Ventricular Tachycardia Cycle Length Research Articles

The importance of scar border zone size in VT presentation and recurrence in post MI patients

Abstract Introduction Available mapping data in post-myocardial infarction patients describe ventricular tachycardia (VT) re-entry circuit characteristics of slow VT, that are typically related to transmural scars. Fast VTs with cycle lengths close to the refractory period may be related to functional re-entry in the scar border zone. Functional re-entry related border zone VTs may be difficult to control by ablation. Purpose The aims of this study are (1) to describe electroanatomical voltage map (EAVM) characteristics in post myocardial infarction (MI) patients with spontaneous and inducible fast VTs and (2) to assess the relation between scar border zone size and ablation outcomes. Methods Consecutive post-MI patients undergoing VT ablation at a tertiary referral center from January 2012 to November 2018 were included. Fast VT was defined as a VT cycle length (VTCL) = ventricular refractory period + max. 30ms. Areas of scar border zone (using 0.5 – 2.1mV/3.0mV cut-offs (according to LV remodeling stage; LVEF<47% and LV end-systolic volume index of >50 ml/m2)) were measured on the EAVM and correlated with clinical outcomes. Results In total, 138 patients were included (86% male; left ventricular ejection fraction 35±10%; 86% remodeled LV). Twenty-three patients (17%) had ≥1 fast VT (mean VTCL 275±52ms) at presentation, mean VTCL of the remaining patients 397±88ms). The median scar border zone size was 27% [IQR 20-38] of the left ventricular endocardial surface. Patients who presented with a spontaneous fast VT had a larger border zone than patients with slower VT (32% [IQR 28 – 41] vs. 25% [IQR 16 – 36], p=0.01). After ablation, 79 (57%) patients remained inducible for any VT, including 59/79 (75%) for a fast VT (median VTCL fast VT 260ms [IQR 236 -280]). Patients who remained inducible for fast VTs had a larger border zone than patients who remained inducible for slower VTs (35% [IQR 27 – 44] vs. 26% [IQR 20 – 36], p<0.001). During a median follow-up of 26 months [IQR 8 – 47], 45 patients (33%) had a VT recurrence (mean VTCL 357±98ms). Patients with a below median (27%) scar border zone area had a lower VT recurrence rate compared to patients with an above median scar border zone area (recurrence rate: 16/66 (24%) vs. 29/72 (40%), p=0.03). Kaplan-Meier survival analysis showed better free VT survival in the below median border zone patients (Log-rank: p<0.05) (Figure 1). Conclusion Patients who present with spontaneous fast VTs or who remain inducible for fast VTs after ablation have larger scar border zones during EAVM compared to patients with presenting or remaining slower VTs. A larger border zone appeared to be associated with higher VT-recurrence rates. The scar border zone may play an important role as VT substrate for (fast) VTs and may not be easily targeted by current ablation techniques.VT-free survival stratified by median BZ

