Origin Of Ventricular Tachycardia Research Articles

Electro‐anatomically confirmed sites of origin of ventricular tachycardia and premature ventricular contractions and occurrence of R wave in lead aVR: A proof of concept study

AbstractBackgroundThe R wave in lead aVR, during the wide QRS complex tachycardia, is commonly observed in a ventricular tachycardia (VT) arising from certain locations in the ventricles.ObjectivesThis was a retrospective and a proof of concept study to correlate the sites of origin of VT and premature ventricular contractions (PVCs) with the occurrence of R wave in lead aVR.MethodsPatients with VT or high density of PVCs were included. Surface and intracardiac electrograms were recorded during the arrhythmia. VTs and PVCs arising from the inferior, inferolateral, or apical region of the ventricles were grouped into Zone 2. Those arising from the other areas of the ventricles were grouped into Zone 1.ResultsSixty‐four patients were included in the study. The mean age was 57 years. There were 47 males. Among 64 patients with VT or PVCs, 28 patients had an R wave in aVR (43.7%), In 26 of 28 patients with an R wave in aVR, the site of origin of the arrhythmia was in Zone 2. The R wave in aVR was absent in 36 patients, 34 of whom had the origin of arrhythmia focus in Zone 1. The presence of an R wave in aVR correctly identified Zone 2 as a site of origin of the arrhythmia with high sensitivity (93%) and specificity (94%).ConclusionsThe presence of an R wave in aVR during wide QRS complex tachycardia or PVC is a valuable observation for identifying the site of origin of the arrhythmia and hence in distinguishing supraventricular tachycardia with aberrancy from VT.

Right ventricular outflow tract cardiomyocytes possess distinct calcium handling and contractile properties

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Rembrandt Research Grant 2021 Background The right ventricular outflow tract (RVOT) is the predominant site of origin of idiopathic ventricular tachycardia. Idiopathic ventricular tachycardias are typically sensitive to adenosine, consistent with triggered activity caused by delayed afterdepolarizations due to intracellular Ca2+ overload. The distinct properties of RVOT myocytes explaining increased susceptibility to Ca2+ overload and triggered activity are unknown. Purpose To identify distinct RVOT electrophysiological properties including Ca2+ handling and its molecular underpinnings. Methods and Results Experiments were performed using freshly isolated cardiomyocytes from the RVOT and right ventricular (RV) apex of adult rabbit hearts. To identify distinct RVOT electrophysiological properties, we employed the perforated patch clamp methodology and measured action potentials and L-type Ca2+ current. Action potentials of RVOT myocytes were significantly shorter compared to RV myocytes, particularly at lower pacing frequency. L-type Ca2+ current peak density was significantly lower in RVOT myocytes compared to RV myocytes (34.0 ± 9.1% at 0 mV). However, voltage-dependencies of L-type Ca2+ current activation and inactivation were not statistically different. Next we measured intracellular Ca2+ transients using the fluorescent Ca2+ indicator indo-1 and found that Ca2+ transient amplitudes were significantly lower in RVOT myocytes compared to RV myocytes. To investigate a relationship between RVOT myocyte Ca2+ handling and contractility, we performed unloaded sarcomere shortening measurements using the Cytocypher Multicell system. Shortening of relaxation time following increased pacing frequency (1-2 Hz) was significantly larger for RVOT myocytes compared to RV myocytes. To identify molecular factors explaining the distinct properties of RVOT myocytes, we performed RNA-seq analysis of differential gene expression using the DESeq2 method. RVOT and RV transcriptomic profiles consisted of 30 differentially expressed genes (adjusted p ≤ 0.05). One of genes significantly higher expressed by the RV was synaptotagmin (SYT1), a Ca2+ sensor and positive regulator of the cardiac L-type Ca2+ channel through inhibition of syntaxin 1A [Ref. 1, 2]. Conclusion RVOT cardiomyocytes possess distinct electrophysiological and contractile properties, reflected by shorter action potentials, lower Ca2+ transient amplitudes, and larger shortening of relaxation time upon increasing pacing frequency. The RVOT and RV have similar but distinct gene expression signatures. Future experiments will focus on determining the role of SYT1 and other genes in regulation of the L-type Ca2+ current and Ca2+ handling in RVOT myocytes.Distinct properties of RVOT myocytes.Transcriptomic profile of the RVOT.

