Paced QRS morphology mimicking complete left bundle branch block induced by right ventricular pacing is associated with pacing-induced cardiomyopathy.

INTRODUCTION: Right ventricular (RV) pacing sometimes causes left ventricular (LV) systolic dysfunction, also known as pacing-induced cardiomyopathy (PICM). However, the association between specifically paced QRS morphology and PICM development has not been elucidated. This study aimed to investigate the association between paced QRS mimicking a complete left bundle branch block (CLBBB) and PICM development. METHODS: We retrospectively screened 2009 patients who underwent pacemaker implantation from 2010 to 2020 in seven institutions. Patients who received pacemakers for an advanced atrioventricular block or bradycardia with atrial fibrillation, baseline LV ejection fraction (LVEF) ≥ 50%, and echocardiogram recorded at least 6 months postimplantation were included. The paced QRS recorded immediately after implantation was analyzed. A CLBBB-like paced QRS was defined as meeting the CLBBB criteria of the American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society in 2009. PICM was defined as a ≥10% LVEF decrease, resulting in an LVEF of <50%. RESULTS: Among the 270 patients analyzed, PICM was observed in 38. Baseline LVEF was lower in patients with PICM, and CLBBB-like paced QRS was frequently observed in PICM. Multivariate analysis revealed that low baseline LVEF (odds ratio [OR]: 0.93 per 1% increase, 95% confidence interval [CI]: 0.89-0.98, p = 0.006) and CLBBB-like paced QRS (OR: 2.69, 95% CI: 1.25-5.76, p = 0.011) were significantly associated with PICM development. CONCLUSION: CLBBB-like paced QRS may be a novel risk factor for PICM. RV pacing, which causes CLBBB-like QRS morphology, may need to be avoided, and patients with CLBBB-like paced QRS should be followed-up carefully.

Triggers of Ventricular Fibrillation in Patients With Inferolateral J-Wave Syndrome.

BACKGROUND: There are few data on ventricular fibrillation (VF) initiation in patients with inferolateral J waves. OBJECTIVES: This multicenter study investigated the characteristics of triggers initiating spontaneous VF in inferolateral J-wave syndrome. METHODS: A total of 31 patients (age 37 ± 14 years, 24 male) with spontaneous VF episodes associated with inferolateral J waves were evaluated to determine the origin and characteristics of triggers. The J-wave pattern was recorded in inferior leads in 11 patients, lateral leads in 3, and inferolateral leads in 17. RESULTS: The VF triggers (n = 37) exhibited varying QRS durations (176 ± 21 milliseconds, range 119-219 milliseconds) and coupling intervals (339 ± 46 milliseconds, range 250-508 milliseconds) with a right (70%) or left (30%) bundle branch block (BBB) pattern. Trigger patterns were associated with J-wave location: left BBB triggers with inferior J waves and right BBB triggers with lateral J waves. Electrophysiologic study was performed for 22 VF triggers in 19 patients. They originated from the left or right Purkinje system in 6 and from the ventricular myocardium in 10 and were undetermined in 6. Purkinje vs myocardial triggers showed distinct electrocardiographic characteristics in coupling interval and QRS-complex duration and morphology. Abnormal epicardial substrate associated with fragmented electrograms was identified in 9 patients, with triggers originating from the same region in 7 patients. Catheter ablation resulted in VF suppression in 15 patients (79%). CONCLUSIONS: VF initiation in inferolateral J-wave syndrome is associated with significant individual heterogeneity in trigger characteristics. Myocardial triggers have electrocardiographic features distinct from Purkinje triggers, and their origin often colocalizes with an abnormal epicardial substrate.

Electrophysiological features of repetitive focal Purkinje ventricular arrhythmias originating from the proximal cardiac conduction system.