CONTINUOUS LEFT STELLATE GANGLION BLOCK DURING VT ABLATION TO SLOW VT AND IMPROVE ABLATION OUTCOME

Abstract Introduction Perioperative management of advanced patients with indication to ventricular tachycardia (VT) ablation is complex. A PAINESD score ≥ 15 was proposed to identify those who might benefit from pre–emptive mechanical cardiopulmonary support (MCS). We present a case successfully managed with continuous percutaneous left stellate ganglion block (C–PLSGB). Case A 71–year–old diabetic man with severe post–ischemic cardiomyopathy (LVEF 24%, NYHA Class III) and chronic pulmonary disease was admitted for electrical storm with multiple ICD shocks due to poorly tolerated monomorphic VT (MMVT) at 176 bpm resistant to anti–tachycardia pacing (ATP), despite ongoing chronic oral therapy with amiodarone and carvedilol. Poorly tolerated and ATP–resistant MMVTs at 170–180 bpm recurred despite intravenous (iv) amiodarone and lidocaine (20 mcg/kg/min) and oral propranolol. Ultrasound guided C–PLSGB was therefore started; lidocaine was chosen for the continuous infusion due to the short half–life, at the initial dose of 10 mg/h; 6 hours later, his poorly tolerated MMVT recurred at 167 bpm. Therefore, at first we increased iv lidocaine to 30 mcg/kg/min, without benefit, then we increased C–PLSGB at 37.5 mg/h and decreased iv lidocaine to 20 mcg/kg/min due to neurological symptoms. With this regimen, the patient stayed VT free for 2 hours, then the clinical VT recurred at 130 bpm, with good hemodynamic tolerability and ATP–response. C–PLSGB infusion was than increased to 75 mg/h, with no more VT. Endocardial VT ablation was planned. Despite a very high PAINESD score (31) we decided to avoid pre–emptive MCS. We stopped lidocaine (both iv and as C–PLSGB) 2 hours before ablation. As soon as the patient came in the EP room (before instrumentation), the clinical MMVT recurred at 133 bpm. C–PLSGB was then resumed (initially at 100 mg/h for 30 minutes, then at 37.5 mg/h). The MMVT then spontaneously recurred at 133 bpm: it was mapped and ablated in the medio–apical anterior wall, with acute VT interruption. A second VT morphology then appeared, that was mapped and ablated at a more basal site, despite a partial epicardial component of the circuit was identified. C–PLSGB was then stopped and no more VT occurred nor were induced 1 hour later. At 8 months the patient is still alive with no more VT. Conclusion C–PLSGB with individually tailored infusion rates could be used during VT ablation as a mean to reduce VT cycle length and allow for mapping without MCS.

Significant delayed conduction and characteristic ventricular tachycardias in patients with cardiac sarcoidosis and electrical storm.

Electrical storm (ES) of ventricular tachyarrhythmias (VTAs) is an important cause of sudden death in patients with cardiac sarcoidosis (CS). VTAs in CS are associated with myocardial scarring and inflammation. However, little is known about the risk factors of ES in patients with CS and VTAs. The objective of this study is to clarify the characteristics and risk factors for the development of ES in patients with CS. The study population included consecutive 52 patients with CS and sustained VTA. Twenty-five out of 52 patients experienced ES. We evaluated clinical characteristics, imaging modalities, and electrocardiogram (ECG) parameters to determine the risk factors associated with ES. Half of the patients experienced VTAs as the initial symptom of sarcoidosis, and eight patients had ES as the initial VTA episode. There were no differences in cardiac imaging abnormalities between patients with and without ES. Among ECG markers, significant QRS fragmentation (odds ratio [OR]: 7.9, p = .01) and epsilon waves (OR: 12.24, p = .02) were associated with ES. Among the ventricular tachycardia (VT) characteristics, multiple morphologies of monomorphic VTs (OR: 10.9, p < .01), short VT cycle lengths (OR: 12.5, p < .01), and polymorphic VT (OR: 13.5, p < .01) were associated with ES. Bidirectional VTs were detected in 10 patients with ES and one patient without ES. Immunosuppressive therapy relieved ES in some patients. ES was common in patients with CS and VTAs. Significant depolarization abnormalities that appeared as QRS fragmentation, epsilon waves, and specific VT characteristics were associated with ES.

Modified sympathicotomy in patients with refractory ventricular tachycardia and structural heart disease: a single-center experience.

Modified cardiac sympathetic denervation (CSD) with stellate ganglion (SG) sparing is a novel technique for cardiac neuromodulation in patients with refractory ventricular tachycardia (VT). Our aim is to describe the mid- to long-term clinical outcome of the modified CSD with SG sparing in a series of patients with structural heart disease (SHD) and refractory VT. All consecutive patients with SHD and refractory VT undergoing modified CSD were enrolled. Baseline clinical characteristics and periprocedural data were collected for all patients. The primary outcome was any recurrence of sustained VT. We enrolled 15 patients (age: 69.2 ± 7.9years; male 100%) undergoing modified CSD. Left ventricular ejection fraction was 37 ± 11% and all patients had an implantable cardiac defibrillator (ICD); the underlying cardiomyopathy was non-ischemic in 73.3% of them. At least one previous ablation had been attempted in 66.6% of cases. The 73.3% of patients underwent bilateral CSD and the mean effective surgical time was 10.8 ± 2.4min per side; no major periprocedural complication occurred. After a median follow-up time of 15months (IQR: 8.5-24.5months), the primary outcome occurred in 47.6% of cases. All patients experienced a reduction of ICD shocks after CSD (3.1 ICD shocks/patient before vs. 0.3 ICD shocks/patient after CSD; p-value: 0.001). Bilateral CSD and a VT cycle length < 340ms were associated with better outcomes. A modified CSD approach with stellate ganglion sparing appears to be safe, fast, and effective in the treatment of patients with SHD and refractory VTs.