Substrate characterization and outcomes of ventricular tachycardia ablation in amyloid cardiomyopathy: a worldwide study

Abstract Background the electrophysiological substrate underpinning ventricular tachycardia (VT) in cardiac amyloidosis (CA) remains elusive, and outcomes of catheter ablation in this peculiar population are currently unknown. Purpose we sought to describe the electrophysiological substrate and clinical outcomes of VT ablation in a cohort of patients with CA. Methods we included 19 consecutive patients (mean age, 69±10 years; male sex, 89%) with CA (ATTR, n=13; AL, n=6) undergoing catheter ablation for VT/ventricular fibrillation (VF) between 2013 and 2023 in a retrospective, observational, international study, involving 7 referral European and North American electrophysiology units. The primary efficacy outcome was recurrent VT/VF during follow-up, while the primary safety outcome included major procedure-related adverse events. Results the indication for ablation was drug-refractory VT in 16 patients (84%), and PVC-initiated polymorphic VT/VF in 3 (16%). Catheter ablation was performed using endocardial (n=14, 74%) or endo-epicardial approaches (n=5, 26%). Complete endocardial electroanatomical voltage maps of the left and right ventricles were obtained in 14 (74%) and 6 (32%) patients, respectively. Each patient had evidence of low-voltage areas, most commonly involving the interventricular septum (n=12); late potentials were recorded in 13 patients (68%). A median of 1 (1-2) VTs were inducible per patient; in 10 subjects (43% of mappable VTs), activation mapping was consistent with septal VT origin. Complete procedural success was obtained in 13 patients (68%), at the expense of 4 (21%) major procedure-related adverse events. After a median follow-up of 36 (18-54) months, sustained VT/VF recurrence was observed in 9 patients (47%); survival free from VT/VF recurrence was 74% (95%CI, 56-96%) at 12 months, and 53% (95%CI, 34-94%) at 36-month follow-up; the majority of patients remained on antiarrhythmic drugs (Figure). Low-voltage QRS (HR,21.96; p=0.022) and complete procedural success (HR,0.08; p=0.029) were associated with recurrent VT/VF at multivariable analysis (Figure). Conclusions catheter ablation of VT/VF is associated with favorable acute and mid-term arrhythmia control, yet with substantial risk of procedure-related complications and long-term recurrences. Septal substrate and frailty challenge successful management of patients with CA and VT/VF.Multimodality evaluation of LV substrateMain Study Outcomes

Rate of Change of Initial Intrinsicoid Deflection Predicts Endocardial Versus Epicardial Ventricular Tachycardia

BackgroundAssessment of origin of ventricular tachycardias (VTs) arising from epicardial vs endocardial sites are largely challenged by the available criteria and etiology of cardiomyopathy. Current electrocardiographic (ECG) criteria based on 12-lead ECG have varying sensitivity and specificity based on site of origin and etiology of cardiomyopathy. ObjectivesThis study sought to test the hypothesis that epicardial VT has a slower initial rate of depolarization than endocardial VT. MethodsWe developed a method that takes advantage of the fact that electrical conduction is faster through the cardiac conduction system than the myocardium, and that the conduction system is primarily an endocardial structure. The technique calculated the rate of change in the initial VT depolarization from a signal-averaged 12-lead ECG. We hypothesized that the rate of change of depolarization in endocardial VT would be faster than epicardial. We assessed by applying this technique among 26 patients with VT in nonischemic cardiomyopathy patients. ResultsWhen comparing patients with VTs ablated using epicardial and endocardial approaches, the rate of change of depolarization was found to be significantly slower in epicardial (6.3 ± 3.1 mV/s vs 11.4 ± 3.7 mV/s; P < 0.05). Statistical significance was found when averaging all 12 ECG leads and the limb leads, but not the precordial leads. Follow up analysis by calculation of a receiver-operating characteristic curve demonstrated that this analysis provides a strong prediction if a VT is epicardial in origin (AUC range 0.72-0.88). Slower rate of change of depolarization had high sensitivity and specificity for prediction of epicardial VT. ConclusionsThis study demonstrates that depolarization rate analysis is a potential technique to predict if a VT is epicardial in nature.

A Case in Which Identification of Cardiac Scar Tissue by MDCT Was Effective in Ablation for Ventricular Tachycardia – A Secondary Publication

During catheterization of ventricular tachycardia, it is often found difficult to identify the origin of ventricular tachycardia when tachycardia is not induced during the procedure or hemodynamics are disrupted. Late gadolinium enhancement (LGE) in cardiac MRI and late Iodine enhancement (LIE) in cardiac CT are reportedly performed to identify myocardial scar tissue and estimate the origin of ventricular tachycardia preoperatively. However, although LGE is useful for identifying the origin of tachycardia, the slice thickness is large and imaging takes a long time, and if a premature beat occurs or the device is inserted during imaging, a good image cannot be obtained. On the other hand, LIE also has poor resolution, making it difficult to take clear images. In this case report, the origin of ventricular tachycardia was presumed preoperatively using a new image processing method called Subtraction Myocardial Image for Late Iodine Enhancement (SMILIE) using a 320-row Area Detector CT, which was useful during catheter ablation.