Background: Focal Purkinje ventricular arrhythmias (VAs) might originate from the vicinity of the proximal portion of the cardiac conducting system. This study aimed to clarify the features associated with focal Purkinje VAs originating from the proximal conduction system. Methods: A total of 18 patients with focal Purkinje VAs undergoing radiofrequency catheter ablation (RFCA) were retrospectively examined and divided into the proximal type or the non-proximal type. The proximal type was defined as having the origin at the proximal half of the interventricular septum, or the proximal half and the septal side of the anterior wall. The 12-lead electrocardiogram and electrophysiological findings were investigated. Results: Seven patients met criteria for proximal type of focal Purkinje VA. Out of the 7, 4 patients with proximal VAs had multiple QRS morphologies of VAs clinically, whereas out of 11 patients with non-proximal VAs, only 1 had multiple morphologies (p = .047). VA QRS duration was shorter in the proximal type than in the non-proximal type (111.2 ± 19.8 ms vs. 135.7 ± 17.7 ms; p = .003). The absolute axis difference between sinus rhythm and VA was smaller in the proximal type (80.4 ± 46.1°vs. 138.8 ± 59.6°; p = .014). The absolute axis difference ≤134° was useful in distinguishing the two types. Recurrence of VA was recorded in 3 proximal type patients and 3 non-proximal type patients. No procedure-related conduction block was observed. Conclusion: A VA of absolute axis difference ≤134°, and multiple QRS morphologies of clinical VAs indicate a proximal origin. Focal Purkinje VAs from proximal origins can be suppressed by RFCA without severe conduction disturbance.

Subcutaneous implantable cardioverter defibrillator for spontaneous coronary artery dissection with ventricular fibrillation: A report of two cases.

The efficacy of implantable cardioverter defibrillators (ICDs) for secondary prevention in spontaneous coronary artery dissection (SCAD) with ventricular fibrillation (VF) remains unclear. Herein, we report two cases of SCAD. In both cases, VF and ST-elevation myocardial infarction (STEMI) were noted, which were previously reported to increase the risk of VF recurrence and sudden cardiac death (SCD). Hence, a subcutaneous (S)-ICD was implanted for secondary prevention in each case. Previous studies have suggested that among patients with SCAD, those with a history of VF and left ventricular ejection fraction (LVEF) of <50% are at a higher risk of ventricular tachycardia or VF recurrence, whereas those with a history of smoking, STEMI, onset during pregnancy, recurrent SCAD, LVEF <50%, and left coronary artery main trunk lesion or proximal lesion are at a higher risk of SCD. Moreover, S-ICD is associated with fewer complications than transvenous-ICD, and the rate of inappropriate shock is decreasing. Therefore, risk stratification and consideration of S-ICD implantation in high-risk patients may be an important therapeutic strategy for the secondary prevention of SCAD. Learning objective: Previous studies have not shown the efficacy of implantable cardioverter defibrillators (ICDs) for spontaneous coronary artery dissection (SCAD). Meanwhile, it was also suggested that patients with SCAD, including those with a history of ventricular fibrillation (VF) and ST-elevation myocardial infarction, are at high risk of VF recurrence or sudden cardiac death. For the secondary prevention of SCAD with VF, subcutaneous ICD implantation in high-risk patients may be an important strategy.

Two cases of wide QRS complex tachycardia caused by anamorelin.

Anamorelin is prescribed for cancer cachexia treatment. Anamorelin is a ghrelin receptor antagonist and exerts a sodium channel blockade effect, possibly inducing disorders of the cardiac conduction system. We herein report two cases of wide QRS complex tachycardia caused by anamorelin. In both cases, the patients had liver dysfunction. Anamorelin is mainly metabolized in the liver; hence, sodium channel blockade by anamorelin during liver dysfunction can cause serious side effects, including wide QRS complex tachycardia, similar to flecainide toxicity. The differential diagnosis of wide QRS tachycardia caused by anamorelin can be challenging because conventional electrocardiogram criteria cannot be applicable in patients with drug intoxication. It can worsen the situation for the use of antiarrhythmic drugs for wide QRS tachycardia. The appropriate treatment is supportive care until anamorelin is metabolized. To our best knowledge, this is the first study to report the life-threatening adverse effects of anamorelin. Learning objective: Anamorelin is prescribed for cancer cachexia treatment. Anamorelin can cause wide QRS complex tachycardia. Our findings in the two cases we encountered indicate that we should be aware of wide QRS complex tachycardia in patients taking anamorelin, especially if they have liver dysfunction. We should suspect the condition to be the adverse effect of anamorelin and monitor the electrocardiogram and blood test findings regularly to prevent this fatal side effect.

Combined endo- and epicardial pace-mapping to localize ventricular tachycardia isthmus in ischaemic and non-ischaemic cardiomyopathy.

