Catheter ablation of ventricular tachycardia originating from the left posterior papillary muscle guided by the shadow of a multipolar catheter

A 62-year-old man without structural heart disease underwent electrophysiological testing for ventricular tachycardia (VT). Hemodynamically unstable VT was induced after isoproterenol (ISP) provocation. Electroanatomical mapping using a multipolar catheter identified the earliest activation originating from the posterior papillary muscle (PPM) where prepotentials preceding the local ventricular electrogram were observed. Irrigated radiofrequency current guided by the shadow of a multipolar catheter eliminated the VT. This case suggested that multipolar catheters may be helpful for identifying tachycardia origins arising from the PPM.     

Calcium dysregulation increases right ventricular outflow tract arrhythmogenesis in rabbit model of chronic kidney disease

Chronic kidney disease (CKD) increases the risk of arrhythmia. The right ventricular outflow tract (RVOT) is a crucial site of ventricular tachycardia (VT) origination. We hypothesize that CKD increases RVOT arrhythmogenesis through its effects on calcium dysregulation. We analysed measurements obtained using conventional microelectrodes, patch clamp, confocal microscopy, western blotting, immunohistochemical examination and lipid peroxidation for both control and CKD (induced by 150 mg/kg neomycin and 500 mg/kg cefazolin daily) rabbit RVOT tissues or cardiomyocytes. The RVOT of CKD rabbits exhibited a short action potential duration, high incidence of tachypacing (20 Hz)-induced sustained VT, and long duration of isoproterenol and tachypacing-induced sustained and non-sustained VT. Tachypacing-induced sustained and non-sustained VT in isoproterenol-treated CKD RVOT tissues were attenuated by KB-R7943 and partially inhibited by KN93 and H89. The CKD RVOT myocytes had high levels of phosphorylated CaMKII and PKA, and an increased expression of tyrosine hydroxylase-positive neural density. The CKD RVOT myocytes exhibited large levels of I_to, I_Kr, NCX and L-type calcium currents, calcium leak and malondialdehyde but low sodium current, SERCA2a activity and SR calcium content. The RVOT in CKD with oxidative stress and autonomic neuron hyperactivity exhibited calcium handling abnormalities, which contributed to the induction of VT.     

Bidirectional ventricular tachycardia: a hallmark of catecholaminergic polymorphic ventricular tachycardia

Catecholaminergic polymorphic ventricular tachycardia is a familial cardiac arrhythmia that is related to RYR2 or CASQ2 gene mutation. It occurs in patients with structurally normal heart and causes exercise-emotion triggered syncope and sudden cardiac death. We present a 13 year-old girl with recurrent episodes of exercise-related syncope and prior history of sudden death in a first degree relative.     

Catheter ablation of fascicular ventricular tachycardia

Fascicular ventricular tachycardia (VT) is an idiopathic VT with right bundle branch block morphology and left-axis deviation occuring predominantly in young males. Fascicular tachycardia has been classified into three subtypes namely, left posterior fascicular VT, left anterior fascicular VT and upper septal fascicular VT. The mechanism of this tachycardia is believed to be localized reentry close to the fascicle of the left bundle branch. The reentrant circuit is composed of a verapamil sensitive zone, activated antegradely during tachycardia and the fast conduction Purkinje fibers activated retrogradely during tachycardia recorded as the pre Purkinje and the Purkinje potentials respectively. Catheter ablation is the preferred choice of therapy in patients with fascicular VT. Ablation is carried out during tachycardia, using conventional mapping techniques in majority of the patients, while three dimensional mapping and sinus rhythm ablation is reserved for patients with nonmappable tachycardia.     

Ventricular tachycardia in repaired double chambered right ventricle - identification of the substrate and successful ablation

A 35 year old female presented with recurrent ventricular tachycardia 5 years after she had undergone surgical repair of double chambered right ventricle. Electroanatomical mapping showed a localised scar in the apex with double potentials and good pace map. Ablation here resulted in non-inducibility of ventricular tachycardia. We hypothesise that the scarring in the apex is the result of sustained pressure overload and becomes arrhythmogenic similar to the apical scar in patients with mid-ventricular hypertrophic cardiomyopathy.     