Association of ventricular tachycardia morphology induced on electrophysiology study after myocardial infarction: long-term survival and ventricular tachyarrhythmia recurrence

Abstract Background Electrophysiology study (EPS) presents a valuable risk stratification tool to facilitate the implantation of implantable cardioverter-defibrillators (ICDs) to prevent sudden cardiac death from ventricular tachyarrhythmia early after myocardial infarction. Purpose To investigate long-term survival of patients with inducible ventricular tachycardia (VT) at electrophysiology study (EPS) early after ST elevation myocardial infarction (MI) and possible association with site of origin of the induced VT. Methods Consecutive patients with LVEF ≤40% on day 3–5 after MI who underwent EPS were prospectively recruited. Positive EPS was defined as sustained monomorphic VT cycle length ≥200ms for &amp;gt;10 seconds, or shorter duration if hemodynamic compromise occurred. The primary outcome was time to death from any cause. The secondary outcome was time to the composite endpoint of first activation of ICD for ventricular tachyarrhythmia or death. Results A total of 126 patients with inducible VT on EPS early after MI were included with median follow up 6.7 years. 54% had LBBB and 46% had RBBB morphologies during induced VT. The distributions of age, sex, left ventricle ejection fraction, cardiovascular risk factors, infarct artery and EPS characteristics did not differ significantly by induced VT morphology. The estimated risk of death was independently associated with RBBB morphology of VT induced at EPS (adjusted HR 3.2, 95%CI 1.0-10.0, p=0.044). The estimated risk of the composite end-point of spontaneous ventricular tachyarrhythmia recurrence or death was also independently associated with RBBB morphology of VT induced at EPS (HR 1.8, 95%CI 1.0-3.2, p=0.043). Conclusion There is an increased risk of death and spontaneous ventricular tachyarrhythmia recurrence at median follow up of 6.7 years, associated with RBBB morphology of VT (likely origin from left ventricle) induced at EPS early after MI, in those with LVEF &amp;lt;40%. This study is the first to characterise the association between site of origin of VT induced at EPS after myocardial infarction, indicated by RBBB or LBBB morphology, and overall survival as well as activation free survival. The results could help to identify a group of patients that could benefit from closer monitoring post MI and more intense preventative management to improve long-term outcomes.

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.

The effect of scar imaging quality on in-silico pace-mapping of post-infarction ventricular tachycardia

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Wellcome Trust and British Heart Foundation. Background In-silico pacing mapping is a technique which involves using an anatomically-personalised image-based computational model to generate a ‘virtual’ clinical pace map for enhanced pre-procedural ablation planning of post-infarction ventricular tachycardia (VT). Utilising, as it does, a direct clinical ECG (or implanted device) recording of the clinical VT in order to construct the map, it has a number of advantages over other computational methods which attempt to simulate patient-specific VTs to identify ablation targets. However, accurate model construction relies on adequate scar imaging data, which may not be available with current clinical cardiac MR (CMR) sequences. Purpose To investigate the impact of scar imaging quality on the ability of in-silico pace-mapping to determine the VT origin. Methods VTs were simulated in three post-infarction porcine heart models reconstructed from high resolution (1mm isotropic) contrast-enhanced CMR data. Visual analysis of the VT circuits was performed to identify the VT site of origin (exit site) in each case (as the gold standard). The ECG of each simulated VT was computed and used as input for the construction of the in-silico virtual pace-mapping approach. Prior to pace map construction, the scar anatomy was modified to represent three different levels of imaging resolution: high resolution scar mapping (default); low resolution scar (representing standing clinical CMR sequences), obtained by performing dilation and erosion in the scar to close all inner pathways; and, finally, no scar (cardiac anatomy only, representing CT-based reconstructions). In-silico pace-mapping was performed by pacing the heart in N = 1000 sites from randomly chosen locations, on both surfaces and intramurally, within close proximity (&amp;lt;5mm) from the infarct. ECG signals computed following each paced activation wavefront were compared to the VT ECG through correlation analysis to construct the virtual pace map. The distance d between the VT exit site and the pacing location with the strongest correlation was also computed. Results As can be seen in Figure 1, correlation between VT and paced ECGs was found to be strongest at pacing locations near the VT exit site in all models. Correlation coefficients were similar in value and distribution in models with high- (min: -0.49±0.27 and max: 0.92±0.05) and low-resolution scars (min: -0.46±0.29 and max: 0.93±0.05). While the correlation map in the absence of scar had smaller values when compared to the other two models (min: -0.50±0.24 and max: 0.71±0.09), the VT exit was still located near the pacing location with the strongest correlation: d = 9.47±2.83 (high-res), d = 6.63±6.35mm (low-res) and d = 18.60±7.10mm (no scar). Conclusion In-silico pace-mapping successfully detected the VT exit sites regardless the resolution of the scar. This finding suggest that the level of infarct anatomical detail has a minor effect on simulated paced activation to localize VT ablation.