AIMS: A high-density pace-mapping can depict an abrupt transition in paced QRS morphology from a poor to excellent match, unmasking the critical component of ventricular tachycardia (VT) isthmus from the entrance to exit. We sought to assess pace-mapping at multiple sites within the endo- and epicardial scars to identify the VT isthmus in patients with ischaemic (ICM) and non-ischaemic cardiomyopathy (NICM). METHODS AND RESULTS: Colour-coded maps correlating to the percentage matches between 12-lead electrocardiograms during VT and pace-mapping [referred to as correlation score maps (CSMs)] were analysed. We studied 115 CSMs (80 endo- and 35 epicardial CSMs) in 37 patients (17 ICM, 20 NICM). The CSM with an abrupt change (AC) in pacemap score (AC-type) on the endocardium was more frequently observed in ICM than in NICM [11/39 (28%) vs. 1/41 (2%); P = 0.001]. Among 35 CSMs that were analysed by the combined endo- and epicardial mapping, 10 (29%) CSMs exhibited non-AC-type on the endocardium; however, AC-type was present on the opposite epicardium. Although 24 (69%) CSMs did not show AC-type on both the endocardium and epicardium, 16 of them had either an excellent (>90%) or poor (<0%) correlation score on either side, associated with isthmus exit or entrance, respectively. However, the remaining eight CSMs had neither excellent nor poor scores. CONCLUSION: The CSM may provide electrophysiological information to localize the endo- and epicardial VT isthmus. The absence of AC-type CSM on the endocardium, which is frequently observed in NICM, appears to indicate the sub-epicardial or intramural course of the critical isthmus.

Functionally validated SCN5A variants allow interpretation of pathogenicity and prediction of lethal events in Brugada syndrome.

AIMS: The prognostic value of genetic variants for predicting lethal arrhythmic events (LAEs) in Brugada syndrome (BrS) remains controversial. We investigated whether the functional curation of SCN5A variations improves prognostic predictability. METHODS AND RESULTS: Using a heterologous expression system and whole-cell patch clamping, we functionally characterized 22 variants of unknown significance (VUSs) among 55 SCN5A mutations previously curated using in silico prediction algorithms in the Japanese BrS registry (n = 415). According to the loss-of-function (LOF) properties, SCN5A mutation carriers (n = 60) were divided into two groups: LOF-SCN5A mutations and non-LOF SCN5A variations. Functionally proven LOF-SCN5A mutation carriers (n = 45) showed significantly severer electrocardiographic conduction abnormalities and worse prognosis associated with earlier manifestations of LAEs (7.9%/year) than in silico algorithm-predicted SCN5A carriers (5.1%/year) or all BrS probands (2.5%/year). Notably, non-LOF SCN5A variation carriers (n = 15) exhibited no LAEs during the follow-up period. Multivariate analysis demonstrated that only LOF-SCN5A mutations and a history of aborted cardiac arrest were significant predictors of LAEs. Gene-based association studies using whole-exome sequencing data on another independent SCN5A mutation-negative BrS cohort (n = 288) showed no significant enrichment of rare variants in 16 985 genes including 22 non-SCN5A BrS-associated genes as compared with controls (n = 372). Furthermore, rare variations of non-SCN5A BrS-associated genes did not affect LAE-free survival curves. CONCLUSION: In vitro functional validation is key to classifying the pathogenicity of SCN5A VUSs and for risk stratification of genetic predictors of LAEs. Functionally proven LOF-SCN5A mutations are genetic burdens of sudden death in BrS, but evidence for other BrS-associated genes is elusive.

Stellate Ganglion Phototherapy Using Low-Level Laser: A Novel Rescue Therapy for Patients With Refractory Ventricular Arrhythmias.