Cardiomyopathy induced by incessant ventricular tachycardia originating in the vicinity of the His bundle

A 04-year-old boy was referred to our institution with severe, progressive heart failure of 4-months duration associated with a persistent wide QRS tachycardia with left bundle branch block and severe left ventricular dysfunction. Because of incessant wide QRS tachycardia refractory to antiarrhythmic drugs, he was referred for electrophysiological study. The ECG was suggestive of VT arising from the right ventricle near the His area. Electrophysiological study revealed that origin of tachycardia was septum of the right ventricle, near His bundle, however the procedure was not successful and an inadvertent complete atrioventricular conduction block occurred. The same ventricular tachycardia recurred. A second procedure was performed with a retrograd aortic approach to map the left side of the interventricular septum. The earliest endocardial site for ablation was localized in the anterobasal region of left ventricle near His bundle. In this location, one radiofrequency pulse interrupted VT and rendered it not inducible. The echocardiographic evaluation showed partial reversal of left ventricular function in the first 3 months. The diagnosis was idiopathic parahisian left ventricular tachycardia leading to a tachycardia mediated cardiomyopathy, an extremely rare clinical picture in children.     

Catheter ablation of recurrent polymorphic tachycardia: Use of sodium channel blockade to organize the tachycardia: A case report

A 55 year old male presented with recurrent implantable cardioverter defibrillator (ICD) shocks due to polymorphic ventricular tachycardia (PMVT). He had undergone prior catheter ablation for VT three years ago. During the prior attempt he underwent voltage guided substrate ablation. With programmed ventricular extrastimulation (PVES), PMVT was repeatedly induced requiring DC shock. Intravenous procainamide was administered and PVES was repeated which induced sustained monomorphic ventricular tachycardia (MMVT). This VT had pseudo delta waves with maximum deflection index of 0.68, suggestive of epicardial origin. Activation mapping was performed epicardially. Presystolic potentials were recorded in mid anterolateral wall of left ventricular epicardial region. Radiofrequency (RF) ablation at this site terminated the VT. Post ablation there was no inducible tachycardia and patient is free of arrhythmias during 2 years of follow-up.     

Prognostic significance of accelerated ventricular response during radiofrequency ablation of premature ventricular complexes

BackgroundAccelerated ventricular response is frequently observed during radiofrequency ablation (RFA) of premature ventricular complexes (PVCs). We hypothesized that acceleration indicates an appropriate site and adequate injury to the arrhythmogenic tissue, and sought to investigate its value in predicting the outcome.MethodsWe retrospectively analyzed RFA procedures performed for PVCs in our institution from 2011 to 2019.ResultsFifty-eight patients (29 male; age 42.7 ± 15.6 years) underwent 62 RFA procedures. The most common site was the right ventricular outflow tract (67.7%). Acute success was seen in 88.7%. Accelerated ventricular response was observed in 60.0% of the successful procedures. After a median follow-up of 14.0 months (IQR: 6.0–26.6 months), 16 patients had a recurrence. Recurrence was significantly lower in the group with acceleration than in the group without acceleration (12.5% vs. 57.1%; log-rank P < 0.001). The 1-year recurrence rate was 6.5% in the acceleration group and 41.6% in the group without acceleration. On multivariable analysis the adjusted hazard ratio was 0.17 (95% CI, 0.04–0.64; Cox regression P = 0.009). The sensitivity, specificity, positive predictive, and negative predictive values of accelerated response to predict long-term success were 75.7%, 75.0%, 87.5%, and 57.2%, respectively.ConclusionsThe recurrence after PVC ablation is significantly lower when an accelerated response was observed at the successful location during RFA. This can be an additional useful marker of long-term success.     