Influence of standard modifiable risk factors on ventricular tachycardia after myocardial infarction

Abstract Background Sudden cardiac death due to ventricular tachyarrhythmia is the single greatest cause of death within two years after myocardial infarction (MI), especially early in the first 30 days. Purpose We aimed to assess the incidence of inducible ventricular tachycardia (VT) early after MI in those with standard modifiable risk factors (SMuRFs) versus those without. Methods Consecutive patients with LVEF ≤40% on day 3–5 after ST elevation myocardial infarction (STEMI) who underwent electrophysiology study 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 outcomes were inducibility of VT and all-cause mortality. Results A total of 410 patients, of which 126 had inducible VT on EPS, early after myocardial infarction were included. In our multiple regressions model, when smoking history was considered, ex-smokers were identified at increased risk of VT at EPS (adjusted OR 2.0, p=0.033) whilst those who never smoked or were current smokers had comparable risk. It also showed that the presence of any SMuRF apart from current smoker also conferred an increased risk of inducible VT (adjusted OR 1.9, p=0.043). For every 10 years increase in age the risk of death increased by a multiplicative factor of 1.3, for every 10% decrease in LVEF (%) the risk of death increased by a multiplicative factor of 1.9 and in patients with previous IHD, the risk of death was doubled. Neither the number of SMuRFs nor the presence of any SMuRF were associated with mortality. Conclusion In our cohort of patients with LVEF&amp;lt;40% early after STEMI who had an EPS to assess for inducible VT, either the presence of any of the three SMuRFs (hypertension, hypercholesterolemia or diabetes mellitus) or previous smoking doubled the chance of having VT induced. These data provide valuable information that could be integrated into clinical care protocols after myocardial infarction to improve long-term patient outcomes and further reinforces the need to modify SMuRFs in patients with ischemic heart disease.

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.

Abstract 11895: Efficacy of Maintaining Mean Aortic Pressure by Percutaneous Left Ventricular Assist Device for Hemodynamic Support in Ventricular Tachycardia Ablation - Relation to Cycle Length

Introduction: Percutaneous left ventricular assist device (pLVAD) has been used to maintain mean aortic pressure (MAP) during ventricular tachycardia (VT) ablation (ABL) and is a class II recommendation. We sought to assess the ability of pLVAD to maintain MAP and its relationship to VT cycle length (CL). Methods: All patients who underwent CA for VT with pLVAD support within a 3-year period were included. Type of pLVAD was determined by operator. Insertion of device was performed under fluoroscopy via femoral arterial sheath. Acute ablation success was defined as absence of inducible VT at end of procedure. Results: A total of 9 patients were included. Most patients had ischemic cardiomyopathy (Table 1); pLVAD was inserted prophylactically in 66.67% of patients and for refractory VT/VF storm in 22.2%. One patient was had critical AS and underwent balloon valvuloplasty prior to VT ablation. Impella CP was used in 78%, and Impella 2.5 in 22%, mean cardiac output was 2.9 + 0.5 L at mean P flow rate 7.3 + 1.3. CARTO was used in 89% and ESI Navx in 11% for electroanatomic/activation mapping. There were no instances of electromagnetic interference, despite the use of magnetic mapping system in all cases (CARTO in 8, Stereotaxis in 1). Mean PCWP was 17.88 + 10.12 pre-ablation vs 23.57 + 8.30 post-ablation (p=ns). There were 24 VTs, 42% were sustained, with a mean CL 342 + 80 msec, ranging from 223 to 558 msec. Mean MAP pre-ablation was 67.44 + 12.85 mmHg vs 61.86 + 13.27 post-ablation with absent negative correlation to VT CL (p=ns). There was no difference in MAP between VT Cl &gt; 300 msec vs &lt; 300 msec: 66 + 11 vs 59 + 14 mm Hg, (p=ns). Mean dose of phenylephrine was 452 mcg. pLVAD was removed at the end of procedure, there were no femoral site complications. Conclusions: pLVAD utilization maintains stable MAP even with faster VT cycle length in patients undergoing VT ABL under general anesthesia obviating need for high dose pressor support.