OBJECTIVES: This study investigates the effect of stellate ganglion (SG) phototherapy in healthy participants and assesses its efficacy in suppressing electrical storm (ES) refractory to antiarrhythmic drugs and catheter ablation. BACKGROUND: Modulation of the autonomic nervous system has been shown to be an effective adjunctive therapy for ES. METHODS: Ten-minute SG phototherapy was performed twice weekly for 4 weeks in 20 healthy volunteers. To evaluate the acute and chronic effects of SG phototherapy, heart rate variability and serum concentrations of adrenaline, noradrenaline, and dopamine were obtained before phototherapy, immediately after the first phototherapy session, after 8 sessions of phototherapy, and 3 months after the first phototherapy session. In addition, the efficacy of SG phototherapy was evaluated in 11 patients with ES refractory to medication, sedation, and catheter ablation. RESULTS: In healthy participants, serum adrenaline concentration significantly decreased after phototherapy, whereas low-frequency power/high-frequency power significantly decreased during phototherapy. Moreover, the effect on heart rate variability did not last beyond 3 months. In the clinical pilot study, 7 patients had a suppression of ES after SG phototherapy; however, without maintenance therapy, 2 patients had a recurrence of ventricular arrhythmias. Furthermore, it did not control ES in 4 patients. CONCLUSIONS: SG phototherapy reduced sympathetic activity and may be a safe and effective adjunctive therapy to control ES in some patients, but its long-term efficacy remains unknown. Chronic phototherapy might help reduce ES recurrence.

Three-dimensional mapping discovered arrhythmic substrate missed in the initial diagnosis of idiopathic ventricular fibrillation.

During an initial diagnosis of IVF, an arrhythmic substrate may be missed for several reasons such as lack of information; thus, a careful follow-up is important. A three-dimensional mapping may identify a possible missed arrhythmic substrate in IVF.

Novel Diagnostic Observations of Nodoventricular/Nodofascicular Pathway-Related Orthodromic Reciprocating Tachycardia Differentiating From Atrioventricular Nodal Re-Entrant Tachycardia.

OBJECTIVES: This study sought to assess the performance of current diagnostic criteria and identify additional electrophysiological features differentiating orthodromic reciprocating tachycardia (ORT) with a concealed nodoventricular/nodofascicular (NV/NF) pathway from atrioventricular nodal re-entrant tachycardia (AVNRT). BACKGROUND: Diagnosing sustained supraventricular tachycardia (SVT) despite the occurrence of ventriculoatrial block (VAB) is challenging. METHODS: We analyzed electrograms of 25 sustained SVTs (9 NV/NF-ORTs [n = 7/2] and 16 AVNRTs) with VAB and 91 AVNRTs without VAB (for reference). RESULTS: More than 1 SVT, each with a different ventriculoatrial interval, was commonly induced in AVNRT cases (75%) but not in NV/NF-ORT cases (0%; p = 0.0005). Wenckebach VAB was common in NV/NF-ORTs (78%), but VAB patterns varied in AVNRTs. The His-His interval transiently prolonged in the following beat after the VAB in most AVNRTs but rarely did in NV/NF-ORTs (79% vs. 22%; p = 0.01). NV/NF-ORT was diagnosed by His-refractory premature ventricular contractions (n = 5) and the findings during right ventricular overdrive pacing showing an uncorrected/corrected post-pacing interval (PPI)-tachycardia cycle length (TCL) ≤115/110 ms (n = 5/5), orthodromic His capture (n = 6), and V-V-A (ventricle-ventricle-atrial response) response (n = 3). A single form of induced SVT (positive predictive value [PPV]: 69%; negative predictive value [NPV]: 100%), Wenckebach VAB (PPV: 70%; NPV: 87%), stable His-His interval despite VAB (PPV: 70%; NPV: 85%), orthodromic His capture (PPV: 100%; NPV: 97%), and V-V-A response (PPV: 100%; NPV: 95%) characterized NV/NF-ORT, and a PPI-TCL of ≤125 ms (PPV: 100%; NPV: 100%) characterized NV-ORT. CONCLUSIONS: Induction of a single SVT form, Wenckebach VAB, stable His-His interval despite VAB, orthodromic His capture, and V-V-A response appeared to discriminate NV/NF-ORT from AVNRT, with a PPI-TCL of ≤125 ms discriminating NV-ORT from NF-ORT and AVNRT.

Cardiac Emerinopathy: A Nonsyndromic Nuclear Envelopathy With Increased Risk of Thromboembolic Stroke Due to Progressive Atrial Standstill and Left Ventricular Noncompaction.