PO-05-145 A CASE OF SUSPECTED CARDIAC SARCOIDOSIS MIMICKING ISCHEMIC CARDIOMYOPATHY

Cardiac sarcoidosis (CS) is challenging due to varied clinical presentation and limited accuracy of diagnostic criteria. We describe a case of suspected CS in a patient with ischemic cardiomyopathy (ICM) presenting in ventricular tachycardia (VT) storm. To describe the presentation of suspected CS in a patient with ICM and VT. N/A A 73 year old male with ICM and ejection fraction of 35% initially presented with myocardial infarct requiring 3-vessel coronary artery bypass surgery. Months later he developed sustained monomorphic VT which was detected on his pacemaker and underwent upgrade to a dual chamber implantable cardioverter defibrillator. He continued to have frequent VT ultimately presenting in VT storm. He was loaded on amiodarone and referred for radiofrequency catheter ablation. During index ablation, the left ventricular (LV) endocardial bipolar voltage was normal, which was inconsistent with the inferobasal and basal septal scar identified on pre procedural cardiac computed topography (CT) (Figure 1). The clinical VT was mapped to the anterior interventricular vein and targeted from the LV summit since proximity of AIV to the left anterior descending artery precluded ablation from the AIV. His arrhythmic presentation and LV dysfunction was disproportionate to degree of coronary disease. In addition, discordance between clinical VT origin site, bipolar endocardial voltage, and scar on cardiac CT prompted suspicion of an alternate underlying diagnosis, such as an arrhythmogenic inflammatory cardiomyopathy. A positron emission tomography/computed tomography (PET/CT) later obtained showed evidence of patchy 18F-fluorodeoxyglucose uptake along the inferolateral LV, suggestive of CS. He was started on immunosuppressants but developed recurrent VT despite anti arrhythmic therapy and required 2 subsequent ablations. He has since remained quiescent from a VT standpoint on amiodarone with plans for alcohol septal ablation or stereotactic body radiation therapy if VT recurs. Symptoms have improved with steroids and immunosuppressants with no inflammation detected on most recent PET/CT High suspicion of CS should remain in patients presenting with significant arrhythmic burden. Normal endocardial voltage during VT ablation can be suggestive of an acute inflammatory process and should prompt consideration of CS, especially in cases with discordant areas of scar and wall thinning on imaging.

161 ABLATION OF EPICARDIAL VENTRICULAR TACHYCARDIA ORIGINATING IN THE AREA OF PERICARDIAL ADHESIONS INDUCED BY STEREOTACTIC RADIOABLATION IN A PATIENT WITH ISCHEMIC CARDIOMYOPATHY

Abstract This is the case of a 64-year-old male patient with prior inferior wall myocardial infarction, wearing a cardiac resynchronization therapy defibrillator and suffering from recurrent ventricular tachycardia (VT). The patient had undergone a transitory successful endocardial radiofrequency catheter ablation (RFCA) in 2013 and a stereotactic ablative body radiotherapy (SABR) in 2021, targeting the VT originating in the inferior wall myocardial scar. The patient was referred to our institution due to recurrent highly symptomatic slow-VT. A coronary angiography ruled out coronary artery disease (CAD) progression and a RFCA was rescheduled. Given the suspected epicardial origin of VT based on a 12-lead ECG, the decision was made to perform a combined epi-endocardial ablation. SABR-induced pericardial adhesions prevented posterior pericardial access, thus requiring an anterior access approach (Figure 1, Panel A, yellow star). Following epicardial and endocardial electroanatomic mapping (EAM), VT ablation relied on a substrate-based approach. Local abnormal ventricular activities (LAVAs), detected both in the accessible epicardial inferior wall of the left ventricle and at the opposite endocardial site, were eliminated by radiofrequency (RF) current. Upon completion of endocardial ablation, ventricular pacing induced hemodynamically unstable VT, exiting from the epicardial region corresponding to the SABR-induced pericardial adhesions. Mechanical adhesiolysis, using the elbow of the open-irrigated ablation catheter, was performed to disrupt SABR-induced pericardial adhesions in the inferior wall. The epicardial EAM performed with the open-irrigated catheter recorded LAVAs in the infero-posterior wall of the left ventricle, corresponding to the SABR-disrupted pericardial adhesions. A RF current was delivered, targeting LAVAs at this site (Figure 1, Panel B: the central green dot corresponds to the area of disrupted pericardial adhesions). At the end of the procedure, no sustained VT was induced by programmed ventricular stimulation. Conclusion SABR constitutes a novel and promising non-invasive radioablative treatment of VT, potentially associated with cardiac toxicity. To our knowledge, this is the first reported case of combined epicardial and endocardial RFCA of recurrent VT after SABR. Based on the first RFCA report and exclusion of CAD progression, we hypothesized that SABR might have favoured progression of the inferior low voltage area. With this case report, we would like to demonstrate that even if pericardial adhesions could be a consequence of SABR, gentle catheter-driven manoeuvres can be enough to disrupt the adhesions and to achieve full EAM. Further research is mandatory to shed light on SABR's long-term arrhythmogenic role.