Abstract 15869: Antiarrhythmic Effects of Mesenchymal Stromal Cells in a Post-Infarct Swine Model of Ventricular Tachycardia

Introduction: Mesenchymal Stromal Cells (MSC) reduce scar burden in models of ischemic cardiomyopathy. It is unknown whether MSCs exert antiarrhythmic effects. Hypothesis: MSCs reduce inducibility of monomorphic VT (mmVT) or prolong VT cycle length by ≥20 msec in a post-infarct swine model of VT. Methods: Two groups of 8 Yorkshire Swine underwent a 180-minute occlusion of the LAD. Group 1 (n=8) pigs underwent initial MRI scan, electrophysiology study (EPS), and 3D electroanatomic mapping (EAM) with injection of open-label MSCs (200M cells) around the borderzone of the infarct, using a NOGA Myostar catheter (J&amp;J) guided by EAM. Group 1 pigs had repeat EAM, and final EPS 8 weeks later. Group 2 pigs (n=8) were randomized between placebo and MSC and underwent sequential MSC injections (100M cells/procedure), 7 weeks apart, followed by final EPS and MRI 7 weeks later. Scar% = total scar/myocardial mass (grams). Results: MmVT was induced in 5 of 8 (62.5%) at initial EPS (i-EPS) in Group 1 pigs and 3 of 8 (37.5%) at final EPS (f-EPS). In Group 2 all 4 MSC-treated swine had inducible mmVT during i-EPS but only 2 had mmVT at f-EPS. Overall, 9 of 12 MSC-treated pigs had mmVT initially and 5 of 12 pigs had mmVT at f-EPS (p=0.12). For MSC-treated pigs with persistently inducible mmVT (Groups 1 &amp; 2), the baseline VT CL increased in all pigs by ≥20msec and increased from 216 ± 17 msec initially to 274 ± 35 msec at f-EPS (p = 0.001). In Group 1, Scar% was unchanged (22.2±1.6% to 20.5±2.1%) after single MSC treatment (p=0.17). In Group 2 MSC-treated pigs, Scar% decreased from 25.8±2.0% to 17.9±0.6% after 2 MSC treatments (p=0.014). In pigs with mmVT at i-EPS, the scar% was 24.4±1.2%, compared with 19.3±2.0% in pigs without i-EPS inducible mmVT (p=0.025). In pigs with mmVT at f-EPS, scar% was 22.5±1.8% compared with 18.1±1.6% in pigs without mmVT at f-EPS (p=0.048). Placebo-treated pigs showed no change in scar% (22.5±2.6% to 22.4±2.9%, p=0.44) and no change in VT inducibility (3 of 4 pigs at i-EPS and f-EPS). Conclusions: This study demonstrates that MSC injection reduced myocardial scar and either suppressed induction of VT or prolonged VT cycle length, consistent with an antiarrhythmic effect. Lower scar burden was associated with non-inducibility of VT, either at baseline or final EPS.

Machine learning-derived cycle length variability metrics predict spontaneously terminating ventricular tachycardia in implantable cardioverter defibrillator recipients.