BACKGROUND: Mutations in the nuclear envelope genes encoding LMNA and EMD are responsible for Emery-Dreifuss muscular dystrophy. However, LMNA mutations often manifest dilated cardiomyopathy with conduction disturbance without obvious skeletal myopathic complications. On the contrary, the phenotypic spectrums of EMD mutations are less clear. Our aims were to determine the prevalence of nonsyndromic forms of emerinopathy, which may underlie genetically undefined isolated cardiac conduction disturbance, and the etiology of thromboembolic complications associated with EMD mutations. METHODS: Targeted exon sequencing was performed in 87 probands with familial sick sinus syndrome (n=36) and a progressive cardiac conduction defect (n=51). RESULTS: We identified 3 X-linked recessive EMD mutations (start-loss, splicing, missense) in families with cardiac conduction disease. All 3 probands shared a common clinical phenotype of progressive atrial arrhythmias that ultimately resulted in atrial standstill associated with left ventricular noncompaction (LVNC), but they lacked early contractures and progressive muscle wasting and weakness characteristic of Emery-Dreifuss muscular dystrophy. Because the association of LVNC with EMD has never been reported, we further genetically screened 102 LVNC patients and found a frameshift EMD mutation in a boy with progressive atrial standstill and LVNC without complications of muscular dystrophy. All 6 male EMD mutation carriers of 4 families underwent pacemaker or defibrillator implantation, whereas 2 female carriers were asymptomatic. Notably, a strong family history of stroke observed in these families was probably due to the increased risk of thromboembolism attributable to both atrial standstill and LVNC. CONCLUSIONS: Cardiac emerinopathy is a novel nonsyndromic X-linked progressive atrial standstill associated with LVNC and increased risk of thromboembolism.

Closed-loop stimulation as a physiological rate-modulated pacing approach based on intracardiac impedance to lower the atrial tachyarrhythmia burden in patients with sinus node dysfunction and atrial fibrillation.

INTRODUCTION: The effectiveness of rate-modulated pacing for the suppression of atrial fibrillation (AF) is controversial. Closed-loop stimulation (CLS) is a heart rate modulation technique based on the contractility of the right ventricle estimated by sensing myocardial impedance, and CLS can still adapt to the heart rate in conditions where there are no significant changes in acceleration or ventilation, such as emotional stress. We elucidated the association between CLS and atrial tachyarrhythmia (AT) burden in patients with sinus node dysfunction and paroxysmal AF history before pacemaker implantation. METHODS AND RESULTS: We retrospectively reviewed all consecutive patients who underwent pacemaker implantation for sinus node dysfunction with an AF history before implantation. Overall, 146 patients were analyzed, with fixed-rate pacing (FP) in 82, CLS in 31, and non-CLS rate modulation in 33 patients. The AF/AT episodes were detected in 98 patients during a 12-month period. The median AF/AT burden was 1.6% (interquartile: 0.0%, 11.0%) in FP; 0% (0.0%, 2.5%) in CLS, and 1.0% (0.1%, 9.3%) in non-CLS. The AF/AT burden was significantly lower for CLS than for FP and non-CLS rate modulation (P < .01 and P = .04, respectively). CLS was associated with lower risks of AF/AT occurrence (hazard ratio [HR], 0.31; P = .02) and AF/AT burden more than 5% (HR, 0.28; P = .05), even after adjusting for potential confounders. This association was independent of the percentage of atrial pacing. CONCLUSION: CLS was associated with lower AF/AT burden after pacemaker implantation in patients with sinus node dysfunction and AF history.

Prognostic impact of lead tip position confirmed via computed tomography in patients with right ventricular septal pacing.

BACKGROUND: Although fluoroscopy-guided right ventricular (RV) lead placement in the ventricular septum is a widely performed procedure, variation in true RV lead tip position confirmed via computed tomography (CT) and its prognostic implications in patients with atrioventricular block (AVB) are not well understood. OBJECTIVE: The purpose of this study was to evaluate the prognostic impact of CT-confirmed RV lead tip position. METHODS: We retrospectively enrolled 228 consecutive patients (age 77 ± 10 years; 125 men) with AVB who underwent fluoroscopy-guided RV septal lead implantation and thoracic CT after pacemaker implantation. Patients were classified into septal and free-wall groups according to RV lead tip position. The primary endpoint was the composite outcome of cardiac death and heart failure hospitalization. RESULTS: The RV lead tip was located at the free wall in 18 patients (8%). The primary endpoint occurred in 37 patients (16%) over median follow-up of 41 months. Electrocardiographic analysis found that R amplitude >0.53 mV in lead I was significantly predictive of free-wall pacing, with sensitivity of 70% and specificity of 77%. Multivariate Cox regression analysis demonstrated that the lead tip in the free wall (hazard ratio 2.93; 95% confidence interval 1.21-7.11; P = .018) was an independent predictor of the primary endpoint. CONCLUSION: Fluoroscopy-guided RV lead placement carries potential risk of unexpected RV free-wall pacing and may increase the risk of cardiac death and heart failure-related hospitalization in patients undergoing RV septal pacing due to AVB and receiving thoracic CT for medical reasons.