987 VENTRICULAR TACHYCARDIA CATHETER ABLATION: THE ROLE OF ARRHYTHMIA INTERRUPTION DURING RADIOFREQUENCY EROGATION.

Abstract Background Due to the complexity of the underlying substrate and to the difficulty in characterizing the arrhythmia mechanism and circuitry, every ventricular tachycardia (VT) catheter ablation (CA) represents a challenge. Nowadays VT CA is an increasingly recommended and used procedure. Objective Investigate whether VT interruption during radiofrequency (RF) delivery can be regarded as a marker indicating a lower risk VT recurrence at follow-up. Methods We conducted a retrospective cohort study and we enrolled 69 patients with VTs treated with CA using RF energy, from November 2018 to July 2022. First, in all patient substrate and late potential map was performed; than VT induction was attempted. In patients in whom activation mapping could be performed, we first targeted VT interruption, followed by substrate modification (fragmented/late potential elimination and/or dechanneling of the entire pathologic zone) [group1]. In 15 patients, it was not possible to perform activation mapping due to the poor hemodynamic VT tolerance and/or to the absence of VT inducibility with programmed ventricular stimulation. In these cases, substrate CA was performed, aiming to eliminate fragmented and/or late potentials [group2]. Recurrences were assessed with ICD in office interrogations and remote monitoring for a median of 12 (IQR 5-20) months of follow-up. Results Sixty-nine patients were included in the study. Respectively for the group1 and for the group2, the mean age at baseline was 60 ± 18,3 and 63 ± 12,3 p &amp;gt; 0,05) and the mean left ventricular ejection fraction was 41,3 ± 12,6% and 38,2 ± 11,8% (p &amp;gt; 0,05). In 41 (59%) patients, the indication for the procedure was electrical storm refractory to pharmacological therapies or multiple ICD shocks due to VT/VF. 12 (17%) patients underwent endo-epicardial CA due to the presumed epicardial VT origin and only 9 (13%) underwent right ventricular CA. Among the 31 patients in which it was possible to interrupt the arrhythmia through RF delivery, we observed 9 (23%) sustained VT recurrence at follow-up. Among the 38 patients in which VT was not interrupted with RF delivery or the VT had poor hemodynamic tolerance, there were 16 (42%) sustained VT recurrences at follow-up. Risk of recurrence at follow-up was numerically lower in patients in which VT was interrupted with RF delivery during the procedure, but not statistically significant (p value &amp;gt; 0,05). Conclusions In patients undergoing CA for VTs, activation mapping is useful to enhance the understanding of the arrhythmia circuitry. Our preliminary results seem to suggest that VT interruption during RF delivery may represent a positive prognostic marker, pointing to better outcomes and lower recurrence rates, even if the results were not statistically significant. Further investigations with a larger cohort of patients is required to confirm these findings.

Reversible QRS fragmentation in Takotsubo cardiomyopathy.

An 80-year-old lady with a history of diabetes mellitus presented to the emergency room with palpitations. Electrocardiogram revealed ST-segment elevation over the inferior and lateral leads. Notably, the QRS complexes across precordial leads V4-6 and aVR were fragmented. A positive deflection was seen in lead V1, embedded within the QRS complex, which is resemblant to the Epsilon wave morphology (Figure 1, left columns). Despite such findings and raised serum troponin, she was free from chest pain. Transthoracic echocardiography showed left ventricular (LV) apical ballooning with severe hypokinesis, corroborated by invasive left ventriculography. Coronary angiography revealed no occlusive lesion. The diagnosis was Takotsubo cardiomyopathy (TTC). (Figure 2). The finding of fragmented QRS in TTC is of electrophysiological interest. Arrhythmic manifestations complicating TTC affects up to one-quarter of patients, and half is life-threatening (13.5%).1 Symptomatic atrioventricular block and less commonly sinus nodal dysfunction may mandate cardiac pacing and are due to a secondary increase in vagal tone in sympathetic overdrive. The origin of ventricular tachycardia (VT)/ fibrillation remained controversial in TTC. While QT prolongation is well-recognized in TTC that provided a substrate for polymorphic VT, the origin of monomorphic VT was believed to be catecholaminergic or automatic, and unlikely reentrant based on classical lack of myocardial fibrosis detectable as late gadolinium MRI enhancement in TCC.2, 3 However, latest research provided revoking evidence by identifying diffuse fibrosis/ micronecrosis through T1-mapping in TTC.4 QRS fragmentation, a marker of myocardial fibrosis, is predictive of sudden cardiac death in patients with ischemic and non-ischemic cardiomyopathy. Its presence in the inferior leads, in particular, was identified as an ominous sign in patients with known cardiomyopathy for subsequent sudden death,5 while lateral lead predominance conferred excess risks in subjects without structural heart disease. Whether fragmented QRS has a prognostic role in Takotsubo cardiomyopathy remained unclear. Furthermore, myocardial edema during a hyperacute phase in TTC may predispose to transient electrical inhomogeneity.2 On the contrary, the Epilson wave, an electrocardiographic finding characteristic of arrhythmogenic right ventricular cardiomyopathy, together with QRS fragmentation are both indicators of delayed ventricular depolarization. While the Epilson wave has been reported in myocarditis, how it is related to myocardial edema in the hyperacute phase of TTC and whether it may have a prognostic role remained obscure. In our patient, no significant nodal dysfunction or ventricular tachyarrhythmia occurred. She was treated with aspirin (80 mg daily), lisinopril (2.5 mg daily), bisoprolol fumarate (1.25 mg daily), and atorvastatin (20 mg daily). Three months later, reassessment echocardiography showed recovered LV systolic function with an ejection fraction of 65%, and resolution of apical ballooning. These were accompanied by a complete reversal of QRS fragmentation and the disappearance of the Epsilon wave-like morphology (Figure 1, rights columns). Ambulatory Holter assessment showed nil evidence of electrical instability. This succinct Spotlight thus re-capitulates the fundamental electro-pathophysiological basis implicated in the natural course of TTC, in which further research is needed. Li Shu Fan Medical Fellowship for Internal Medicine 2021/22 (Y.H.C.) None declared.

