.3 ± 0.25 mm, WT-MI-DAN 5.5 ± 0.14 mm, P<0.01). VT test by epinephrine (2mg/kg, i.p.) showed that VT was induced in all WT-MI group, although it was significantly inhibited in WT-MI-DAN group. An increase in diastolic Ca 2+ spark frequency and a decrease in sarcoplasmic reticulum Ca 2+ content were observed in isolated cardiomyocytes from WT-MI group whereas both were significantly ameliorated in WT-MI-DAN group. Conclusions: Dantrolene improves the diastolic Ca 2+ leakage from sarcoplasmic reticulum of damaged cardiomyocytes. Chronic administration of dantrolene after MI inhibits VT and ameliorates LV remodeling, leading to improved prognosis after MI. RyR2-targeting therapy could be a novel strategy for the treatment of post MI.

Correlation of extent of left ventricular endocardial unipolar low-voltage zones with ventricular tachycardia in nonischemic cardiomyopathy

BackgroundEndocardial electrogram (EGM) characteristics in nonischemic cardiomyopathy (NICM) have not been explored adequately for prognostication. ObjectiveWe aimed to study correlation of bipolar and unipolar EGM characteristics with left ventricular ejection fraction (LVEF) and ventricular tachycardia (VT) in NICM. MethodsElectroanatomic mapping of the left ventricle was performed. EGM characteristics were correlated with LVEF. Differences between groups with and without VT and predictors of VT were studied. ResultsIn 43 patients, unipolar EGM variables had better correlation with baseline LVEF than bipolar EGM variables: unipolar voltage (r = +0.36), peak negative unipolar voltage (r = −0.42), peak positive unipolar voltage (r = +0.38), and percentage area of unipolar low-voltage zone (LVZ; r = −0.41). Global mean unipolar voltage (hazard ratio [HR], 0.4; 95% confidence interval [CI], 0.2–0.8), extent of unipolar LVZ (HR, 1.6; 95% CI, 1.1–2.3), and percentage area of unipolar LVZ (HR, 1.6; 95% CI, 1.1–2.3) were significant predictors of VT. For classification of patients with VT, extent of unipolar LVZ had an area under the curve of 0.82 (95% CI, 0.69–0.95; P < .001), and percentage area of unipolar LVZ had an area under the curve of 0.83 (95% CI, 0.71–0.96; P = .01). Cutoff of >3 segments for extent of unipolar LVZ had the best diagnostic accuracy (sensitivity, 90%; specificity, 67%) and cutoff of 33% for percentage area of unipolar LVZ had the best diagnostic accuracy (sensitivity, 95%; specificity, 60%) for VT. ConclusionIn NICM, extent and percentage area of unipolar LVZs are significant predictors of VT. Cutoffs of >3 segments of unipolar LVZ and >33% area of unipolar LVZ have good diagnostic accuracies for association with VT.

Ser194Leu DSG2 mutation, associated with arrhythmogenic left ventricular cardiomyopathy and ventricular tachycardia.

Arrhythmogenic cardiomyopathy (AC) is an inherited cardiomyopathy characterized by fibro-fatty replacement of cardiomyocytes, leading to life-threatening ventricular arrhythmia and heart failure. Pathogenic variants of desmoglein2 gene (DSG2) have been reported as genetic etiologies of AC. In contrast, many reported DSG2 variants are benign or variants of uncertain significance. Correct genetic variant classification is crucial for determining the best medical therapy for the patient and family members. Pathogenicity of the DSG2 Ser194Leu variant that was identified by whole exome sequencing in a patient, who presented with ventricular tachycardia and was diagnosed with AC, was investigated by electron microscopy and immunohistochemical staining of endomyocardial biopsy sample. Electron microscopy demonstrated a widened gap in the adhering junction and a less well-organized intercalated disk region in the mutated cardiomyocytes compared to the control. Immunohistochemical staining in the proband diagnosed with AC showed reduced expression of desmoglein 2 and connexin 43 and intercalated disc distortion. Reduced expression of DSG2 and Connexin 43 were observed in cellular cytoplasm and gap junctions. Additionally, we detected perinuclear accumulation of DSG2 and Connexin 43 in the proband sample. Ser194Leu is a missense pathogenic mutation of DSG2 gene associated with arrhythmogenic left ventricular cardiomyopathy.