Implantable cardioverter defibrillator (ICD) therapies have been associated with increased mortality and should be minimized when safe to do so. We hypothesized that machine learning-derived ventricular tachycardia (VT) cycle length (CL) variability metrics could be used to discriminate between sustained and spontaneously terminating VT. In this single-centre retrospective study, we analysed data from 69 VT episodes stored on ICDs from 27 patients (36 spontaneously terminating VT, 33 sustained VT). Several VT CL parameters including heart rate variability metrics were calculated. Additionally, a first order auto-regression model was fitted using the first 10 CLs. Using features derived from the first 10 CLs, a random forest classifier was used to predict VT termination. Sustained VT episodes had more stable CLs. Using data from the first 10 CLs only, there was greater CL variability in the spontaneously terminating episodes (mean of standard deviation of first 10 CLs: 20.1 ± 8.9 vs. 11.5 ± 7.8 ms, P < 0.0001). The auto-regression coefficient was significantly greater in spontaneously terminating episodes (mean auto-regression coefficient 0.39 ± 0.32 vs. 0.14 ± 0.39, P < 0.005). A random forest classifier with six features yielded an accuracy of 0.77 (95% confidence interval 0.67 to 0.87) for prediction of VT termination. Ventricular tachycardia CL variability and instability are associated with spontaneously terminating VT and can be used to predict spontaneous VT termination. Given the harmful effects of unnecessary ICD shocks, this machine learning model could be incorporated into ICD algorithms to defer therapies for episodes of VT that are likely to self-terminate.

Influence of standard modifiable risk factors on ventricular tachycardia after myocardial infarction

BackgroundInducible ventricular tachycardia (VT) at electrophysiology study (EPS) predicts sudden cardiac death because of ventricular tachyarrhythmia, the single greatest cause of death within 2 years after myocardial infarction (MI).ObjectivesWe aimed to assess the association between standard modifiable risk factors (SMuRFs) and inducible VT at EPS early after MI.MethodsConsecutive patients with left ventricle ejection fraction ≤40% on days 3–5 after ST elevation MI (STEMI) who underwent EPS were prospectively recruited. Positive EPS was defined as induced sustained monomorphic VT cycle length ≥200 ms for ≥10 s or shorter if hemodynamically compromised. The primary outcome was inducibility of VT at EPS, and the secondary outcome was all-cause mortality on follow-up.ResultsIn 410 eligible patients undergoing EPS soon (median of 9 days) after STEMI, 126 had inducible VT. Ex-smokers experienced an increased risk of inducible VT [multivariable logistic regression adjusted odds ratio (OR) 2.0, p = 0.033] compared with current or never-smokers, with comparable risk. The presence of any SMuRFs apart from being a current smoker conferred an increased risk of inducible VT (adjusted OR 1.9, p = 0.043). Neither the number of SMuRFs nor the presence of any SMuRFs was associated with mortality at a median follow-up of 5.4 years.ConclusionsIn patients with recent STEMI and impaired left ventricular function, the presence of any SMuRFs, apart from being a current smoker, conferred an increased risk of inducible VT at EPS. These results highlight the need to modify SMuRFs in this high-risk subset of patients.

Correlation relationships of the reentrant ventricular tachycardia circuit

IntroductionA quantitative analysis of the components of reentrant ventricular tachycardia (VT) circuitry could improve understanding of its onset and perpetuation. MethodIn 19 canine experiments, the left anterior descending coronary artery was ligated to generate a subepicardial infarct. The border zone resided at the epicardial surface of the anterior left ventricle and was mapped 3–5 days postinfarction with a 196–312 bipolar multielectrode array. Monomorphic VT was inducible by extrastimulation. Activation maps revealed an epicardial double-loop reentrant circuit and isthmus, causing VT. Several circuit parameters were analyzed: the coupling interval for VT induction, VT cycle length, the lateral isthmus boundary (LIB) lengths, and isthmus width and angle. ResultsThe extrastimulus interval for VT induction and the VT cycle length were strongly correlated (p < 0.001). Both the extrastimulus interval and VT cycle length were correlated to the shortest LIB (p < 0.005). A derivation was developed to suggest that when conduction block at the shorter LIB is functional, the VT cycle length may depend on the local refractory period and the delay from wavefront pivot around the LIB. Isthmus width and angle were uncorrelated to other parameters. ConclusionsThe shorter LIB is correlated to VT cycle length, hence its circuit loop may drive reentrant VT. The extrastimulation interval, VT cycle length, and shorter LIB are intertwined, and may depend upon the local refractory period. Isthmus width and angle are less correlated, perhaps being more related to electrical discontinuity caused by alterations in infarct shape at depth.