Efficacy of Endocardial Ablation of Drug-Resistant Ventricular Fibrillation in Brugada Syndrome: Long-Term Outcome.

Background Both endocardial trigger elimination and epicardial substrate modification are effective in treating ventricular fibrillation (VF) in Brugada syndrome. However, the primary approach and the characteristics of patients who respond to endocardial ablation remain unknown. Methods Among 123 symptomatic Brugada syndrome patients (VF, 63%; syncope, 37%), ablation was performed in 21 VF/electrical storm patients, the majority of whom were resistant to antiarrhythmic drugs. Results Careful endocardial mapping revealed that 81% of the patients had no specific findings, whereas 19% of the patients, who experienced the most frequent VF episodes with notching of the QRS in lead V1, had delayed low-voltage fractionated endocardial electrograms. Ablation of VF triggers followed by endocardial substrate modification was performed in the right ventricular outflow tract in 85% of the cases and in the right ventricle in 15%. VF triggers could not be completely eliminated in 1 patient and VF became noninducible in 14 (88%) patients among 16 patients who underwent VF induction with normalization of Brugada-type ECG in 3. During follow-up (56.14±36.95 months), VF recurrence was observed in 7 patients. Importantly, all patients who had nothing of QRS in lead V1 did not respond to endocardial ablation despite presence of VF-triggering ectopic beats during ablation. Conclusions With careful documentation of VF-triggering ectopic beats and detailed endocardial mapping, endocardial VF trigger elimination followed by endocardial substrate modification has an excellent long-term outcome, whereas presence of QRS notching in lead V1 was associated with high VF recurrence suggesting epicardial substrate ablation as effective initial approach.

New Substrate-Guided Method of Predicting Slow Conducting Isthmuses of Ventricular Tachycardia: Preliminary Analysis to the Combined Use of Voltage Limit Adjustment and Fast-Fourier Transform Analysis.

BACKGROUND: Several conducting channels of ventricular tachycardia (VT) can be identified using voltage limit adjustment (VLA) of substrate mapping. However, the sensitivity or specificity to predict a VT isthmus is not high by using VLA alone. This study aimed to evaluate the efficacy of the combined use of VLA and fast-Fourier transform analysis to predict VT isthmuses. METHODS AND RESULTS: VLA and fast-Fourier transform analyses of local ventricular bipolar electrograms during sinus rhythm were performed in 9 postinfarction patients who underwent catheter ablation for a total of 13 monomorphic VTs. Relatively higher voltage areas on an electroanatomical map were defined as high voltage channels (HVCs), and relatively higher fast-Fourier transform areas were defined as high-frequency channels (HFCs). HVCs were classified into full or partial HVCs (the entire or >30% of HVC can be detectable, respectively). Twelve full HVCs were identified in 7 of 9 patients. HFCs were located on 7 of 12 full HVCs. Five VT isthmuses (71%) were included in the 7 full HVC+/HFC+ sites, whereas no VT isthmus was found in the 5 full HVC+/HFC- sites. HFCs were identical to 9 of 16 partial HVCs. Eight VT isthmuses (89%) were included in the 9 partial HVC+/HFC+ sites, whereas no VT isthmus was found in the 7 partial HVC+/HFC- sites. All HVC+/HFC+ sites predicted VT isthmus with a sensitivity of 100% and a specificity of 80%. CONCLUSIONS: Combined use of VLA and fast-Fourier transform analysis may be a useful method to detect VT isthmuses.

Amiodarone-induced Thyrotoxicosis with Cardiopulmonary Arrest.