Clinical Outcomes in Patients With Dilated Cardiomyopathy and Ventricular Tachycardia

BackgroundRecurrent ventricular tachycardia (VT) due to dilated cardiomyopathy (DCM) is difficult to treat, and long-term outcome data are limited. ObjectivesThe aim of this study was to identify predictors of mortality or heart transplantation (HTx) and VT recurrence. MethodsConsecutive patients with DCM accepted for radiofrequency catheter ablation (RFCA) of VT at 9 centers were prospectively enrolled and followed. ResultsOf 281 consecutive patients (mean age 60 ± 13 years, 85% men, mean left ventricular ejection fraction [LVEF] 36% ± 12%), 35% had VT storm, 20% had incessant VT, and amiodarone was unsuccessful in 68%. During follow-up of 21 months (IQR: 6-30 months), 67 patients (24%) died or underwent HTx, and 138 (49%) had VT recurrence (45 within 30 days, defined as early); the 4-year rate of VT recurrence or mortality or HTx was 70%. Independent predictors of mortality or HTx were early VT recurrence (HR: 2.92; 95% CI: 1.37-6.21; P < 0.01), amiodarone at discharge (HR: 3.23; 95% CI: 1.43-7.33; P < 0.01), renal dysfunction (HR: 1.92; 95% CI: 1.01-3.64; P = 0.046), and LVEF (HR: 1.36; 95% CI: 1.0-1.84; P = 0.052). LVEF ≤32% identified patients at risk for mortality or HTx (area under the curve: 0.75). Mortality or HTx per 100 person-years was 40.4 events after early, compared with 14.2 events after later VT recurrence and 8.5 events with no VT recurrence after RFCA (P < 0.01 for both). Patients with early recurrence and LVEFs ≤32% had a 1-year rate of mortality or HTx of 55%. VT recurrence was predicted by prior implantable cardioverter-defibrillator shocks, basal anteroseptal VT origin, and procedural failure but not LVEF. ConclusionsPatients with DCM needing RFCA for VT are a high-risk group. Following RFCA, approximately one-half remain free of VT recurrence. Early VT recurrence with LVEF ≤32% identifies those at very high risk for mortality or HTx, and screening for mechanical support or HTx should be considered. Late VT recurrence after RFCA does not predict worse outcome.

Automated detection of scar-related ventricular tachycardia origins from implanted device electrograms: a combined computational-AI platform

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): EPSRC Background Existing strategies that identify ventricular tachycardia (VT) ablation targets either employ invasive and time-consuming electrophysiological (EP) mapping, or non-invasive modalities that utilise standard electrocardiogram (ECG) signals. Success of these pre-procedure ablation approaches in localising re-entrant VTs often relies on VT induction, which could be avoided by utilising recordings of clinical VT episodes stored as electrograms (EGMs) in implanted devices. Such a non-invasive approach that localises VT substrates from EGMs may aid ablation planning, enhancing safety and speed. Purpose Our goal is to automate scar-related VT localisation by utilising EGM recordings of VT episodes from implanted devices. To achieve this, deep-learning algorithms will be trained on computational data to return VT sites of origin from implanted device EGMs. Ultimately, we intend to utilise this computational-artificial intelligence (AI) framework to detect ablation targets of clinical VT episodes and guide pre-procedure ablation planning non-invasively. Methods A comprehensive library of ECGs and EGMs from simulated paced beats (~15000) and scar-related VTs (500) was generated across five detailed torso models within a fast EP computational environment, combining reaction-eikonal and lead field methods. ECG (or EGM) traces from simulated paced beats were used to initially pre-train two convolutional neural network (CNN) long short-term (LSTM) attention-based architectures. Subsequently, signals of the in-silico, re-entrant VTs were used to re-train the networks to output the sites of origin of these episodes in a standardised ventricular coordinate space. Finally, the retrained CNN architectures were tested on re-entrant VTs of unseen models, and median localisation errors (LEs) were estimated against known VT origins from simulations. Results The performance of the networks to localise scar-related VT episodes was asserted for each torso model. When a torso model was only seen during initial training on simulated paced beats, implanted device EGMs and ECGs successfully localised VT sources with LEs 10.04 – 16.36 mm and 10.05 – 12.79 mm, respectively. When a torso model was not seen during pacing or VT training, recreating potential clinical application settings where ECGs or EGMs of clinical VTs would be the only inputs to the networks, LEs ranged 12.42 - 22.79 mm and 12.41 - 19.68 mm for EGM and ECG-based testing, respectively. Conclusions Our study successfully detected VT ablation substrates with accuracy that could be beneficial in clinical ablation settings. The proposed computational-AI framework may be used to automate the localisation of scar-related VTs from clinical ECGs or EGM recordings from implanted devices, ultimately aiding ablation planning.