Efficacy of RyR2 inhibitor EL20 in induced pluripotent stem cell-derived cardiomyocytes from a patient with catecholaminergic polymorphic ventricular tachycardia

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited cardiac arrhythmia syndrome that often leads to sudden cardiac death. The most common form of CPVT is caused by autosomal-dominant variants in the cardiac ryanodine receptor type-2 (RYR2) gene. Mutations in RYR2 promote calcium (Ca²⁺) leak from the sarcoplasmic reticulum (SR), triggering lethal arrhythmias. Recently, it was demonstrated that tetracaine derivative EL20 specifically inhibits mutant RyR2, normalizes Ca²⁺ handling and suppresses arrhythmias in a CPVT mouse model. The objective of this study was to determine whether EL20 normalizes SR Ca²⁺ handling and arrhythmic events in induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from a CPVT patient. Blood samples from a child carrying RyR2 variant RyR2 variant Arg-176-Glu (R176Q) and a mutation-negative relative were reprogrammed into iPSCs using a Sendai virus system. iPSC-CMs were derived using the Stemdiff^TM kit. Confocal Ca²⁺ imaging was used to quantify RyR2 activity in the absence and presence of EL20. iPSC-CMs harbouring the R176Q variant demonstrated spontaneous SR Ca²⁺ release events, whereas administration of EL20 diminished these abnormal events at low nanomolar concentrations (IC₅₀ = 82 nM). Importantly, treatment with EL20 did not have any adverse effects on systolic Ca²⁺ handling in control iPSC-CMs. Our results show for the first time that tetracaine derivative EL20 normalized SR Ca²⁺ handling and suppresses arrhythmogenic activity in iPSC-CMs derived from a CPVT patient. Hence, this study confirms that this RyR2-inhibitor represents a promising therapeutic candidate for treatment of CPVT.     

The first human experience of a contact force sensing catheter for epicardial ablation of ventricular tachycardia

Contact force (CF) is one of the major determinants for sufficient lesion formation. CF-guided procedures are associated with enhanced lesion formation and procedural success. We report our initial experience in epicardial ventricular tachycardia (VT) ablation with a force-sensing catheter using a new approach with an angioplasty balloon. Two patients with arrhythmogenic right ventricular cardiomyopathy who underwent prior unsuccessful endocardial ablation were treated with epicardial VT ablation. CF data were used to titrate force, power and ablation time.     

抗心律失常药对豚鼠左心室流出道自律细胞电活动的影响

目的:研究抗心律失常药对豚鼠左心室流出道自律细胞电活动的影响。方法:采用标准玻璃微电极细胞内记录技术,记录并分析了四类抗心律失常药及腺苷对离体豚鼠左心室流出道自发慢反应电位的效应。结果:ⅠA类抗心律失常药1μmol/L奎尼丁可使左心室流出道自发慢反应电位的放电频率(RPF)和4相自动去极速度(VDD)减慢(P0.05),动作电位幅度(APA)降低(P0.05),0相最大去极速度(Vmax)减慢(P0.05),复极50%(APD50)和90%时间(APD90)延长(P0.05);ⅠB类抗心律失常药1μmol/L利多卡因灌流标本后,RPF和VDD减慢(P0.05),最大复极电位(MDP)绝对值和APA减小(P0.05),Vmax减慢(P0.05),APD50和APD90缩短(P0.05);ⅠC类抗心律失常药0.5μmol/L普罗帕酮可使RPF(P0.01)和VDD(P0.05)减慢,APA降低(P0.05),Vmax减慢(P0.01),APD50(P0.01)和APD90(P0.05)延长;Ⅱ类抗心律失常药5μmol/L普萘洛尔可使RPF和VDD减慢(P0.01),MDP绝对值和APA减小(P0.01),Vmax减慢(P0.05),APD50和APD90延长(P0.01);Ⅲ类抗心律失常药1μmol/L胺碘酮可使RPF和VDD减慢(P0.01),APA降低(P0.01),Vmax减慢(P0.05),APD50(P0.01)和APD90(P0.05)延长;Ⅳ类抗心律失常药1μmol/L维拉帕米可使RPF和VDD减慢(P0.01),MDP绝对值和APA减小(P0.05),Vmax减慢(P0.05),APD50和APD90延长(P0.05);50μmol/L腺苷可使RPF和VDD减慢(P0.05),APA降低(P0.05),Vmax减慢(P0.01),APD50和APD90缩短(P0.05)。结论:抗心律失常药均可显著降低左心室流出道组织的自律性,通过改变APD50和APD90影响有效不应期而起到抗心律失常作用。     