P 023: Idiopathic left fascicular ventricular tachycardia in pregnancy

Ventricular tachycardia (VT) can occasionally cause complications in pregnancy. In structurally normal heart, VT that arises in the left ventricle is uncommon and is termed as idiopathic left fascicular VT (ILVT). We report a case of 32-year-old lady, gravida 4 para 3 who presented to us at 34 weeks of pregnancy with symptomatic stable cardiac arrythmia with heart rate of 160 beats per minute. Electrocardiogram showed wide complex tachycardia with positive initial R wave at aVR and capture beats suggestive of ILVT. Echocardiogram was normal. She received IV verapamil 25 mg in total which failed to revert to sinus rhythm and hence, she underwent emergency Caesarean section followed by synchronized cardioversion urgently in operation theatre. Post cardioversion ECG showed sinus rhythm with memory T waves at chest leads. She was scheduled radiofrequency ablation later. This case highlights the importance of attaining the diagnosis of ILVT with distinctive ECG changes. Left ventricular outflow tract (LVOT) VT morphology depends on the site of origin, with either LBBB or early precordial transition in leads V1 to V2 or RBBB pattern in V1 with broad monophasic R in the precordial leads. In addition, there will be an R:S amplitude ratio of 30% or more or an R:QRS duration ratio of 50% in leads V1–2 with other features like capture beats and fusion beats. ILVT responds well with verapamil and can be cured with cardiac ablation, with success rates of more than 90%. ILVT though difficult to diagnose, it has distinctive ECG features which can lead to its diagnosis for appropriate treatment to be given accordingly. ILVT in pregnant patients generally has a good prognosis.

Left Fascicular Ventricular Tachycardia: What Is Forgotten in the Differential Diagnosis?

Left Fascicular Ventricular Tachycardia: What Is Forgotten in the Differential Diagnosis?

Trans-apical catheter ablation of ventricular tachycardia in a patient with metallic aortic and mitral valves

We present a patient with a history of heart failure and metallic aortic and mitral valves surgeries, who required ablation for a drug-refractory left ventricular tachycardia. But the metallic valves prohibited the insertion of catheters via retrograde or via trans-septal approaches. Therefore, we decided to perform catheter ablation by direct left ventricle puncture through a minithoracotomy. The arrhythmia was successfully ablated via of trans-apical approach and did not recur at six months follow-up.

Upper turnaround point in a reentry circuit of the idiopathic left posterior fascicular ventricular tachycardia.

The anatomic extent of the reentry circuit in idiopathic left posterior fascicular ventricular tachycardia (LPF-VT) is yet to be fully elucidated. We hypothesized that entrainment mapping could be used to delineate the reentry circuit of an LPF-VT, especially including the upper turnaround point. Twenty-three consecutive LPF-VT patients (mean age, 29±9 years, 18 males) were included. We performed overdrive pacing with entrainment attempts at the left bundle branch (LBB) and the left His bundle (HB) region. Overdrive pacing from the LBB region showed concealed fusion in all 23 patients (post-pacing interval [PPI], 322.1±64.3ms; tachycardia cycle length [TCL], 319.0±61.6ms; PPI-TCL, 3.1±4.6ms) with a long stimulus-to-QRS interval (287.9±58.0ms, approximately 90% of the TCL). Pacing from the same LBB region at a slightly faster pacing rate showed manifest fusion with antidromic conduction to the LBB and minimal in-and-out time to the LBB potential (PPI-TCL, 21.3±13.7ms). Overdrive pacing from the left HB region showed manifest fusion with a long PPI-TCL (53.9±22.5ms). Our pacing study results suggest that the upper turnaround point in a reentry circuit of the LPF-VT may extend to the proximal His-Purkinje conduction system near the LBB region but below the left HB region. The LPF may constitute the retrograde limb of the reentry circuit.

Efficacy of High-Density Three-Dimensional Mapping for Verapamil-Sensitive Left Posterior Fascicular Ventricular Tachycardia in Pediatric Patients.