Selective and non-selective right bundle pacing for the diagnosis of bundle branch reentry ventricular tachycardia.

Bundle branch reentry ventricular tachycardia (BBRVT) can be seen in patients with conduction disease. In this report, we describe the use of conduction system pacing for its diagnosis. BBRVT was induced in two patients with infra-nodal conduction disease. Bundle branch reentry ventricular tachycardia with a left bundle branch block morphology was observed in the first patient (type A), whereas the second patient had a right bundle branch block morphology (type C).The diagnosis of BBRVT was confirmed in both patients by ventriculo-atrial dissociation, and the interdependence of the conduction system and the ventricular tachycardia cycle length variations.Selective and non-selective RB pacing was observed in the two patients during apical right ventricular pacing for entrainment of BBRVT with evidence of manifest entrainment with non-selective RB capture in the first patient, and concealed entrainment by selective RB capture in the second patient. Other criteria for entrainment including a short post-pacing interval at the right bundle pacing site were noted. Right bundle pacing is feasible in patients with BBRVT and may be a helpful manoeuver for the diagnosis of BBRVT.

Optimizing electrophysiology studies to prevent sudden cardiac death after myocardial infarction.

This study assessed associations of minimum final extrastimulus coupling interval utilized within electrophysiology study (EPS) after myocardial infarction (MI) and possible site of origin of induced ventricular tachycardia (VT) with long-term occurrence of spontaneous ventricular tachyarrhythmia and long-term survival. This prospective study recruited consecutive patients with left ventricular ejection fraction (LVEF) ≤ 40% who underwent EPS days 3-5 after MI between 2004 and 2017. Positive EPS was defined as sustained monomorphic VT cycle length ≥200 ms for ≥10 s or shorter duration if haemodynamic compromise occurred. Each of the four extrastimuli was shortened by 10 ms at a time, until it failed to capture the ventricle (ventricular refractoriness) or induced ventricular tachyarrhythmia. Outcomes included spontaneous ventricular tachyarrhythmia occurrence and all-cause mortality. Shorter coupling interval length of final extrastimulus that induced VT was associated with higher risk of spontaneous ventricular tachyarrhythmia (P < 0.001). Significantly higher rates of spontaneous ventricular tachyarrhythmia (65.2% vs. 23.2%; P < 0.001) were observed for final coupling interval at EPS <200 ms vs. >200 ms. Right bundle branch block (RBBB) morphology of induced VT, with possible site of origin from the left ventricle, was associated with all-cause mortality [hazard ratio (HR) 3.2, P = 0.044] and a composite of spontaneous ventricular tachyarrhythmia recurrence or mortality (HR 1.8, P = 0.043). Ventricular tachycardia induced with shorter coupling intervals was associated with higher risk of spontaneous ventricular tachyarrhythymia on follow-up, indicating that the final extrastimulus coupling interval at EPS early after MI should be determined by ventricular refractoriness. Induced VT with possible origin from left ventricle was associated with increased risk of spontaneous ventricular tachyarrhythmia recurrence or death.

Characteristics of the phenotype of mixed cardiomyopathy in patients with implantable cardioverter-defibrillators