Periaortic scar-related ventricular tachycardia in patients with aortic valve replacement: transcatheter ablation is feasible and decisive

Abstract Funding Acknowledgements Type of funding sources: None. Background Aortic valve replacement (AVR) is a common procedure. While conduction disturbances are well-recognized complications, ventricular tachycardias (VTs) have not been widely reported neither described mainly because prosthetic valves represent a potential practical problem in the access to the ventricles, and this may limit the use of radiofrequency ablation (RF). Purpose and Methods We report three cases of periaortic scar-related VT in patients with AVR. Results The first case was a 85 years old (yo) man, with both aortic and mitral biological valve replacement. The left ventricular ejection fraction (LVEF) was normal and the clinical VT (left bundle branch block (BBB) and inferior axis, cycle length (CL) = 305 ms) was induced. Left ventricle (LV) was mapped with a retrograde transaortic approach: to cross safely the prosthesis, a 6-French (F) pigtail catheter was first placed in the ventricle; a 8.5-F Braided Guiding Introducer (SL1) was placed across the valve over a guidewire. The 8.5-F ablation catheter allowed to locate the VT origin underneath the septal portion of prosthetic aortic valve (PAV). The second case was a 85 yo man, with bioprosthetic AVR and replacement of the ascending aorta. LVEF was 40% with mild PAV degeneration. The clinical VT had left BBB morphology and inferior axis (CL = 352 ms). Transaortic approach was hampered by an unfavorable entry angle and by valve degeneration. Then we opted for the technique commonly used during transcatheter AVR: the access to the LV was obtained using a 6-F coronary catheter (AL1) and a stright tip 0.034" angiographic guidewire; subsequently a 8.5-F, 81 cm long, introducer sheath (SL0) was positioned across the PAV. The reentry circuit was mapped in the high anterior region, just below the PAV insertion. The third case was a 65 yo man, with mechanical PAV. LVEF was normal and the clinical VT had right BBB and left inferior axis (CL = 290 ms). After transseptal puncture, a steerable introducer was placed in left atrium. The mapping catheter allowed to identify early and fractional potentials in the anterior portion of PAV. In all cases, RF applications was delivered at the earliest ventricular activation site with termination of the VTs. Thereafter, no VTs could be induced. At 12 months follow-up, the patients are free of any VT relapses. Conclusions The most common origin of sustained monomorphic VT occurring after PAV is the surgical scar and catheter ablation is a feasible option. In case of mechanical PAV, the only practicable access is the transeptal one; on the contrary, with biological PAV the transaortic approach can also be used. In difficult cases, the access to the LV can be obtained with the technique routinely performed during transcatheter AVR.

The outcome spectrum for Dilated Cardiomyopathy and Ventricular Tachycardia: results from the prospective, multicenter, DCM-VT ablation study

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): The study was partially supported by an investigator initiated grant from Biosense Webster (a Johnson &amp; Johnson company) Background Recurrent sustained ventricular tachycardia (VT) due to nonischemic dilated cardiomyopathy (DCM) is difficult to treat and long-term outcome data are limited. Objective We aimed to identify predictors for mortality or heart transplantation (MHT) and VT recurrence. Methods Consecutive DCM patients accepted for VT catheter ablation (RFCA) in 9 centers were prospectively enrolled and followed. Results Of 281 consecutive patients (age 60±13yrs, 85% men, LVEF 36±12%) 35% had VT storm, 20% incessant VT, and 68% failed amiodarone. During a median follow-up of 21 (IQR 6-30) months after RFCA (epicardial in 58%, no RFCA due to inaccessible target in 6.4%), 67(24%) patients died/underwent HT and 138(49%) had VT recurrence (45 within 30 days defined as early); the cumulative 4-year rate of VT or MHT was 70% and of MHT 38%. In multivariable analysis predictors of MHT were early VT recurrence (HR 2.92 (CI1.37-6.21), p&amp;lt;0.01), amiodarone at discharge (HR 3.23 (CI1.43-7.33, p&amp;lt;0.01), renal dysfunction (HR 1.92 (CI1.01-3.64), p=0.046), and LVEF (HR 1.36 (CI 1.0-1.84), p=0.052). A LVEF ≤32% was the optimal threshold to identify patients at risk for MHT (AUC 0.75). MHT per 100 person-years was 40.4 after early VT recurrence and significantly higher, compared to 14.2 after later VT recurrence and to 8.5 after RFCA with no VT recurrence (both p&amp;lt;0.01). Mortality rates for patients with VT recurrence after 30 days were not significantly higher than for patients with no VT recurrences Patients with early recurrence and LVEF≤32% had a 1-year MHT rate of 55% (figure). VT recurrence was predicted by prior ICD shocks, basal antero-septal VT origin, and procedural failure but not LVEF. Conclusion DCM patients needing RFCA for VT are a high-risk group. Following RFCA half remain free of VT recurrences. Early VT recurrence with LVEF&amp;lt;0.32 identifies those with a very high risk and screening for mechanical support/ HT should be considered. Late VT recurrence after RFCA does not predict worse outcome.