In verapamil-sensitive left posterior fascicular ventricular tachycardia (LPF-VT), radiofrequency catheter ablation (RFA) is performed targeting mid-to-late diastolic potential (P1) and presystolic potential (P2) during tachycardia. This study included four patients who had undergone electrophysiological study (EPS) and pediatric patients with verapamil-sensitive LPF-VT who had undergone RFA using high-density three-dimensional (3D) mapping. The included patients were 11-14years old. During EPS, right bundle branch block and superior configuration VT were induced in all patients. VT mapping was performed via the transseptal approach. P1 and P2 during VT were recorded in three of the four patients. All patients initially underwent RFA via the transseptal approach. In three patients, P1 during VT was targeted, and VT was terminated. The lesion size indices in which VT was terminated were 4.6, 4.6, and 4.7. For one patient whose P1 could not be recorded, linear ablation was performed perpendicularly in the area where P2 was recorded during VT. Among the three patients in whom VT was terminated, linear ablation was performed in two to eliminate the ventricular echo beats. In all patients, VT became uninducible in the acute phase and had not recurred 8-24months after RFA. High-density 3D mapping with an HD Grid Mapping Catheter allows recording of P1 and P2 during VT and may improve the success rate of RFA in pediatric patients with verapamil-sensitive LPF-VT.

Surgery for ventricular tachycardia originating from the left ventricular summit.

Ventricular tachycardia (VT) originating from the left ventricular summit region, the most superior region of the left ventricle surrounded by the major coronary arteries and veins, is frequently refractory to pharmacological therapies and endocardial and epicardial catheter ablation. Eleven patients with an age from 31 to 79 (median 56) years old, underwent map-guided surgery for left ventricular summit VT. All patients had undergone 1-5 unsuccessful sessions of catheter ablation for incessant VT, preoperatively. Five patients had suffered VT storm and 1 had a history of cardiopulmonary resuscitation. Four patients had implanted with a defibrillator. Epicardium to endocardium transmural cryothermia was applied at the VT origin determined by intraoperative epicardial mapping with electro-anatomical mapping system. Harmonic scalpel was used to remove the epicardial fat and cryothermia was applied directly to the myocardium, avoiding thermal or mechanical injuries to the coronary vessels. Additional endocardial cryothermia at the VT origin was performed by a cryoprobe introduced into the left ventricular cavity through an aortotomy. There was no surgical mortality or long-term mortality related to VT during a median follow-up period of 60 months (interquartile range: 34-82). Five-year freedom from preoperatively documented left ventricular summit VT and non-documented VT was 91% and 73%, respectively. All the patients with postoperative VT underwent successful catheter ablation. Other patients were free from VT during the follow-up period. Epicardial to endocardial transmural cryothermia at the VT origin guided by intraoperative electro-anatomical mapping with a close collaboration with electrophysiologists was crucial in successful surgery for left ventricular summit VT.

False Tendons in the Left Ventricle: Implications for Successful Ablation of Left Posterior Fascicular Tachycardias

BackgroundThe anatomical substrate for left posterior fascicular ventricular tachycardia (LPF-VT) is still unclear. ObjectivesThe purpose of this study is to describe the endocavitary substrate of the re-entrant loop of LPF-VT. MethodsA total of 26 consecutive patients with LPF-VT underwent an electrophysiology study and radiofrequency ablation. ResultsIntracardiac echocardiography imaging observed a 100% prevalence of false tendons (FTs) at the left posterior septal region in all patients, and 3 different types of FTs could be classified according to their location. In 22 patients, a P1 potential could be recorded via the multielectrode catheter from a FT. In 4 patients without a recorded P1 during LPF-VT, the earliest P2 potentials were recorded from a FT in 3 patients, and from a muscular connection between 2 posteromedial papillary muscles in 1 patient. Catheter ablation focused on the FTs with P1 or earliest P2 (in patients without P1) was successful in all 26 patients. After 19 ± 8.5 months of follow-up, no patients had recurrence of LPF-VT. ConclusionsFTs provide an electroanatomical substrate for LPF-VT and a “culprit FT” may be identified as the critical structure bridging the macro–re-entrant loop. Targeting the “culprit FT” is a novel anatomical ablation strategy that results in long-term arrhythmia-free survival.