A case of successful radiofrequency catheter ablation for atrial tachycardia originating from the inferior vena cava using high-resolution mapping

A 60-year-old man presented with sustained supraventricular tachycardia. Atrial tachycardia (AT), with the earliest atrial activation (EAA) occurring at the ostium of the coronary sinus, was reproducibly induced.Three-dimensional electroanatomical mapping (3DEAM) using a 3.5-mm distal electrode tip linear catheter (Thermocool) and radiofrequency energy (RF) was performed at the fractionated atrial electrogram site. It preceded at 30 ms to the EAA but did not terminate AT. Further 3DEAM using a multielectrode mapping catheter (Pentaray) demonstrated a centrifugal propagation pattern at the boundary zone between the right atrium and inferior vena cava. RF application here terminated AT, which then became non-inducible.     

Distinctive electrophysiological characteristics of right ventricular out‐flow tract cardiomyocytes

Ventricular arrhythmias commonly originate from the right ventricular out‐flow tract (RVOT). However, the electrophysiological characteristics and Ca²⁺ homoeostasis of RVOT cardiomyocytes remain unclear. Whole‐cell patch clamp and indo‐1 fluorometric ratio techniques were used to investigate action potentials, Ca²⁺ homoeostasis and ionic currents in isolated cardiomyocytes from the rabbit RVOT and right ventricular apex (RVA). Conventional microelectrodes were used to record the electrical activity before and after (KN‐93, a Ca²⁺/calmodulin‐dependent kinase II inhibitor, or ranolazine, a late sodium current inhibitor) treatment in RVOT and RVA tissue preparations under electrical pacing and ouabain (Na⁺/K⁺ ATPase inhibitor) administration. In contrast to RVA cardiomyocytes, RVOT cardiomyocytes were characterized by longer action potential duration measured at 90% and 50% repolarization, larger Ca²⁺ transients, higher Ca²⁺ stores, higher late Na⁺ and transient outward K⁺ currents, but smaller delayed rectifier K⁺, L‐type Ca²⁺ currents and Na⁺‐Ca²⁺ exchanger currents. RVOT cardiomyocytes showed significantly more pacing‐induced delayed afterdepolarizations (22% versus 0%, P < 0.05) and ouabain‐induced ventricular arrhythmias (94% versus 61%, P < 0.05) than RVA cardiomyocytes. Consistently, it took longer time (9 ± 1 versus 4 ± 1 min., P < 0.05) to eliminate ouabain‐induced ventricular arrhythmias after application of KN‐93 (but not ranolazine) in the RVOT in comparison with the RVA. These results indicate that RVOT cardiomyocytes have distinct electrophysiological characteristics with longer AP duration and greater Ca²⁺ content, which could contribute to the high RVOT arrhythmogenic activity.     

Intra-septal radiofrequency ablation within the transseptal puncture hole targeting an interatrial connection during a bi-atrial tachycardia

A 74-year-old man after multiple mitral valve surgeries underwent catheter ablation of a bi-atrial tachycardia (BiAT). Ultra-high resolution activation mapping exhibited a reentrant circuit propagating around the inferior to anterior mitral annulus and right atrial (RA) septum with two interatrial connections. At the transeptal puncture site, continuous fractionated electrograms were recorded during the BiAT, and entrainment pacing revealed a post-pacing interval similar to the tachycardia cycle length, which suggested that the interatrial conduction from the RA to the left atrium (LA) was located just at the transseptal puncture site. A radiofrequency application inside the transseptal puncture hole could successfully eliminate the BiAT. The ablation target for BiATs propagating around the mitral annulus and RA septum is generally the anatomical mitral isthmus (MI). Since the present case had multiple incisions on both the RA and LA septum due to mitral valve surgeries, there was the possibility of the occurrence of a BiAT including the RA and LA septum after performing an MI linear ablation. Therefore, the preferable ablation target for the BiAT in the present case appeared to be the interatrial connection. Ultra-high resolution detailed mapping not only on the atrial endocardium but also in the transseptal puncture hole may be useful for identifying a critical interatrial connection of BiAT circuits.