PO-709-03 THE APPLICATION OF THE RE-ENTRY VULNERABILITY INDEX TO DETERMINE VENTRICULAR TACHYCARDIA EXIT FROM DIFFERENT PACING LOCATIONS, IN A PORCINE INFARCT MODEL

The application of high-density electroanatomic (EA) and functional mapping strategies is a new frontier in ventricular tachycardia (VT) ablation. There is no definitive method to identify arrhythmogenic substrate, and ablation outcomes remain suboptimal. The re-entry vulnerability index (RVI) integrates unipolar activation and repolarisation timing, and low RVI values correlate with vulnerable sites of re-entrant VT origin.

The development of a new, simple electrocardiographic method for the estimation of the latest activated left ventricular site

Abstract Background Current cardiac resynchronization therapy (CRT) works by pacing the latest activated left ventricular (LV) site. The estimation of the location of the latest activated LV site (LALVS) may be important to determine the optimal position of the LV electrode during CRT or to predict the patient response to the current CRT technique devised to pace the LALVS usually present in patients with left bundle branch block (LBBB) pattern. Methods We used a modified 12-lead ECG algorithm originally devised and used by other authors* for a different purpose, to identify the segment of origin of ventricular tachycardia in the 16-segment American Heart Association LV model by analyzing the QRS axis in the limb and chest leads. We hypothesized that modifying this ECG algorithm by using the secondary ST vector axis instead of the QRS axis in the limb and chest leads, we can apply this ECG method to estimate the LALVS instead of the site of origin of the ventricular tachycardia. The resultant secondary ST vector is directed 180o away from the LALVS. Using this ECG method we determined the LALVS in 22 patients with LBBB and 20 patients with nonspecific intraventricular conduction disturbance (NICD) patterns and heart failure. To validate the ECG method, we also estimated the LALVS by echocardiography using 3D parametric imaging and 2D speckle tracking. Results The LALVS determined by the electrocardiographic method and echocardiogrpahy in the 16-segment model matched (was in the same or adjacent segment) in 38/42 (90.5%) patients and among these patients complete matching (the LALVSs were in the same segment) was found in 16/38 (42%) and partial matching (the LALVSs were in adjacent segments) in 22/38 (58%) patients. When the LBBB and NICD groups were separated to patients with ≥150 ms and &amp;lt;150 ms QRS duration subgroups, the LALVSs of the ≥150 ms subgroup were almost exclusively in the anterolateral (or anterior) or inferolateral areas and those of the &amp;lt;150 ms subgroup were in the above mentioned areas or sometimes at other sites located remote from these areas. Conclusions The novel, simple surface electrocardiographic method could as reliably estimate the approximate location of LALVS as echocardiography. The possible explanation for the effectivity of CRT in patients with sinus rhythm with intraventricular conduction disturbance and ≥150 ms QRS duration is that their LALVS is at the same most distant areas (anterolateral, anterior, inferolateral) from the initial septal activation site where the LV electrodes are positioned during application of the current CRT technique. Funding Acknowledgement Type of funding sources: None.

B-011-20 EVALUATION OF THE 3-DIMENSIONAL SUBSTRATE OF VENTRICULAR TACHYCARDIA IN A LANGENDORFF PERFUSED HUMAN HEART

The underlying mechanisms of ventricular tachycardia (VT) are not well understood. Most models for VT propagation are based on animal studies or single surface recordings which have limited utility. Human based investigations of VT are often limited by hemodynamic collapse and lack viable ways to assess the myocardial electrical propagation. The authors seek to provide a novel method for the experimental evaluation of VT in human hearts with correlation to high resolution MRI fibrosis imaging. Human donor hearts were obtained from discarded transplant specimens. Following explant, the hearts were cannulated to the Langendorff apparatus and ventricular tachycardia was induced using a programmed ventricular stimulation protocol. Custom built 3D printed epicardial and endocardial mapping probes were deployed to map whole ventricular contraction. The hearts were imaged using high-resolution late gadolinium enhancement 4T MRI for fibrosis quantitation. A total of 8 human hearts underwent complete mapping procedures with 3 spontaneously beating VT hearts and 5 control hearts. High resolution mapping demonstrated VT originated from epicardial regions in all 3 hearts. Site of origin of VT was identified in all 3 human hearts and correlated to MRI fibrosis mapping. This study highlights new methods for the interrogation of ventricular tachycardia substrates using a novel human Langendorff heart model. The integration of mapping and imaging techniques in this study provides new insights into the mechanisms underlying VT. These efforts may help clinicians to provide more targeted ablation procedures.

A Novel Use of Noninvasive Registered Electrocardiographic Imaging Map for Localization of VT and PVC

A 33-year-old woman presented with sustained monomorphic ventricular tachycardia (VT). The 12-lead electrocardiogram, 3-dimensional (3D) picture of chest electrodes, and cardiac magnetic resonance were used to create a noninvasive 3D electrocardiographic imaging map to identify the most likely site of VT origin. This map was integrated with a 3D mapping system to aid in VT ablation. (Level of Difficulty: Advanced.)