Subxiphoid epicardial access facilitated by saline infusion or carbon dioxide insufflation through a right atrial appendage controlled exit

Abstract Funding Acknowledgements Type of funding sources: None. Background Subxiphoid percutaneous access to the pericardial space for mapping and ablation of atrial and ventricular arrhythmia carries the potential risk of cardiac perforation and coronary artery laceration. Widening the pericardial space with saline solution or carbon dioxide (CO2) insufflation by intentional coronary vein exit prior to subxiphoid puncture reduces the risk of organ lesion. However, cannulation of a coronary branch is often difficult and adds complexity to the ablation procedure. Purpose To determine the feasibility and the safety of subxiphoid epicardial access facilitated by controlled pericardial saline infusion or neumopericardium through a right atrial appendage exit. Methods The right atrial appendage was transvenously cannulated using a steerable sheath following anatomical characterization of the right atrium on an electroanatomical navigation system. A 0.014" angioplasty guide was introduced with the proximal rigid end placed distally and progressed until the appendage was perforated and the guide-wire placed into the pericardial space. A double lumen microcatheter was then progressed over the wire. Saline solution (100-400 mL) or CO2 (100-500 cc) were infused through the microcatheter to achieve sufficient pericardial space widening or hemodynamic deterioration. Finally, pericardial access was obtained using the conventional subxiphoid approach. Results 17 consecutive patients (62±10 years, 15 male) with left atrial flutter (LAF n=11) or ventricular tachycardia (VT n=6) refractory to endocardial ablation were prospectively included. All patients with atrial flutter (uninterrupted oral anticoagulation plus heparin for ACT &amp;gt;300 sec) and ventricular tachycardia (heparin for ACT &amp;gt;300 sec) were fully anticoagulated at the time of the procedure. It was not possible to access epicardium in 4 patients due to adhesions (VT=3 LFA=1). The first 4 patients with successful access had saline infused and the remaining 9 patients had CO2 insufflated. Epicardial tachycardia ablation was successfully achieved in 8 patients (5 AFLs and 3 VTs) and partially successful in 1 patient (1AFL). A pericardial drainage was left in 6 patients before leaving the EP laboratory and removed in the remaining. There was no apparent right ventricular puncture, coronary artery laceration or other major complications. One patient had cardiac tamponade during the procedure and 2 other patients presented tamponade after the procedure following discharge from the interventional lab. One patient presented neumomediastinum and other patient presented subcutaneous emphysema, which resolved uneventful in 24 hours. Conclusions Saline infusion or carbon dioxide insufflation through a right atrial appendage controlled exit facilitates subxiphoid epicardial access for ablation of refractory atrial and ventricular arrhythmias. This approach can be performed in the majority the patients and appears to be safe.

RyR2-targeting therapy prevents left ventricular remodeling and ventricular tachycardia in post-infarction heart failure

BackgroundDantrolene binds to the Leu601-Cys620 region of the N-terminal domain of cardiac ryanodine receptor (RyR2), which corresponds to the Leu590-Cys609 region of the skeletal ryanodine receptor, and suppresses diastolic Ca2+ leakage through RyR2. ObjectiveWe investigated whether the chronic administration of dantrolene prevented left ventricular (LV) remodeling and ventricular tachycardia (VT) after myocardial infarction (MI) by the same mechanism with the mutation V3599K of RyR2, which indicated that the inhibition of diastolic Ca2+ leakage occurred by enhancing the binding affinity of calmodulin (CaM) to RyR2. Methods and resultsA left anterior descending coronary artery ligation MI model was developed in mice. Wild-type (WT) were divided into four groups: sham-operated mice (WT-Sham), sham-operated mice treated with dantrolene (WT-Sham-DAN), MI mice (WT-MI), and MI mice treated with dantrolene (WT-MI-DAN). Homozygous V3599K RyR2 knock-in (KI) mice were divided into two groups: sham-operated mice (KI-Sham) and MI mice (KI-MI). The mice were followed for 12 weeks.Survival was significantly higher in the WT-MI-DAN (73%) and KI-MI groups (70%) than the WT-MI group (40%). Echocardiography, pathological tissue, and epinephrine-induced VT studies showed that LV remodeling and VT were prevented in the WT-MI-DAN and KI-MI groups compared to the WT-MI group. An increase in diastolic Ca2+ spark frequency and a decrease in the binding affinity of CaM to the RyR2 were observed at 12 weeks after MI in the WT-MI group, although significant improvements in these values were observed in the WT-MI-DAN and KI-MI groups. ConclusionsPharmacological or genetic stabilization of RyR2 tetrameric structure improves survival after MI by suppressing LV remodeling and proarrhythmia.

A rapid wide complex tachycardia

A rapid wide complex tachycardia

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.

Left bundle branch re-entrant ventricular tachycardia in septal myocarditis with QRS narrowing after ablation.

Left bundle branch re-entrant ventricular tachycardia in septal myocarditis with QRS narrowing after ablation.