We describe a case of amiodarone-induced thyrotoxicosis (AIT) with cardiopulmonary arrest (CPA) in a 49-year-old woman. The patient had been treated with amiodarone for non-sustained ventricular tachycardia. Two weeks prior to her admission, she developed thyrotoxicosis and prednisolone (PSL, 30 mg daily) was administered with the continuation of amiodarone. However, she was admitted to our hospital for CPA. We performed total thyroidectomy to control her thyrotoxicosis and the pathological findings were consistent with type 2 AIT. She gradually improved and was discharged on day 84. This case demonstrates the importance of considering immediate total thyroidectomy for patients with uncontrollable AIT.

Fascicular Ventricular Tachycardia Originating From Papillary Muscles: Purkinje Network Involvement in the Reentrant Circuit.

BACKGROUND: Verapamil-sensitive fascicular ventricular tachycardia (FVT) has been demonstrated to be a reentrant mechanism using the Purkinje network as a part of its reentrant circuit. Although the papillary muscles (PMs) are implicated in arrhythmogenic structure, reentrant FVT originating from the PMs has not been well defined. METHODS AND RESULTS: We studied 13 patients in whom FVT was successfully eliminated by ablation at the posterior PMs (n=8; PPM-FVT) and anterior PMs (n=5; APM-FVT). Although intravenous administration of verapamil (5 mg) terminated ventricular tachycardia (VT) in 6 patients, VT was only slowed in the remaining 7 patients. PPM-FVT exhibited right bundle branch block and superior right axis (extreme right axis) or horizontal axis deviation. APM-FVT exhibited right bundle branch block configuration and right axis deviation with deep S wave in leads I, V5, and V6. VT was reproducibly induced by programmed atrial or ventricular stimulation. His-ventricular interval during VT was shorter than that during sinus rhythm. Ablation at the left posterior or anterior fascicular regions often changed the QRS morphology but did not completely eliminate it. Mid-diastolic Purkinje potentials were recorded during VT around the PMs, where ablation successfully eliminated the tachycardia. All patients have been free from recurrent VT after ablation. CONCLUSIONS: Reentrant circuit of verapamil-sensitive FVT can involve the Purkinje network lying around the PMs. PM-FVT is a distinct entity that is characterized by distinctive electrocardiographic characteristics and less sensitivity to verapamil administration compared with common type FVT. Ablation targeting the mid-diastolic Purkinje potentials around the PMs during tachycardia can be effective in suppressing this arrhythmia.

Non-Reentrant Fascicular Tachycardia: Clinical and Electrophysiological Characteristics of a Distinct Type of Idiopathic Ventricular Tachycardia.

BACKGROUND: The most common form of idiopathic Purkinje-related ventricular tachycardia (VT) is the reentrant type. We describe the clinical and electrophysiological characteristics of focal non-reentrant fascicular tachycardia. METHODS AND RESULTS: Among 530 idiopathic VT patients who were referred for ablation, we identified 15 (2.8%) with non-reentrant fascicular tachycardia (11 men, 45±21 years). Sinus rhythm ECG showed normal conduction intervals with a His-ventricular interval of 41±4 ms. All patients had monomorphic VT (cycle length: 337±88 ms) with a relatively narrow QRS (123±12 ms), and they did not respond to verapamil during the initial presentation. VT exhibited right bundle-branch block/superior axis configuration in 11 patients (73%) and inferior axis in 3 (20%). In 1 patient (7%), VT exhibited left bundle-branch block/superior axis configuration. During ablation, spontaneous VT occurred in 3 patients (20%) and nonentraintable VT or identical premature ventricular complex was induced in 9 (60%). A high-frequency presystolic Purkinje potential was recorded during VT/premature ventricular complex, preceding the QRS by 25±16 ms. VT recurrence was observed in 4 patients (27%), and among them, 3 underwent pacemap-guided ablation during the first session. A second ablation with activation mapping guidance eliminated the VT during the 88±8-month follow-up. CONCLUSIONS: Among idiopathic VT cases referred for ablation, 2.8% were focal non-reentrant fascicular tachycardia, which had distinct clinical characteristics and usually originated from the left posterior fascicle, and less commonly from the left anterior fascicle and right ventricular Purkinje network. Catheter ablation is effective, whereas pacemap-guided approach is less efficacious.