Catheter ablation of idiopathic left fascicular ventricular tachycardia: Implications of false tendons for mapping and ablation.

The anatomical substrate for idiopathic left ventricular tachycardia (ILVT) remains speculative. Purkinje networks surrounding false tendons (FTs) might be involved in the reentrant circuit of ILVT. The objective was to evaluate the anatomical and electrophysiological features of false tendons FTs in relation to ILVT. Intracardiac echocardiography (ICE) was conducted on patients with ILVT. The relationship of the FTs with ILVT was determined using electro-anatomical mapping. Electrophysiological evaluation and radiofrequency ablation were conducted in 23 consecutive patients with ILVT. FTs were identified in 19/23 cases (82.6%) with P1 potentials during VT recorded at the FT in 14 of these patients (73.7%). Three FT types were identified. In type 1, the FT attached the septum to the base of the posteromedial papillary muscle (PPM) (4/19); type 2 FTs ran between the septum and the PPM apex (3/19), while in type 3, the connection occurred between the septum and apex (11/19) or between the septum and the LV free wall (1/19). The effective ILVT ablation sites were situated at the FT-PPM (3/19) and the FT-septum (16/19) attachment sites. This series demonstrates the association between Purkinje fibers and FTs during catheter ablation of ILVT and verifies that left ventricular FTs are an important substrate in this type of tachycardia.

Substrate Mapping Alters Ventricular Tachycardia Inducibility.

Initiation of ventricular tachycardia (VT) by programmed electrical stimulation (PES) has an important role to allow mapping and assess ablation end points. We hypothesized that substrate mapping may alter VT inducibility by mechanical bumping of critical sites. Subjects with left ventricular scar-related VT that was inducible by PES who were undergoing ablation were included. PES was repeated after substrate mapping (Group I) or after time under sedation/anesthesia during which additional imaging and transeptal puncture were performed without substrate mapping (Group II). The response to the second PES was categorized as type I if the same VT was induced, type II if a different VT was induced, and type III if VT was not inducible. Twenty-eight patients (median age 66 years, 61% ischemic cardiomyopathy), 14 in Group I and 14 in Group II, were included. Age, time between initial and second PES, type of cardiomyopathy, ejection fraction, and anesthesia methods were not different between the 2 groups. Initial VT cycle length, however, was shorter in Group I (305 millisecond [range, 235-600] versus 350 millisecond [range, 235-600], P=0.016). Also, Group I required more extrastimuli to induce VT in PES 1 (2 [1-4] versus 2 [1-3], P=0.022). In Group I, following substrate mapping, the second PES induced the same VT in 3 patients (21%), a different VT in 9 (64%), and no VT in 2 (14%) patients. In contrast, in Group II the same VT was induced in 10 (71%) patients, a different VT in 3 (21%) and no VT in 1 (7%) patient (P=0.017). Mechanical effects of substrate mapping commonly alter inducibility of VT. This has important implications for catheter ablation procedure planning and acute assessment of outcome and can potentially account for some recurrent VTs that are not recognized at the time of the procedure.

Electrophysiological characteristics and long-term outcome of substrate-based catheter ablation for left posterior fascicular ventricular tachycardia targeting fragmented antegrade Purkinje potentials during sinus rhythm.

The aim of this study was to investigate the electrophysiological characteristics and long-term outcome of patients undergoing substrate-based ablation of left posterior fascicular ventricular tachycardia (LPF-VT) guided by targeting of fragmented antegrade Purkinje potentials (FAPs) during sinus rhythm. This study retrospectively analysed 50 consecutive patients referred for ablation. Substrate mapping during sinus rhythm was performed to identify the FAP that was targeted by ablation. FAPs were recorded in 48 of 50 (96%) patients during sinus rhythm. The distribution of FAPs was located at the proximal segment of posterior septal left ventricle (LV) in two (4.2%) patients, middle segment in 33 (68.8%) patients, and distal segment in 13 (27.1%) patients. In 32 of 48 (66.7%) patients, the FAP displayed a continuous multicomponent fragmented electrogram, while a fragmented, split, and uncoupled electrogram was recorded in 16 (33.3%) patients. Entrainment attempts at FAP region were performed successfully in seven patients, demonstrating concealed fusion and the critical isthmus of LPF-VT. Catheter ablation targeting at the FAPs successfully terminated the LPF-VT in all 48 patients in whom they were seen. Left posterior fascicular (LPF) block occurred in four (8%) patients after ablation. During a median follow-up period of 61.2 ± 16.8 months, 47 of 50 (94%) patients remained free from recurrent LPF-VT. Ablation of LPF-VT targeting FAP during sinus rhythm results in excellent long-term clinical outcome. FAPs were commonly located at the middle segment of posterior septal LV. Region with FAPs during sinus rhythm was predictive of critical site for re-entry.

Repetitive multiform narrow complex tachycardia

A 73-year-old man presented to the emergency department with palpitations. After experiencing transient exertional palpitations and dyspnea a few months earlier, investigation revealed moderate left ventricular dysfunction and extensive coronary artery disease with evidence of prior inferior infarction. He underwent bypass grafting and remained symptom free with normalization of his ejection fraction until the current presentation. Figure 1 demonstrates his presenting rhythm that did not respond to adenosine but terminated with intravenous diltiazem. What is the most likely mechanism of the tachycardia? Figure 1 shows a regular narrow complex tachycardia with 3 distinct alternating QRS morphologies: (1) right bundle branch block (RBBB), V1 R 120 ms, V4 precordial transition, left superior axis; (2) RBBB, V1 rsRʹ 100 ms, positive precordial concordance, left superior axis; and (3) RBBB, V1 R 100 ms, positive precordial concordance, left superior axis. The RBBB and left superior axis of all 3 morphologies suggest that the ventricles are activated via the left posterior fascicle, or at the very least, there is early engagement of this fascicle. While supraventricular tachycardia with aberrant conduction is theoretically possible, varying ventricular morphologies in this fashion, lack of termination with adenosine, and the relatively narrow QRS duration (<130 ms) would make this less likely. Together with the response to diltiazem, the overall evidence suggests ventricular tachycardia involving the left posterior fascicle. The classic form of idiopathic fascicular ventricular tachycardia involves the left posterior fascicle, in which there is slow antegrade conduction along abnormal Purkinje fibers in the mid-septum (resulting in P1 potentials) and conduction over the left posterior fascicle (resulting in P2 potentials).1Nogami A. Naito S. Tada H. et al.Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia.J Am Coll Cardiol. 2000; 36: 811-823Crossref PubMed Scopus (218) Google Scholar In any individual patient, variable relationships of the abnormal Purkinje fiber to the left posterior fascicle can result in a more basal or apical site of breakout to the left ventricle; these differences can often be suggested on the surface electrocardiogram by the width of the QRS complex and the precordial transition.2Liu Q. Shehata M. Jiang R. et al.Macroreentrant loop in ventricular tachycardia from the left posterior fascicle: new implications for mapping and ablation.Circ Arrhythm Electrophysiol. 2016; 9e004272Crossref Scopus (7) Google Scholar,3Ma W. Lu F. Shehata M. et al.Catheter ablation of idiopathic left posterior fascicular ventricular tachycardia: predicting the site of origin via mapping and electrocardiography.Circ Arrhythm Electrophysiol. 2017; 10e005240Crossref PubMed Scopus (1) Google Scholar Sung et al4Sung R.K. Kim A.M. Tseng Z.H. et al.Diagnosis and ablation of multiform fascicular tachycardia.J Cardiovasc Electrophysiol. 2013; 24: 297-304Crossref PubMed Scopus (29) Google Scholar described multiform fascicular QRS complexes due to alternate conduction over the left anterior fascicle and the left posterior fascicle from the septal fascicle, but the QRS forms described in the present report are different. Idiopathic fascicular ventricular tachycardia typically occurs in patients with structurally normal hearts, which was not the case in the present report. However, abnormal Purkinje fibers have also been implicated in a minority of patients with ischemic ventricular tachycardia and extension of inferoposterior scar to the left posterior fascicle.5Bogun F. Good E. Reich S. et al.Role of Purkinje fibers in post-infarction ventricular tachycardia.J Am Coll Cardiol. 2006; 48: 2500-2507Crossref PubMed Scopus (121) Google Scholar In this case, it was hypothesized that different QRS morphologies were due to varying sites of left ventricular breakout (Figure 2). The patient underwent electrophysiology study, where multiple episodes of ventricular tachycardia were able to be induced with ventricular extrastimuli similar to those seen on presentation. Ablation of the left posterior fascicle was undertaken, with subsequent noninducibility and no further episodes after 12 months of follow-up.

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

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. 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. 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.