Background or PurposeThe prognosis of mixed cardiomyopathy (CMP) in patients with implanted cardioverter-defibrillators (ICDs) has not been investigated. We aim to study the demographic, clinical, device therapies and survival characteristics of mixed CMP in a cohort of patients implanted with a defibrillator.MethodsThe term mixed CMP was used to categorise patients with impaired left ventricular ejection fraction attributed to documented non-ischemic triggers with concomitant moderate coronary artery disease. This is a single center observational cohort of 526 patients with a mean follow-up of 8.7 ± 3.5 years.ResultsThere were 42.5% patients with ischemic cardiomyopathy (ICM), 26.9% with non-ischemic cardiomyopathy (NICM) and 30.6% with mixed CMP. Mixed CMP, compared to NICM, was associated with higher mean age (69.1 ± 9.6 years), atrial fibrillation (55.3%) and greater incidence of comorbidities. The proportion of patients with mixed CMP receiving device shocks was 23.6%, compared to 18.4% in NICM and 27% in ICM. The VT cycle length recorded in mixed CMP (281.6 ± 43.1 ms) was comparable with ICM (282.5 ± 44 ms; p = 0.9) and lesser than NICM (297.7 ± 48.7 ms; p = 0.1). All-cause mortality in mixed CMP (21.1%) was similar to ICM (20.1%; p = 0.8) and higher than NICM (15.6%; p = 0.2). The Kaplan–Meier curves revealed hazards of 1.57 (95% CI: 0.91, 2.68) for mixed CMP compared to NICM.ConclusionIn a cohort of patients with ICD, the group with mixed CMP represents a phenotype predominantly comprised of the elderly with a higher incidence of comorbidities. Mixed CMP resembles ICM in terms of number of device shocks and VT cycle length. Trends of long-term prognosis of patients with mixed CMP are worse than NICM and similar to ICM.

Arrhythmogenicity of anti-tachycardia pacing in patients with implantable cardioverter defibrillator

BackgroundAnti-tachycardia pacing therapy (ATP) has shown comparable efficacy to shock therapy in ventricular tachycardia (VT) termination with better quality of life. However, some ATPs may lead to VT acceleration or degeneration to ventricular fibrillation (VF), which will result in more ICD shocks. The aim of this study was to investigate the predictors of VT acceleration by ATP therapy in a real-life patient cohort.ResultsWe retrospectively reviewed 448 monomorphic VT episodes that required ATP therapy in 60 patients with structural heart diseases implanted with ICD or CRTD. The clinical data of the patients and the episodes’ details were evaluated. We found that patients with a higher ejection fraction (EF) were more likely to be cardioverted by ATP therapy (P: 0.024). VT acceleration was more frequent in patients with lower EF (mean 31.24 ± 4.08) compared with the non-accelerated patients with higher EF (mean 37.00 ± 9.4, P: 0.016). The percentage of accelerated episodes was 8.5%. VT episodes with a mean cycle length (CL) < 310 ms are more likely to accelerate (sensitivity 76.3%, specificity 67.7%, PPV value 45%, NPV 86%, and AUC 0.790). There was a statistically significant difference in the accelerated VT episodes as compared to non-accelerated episodes regarding the number of ATP bursts (mean 3.66 ± 2.22 vs. 1.76 ± 1.35, P: < 0.001), ramp (23.7% vs. 4.2%, P: < 0.001), scanning (55.3% vs. 31.3%, P: 0.003) and burst adaptive cycle length (mean 83.55 ± 2.92 vs. 84.64 ± 2.61, P: 0.016). In a multivariate analysis, the VT CL, number of ATP bursts and ramp pacing predicted VT acceleration by ATP therapy.ConclusionsVentricular tachycardia in patients with low LV EF and fast VTs with a CL less than 310 ms were more likely to accelerate with ATP therapy. The number of ATP bursts and the use of ramp had a significant effect on VT acceleration. To avoid VT acceleration by ATP therapy, ramp pacing better be avoided, especially in fast VTs, and lesser number of bursts should be delivered.

Catheter ablation as first line treatment in patients with ischemic cardiomyopathy, tolerated ventricular tachycardia and left ventricular ejection fraction over 35%: long term outcomes

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Patients with ischemic cardiomyopathy (ICM) and monomorphic, sustained ventricular tachycardia (VT) are considered to be at risk for arrhythmia-related sudden cardiac death (SCD). Prior studies have suggested that patients with well-tolerated VTs and preserved or moderately reduced left ventricular ejection fraction (LVEF) and successful VT ablation may not benefit from cardioverter defibrillator implantation (ICD Current guidelines indicate that in selected patients catheter ablation should be considered instead of ICD, but supporting evidence is limited. Aim This study aims to analyze arrhythmia outcomes of ICM patients referred for VT ablation without prior ICD implantation according to LVEF, hemodynamical stability during VT and ablation outcome. Methods ICM patients without prior ICD implantation undergoing VT ablation in a tertiary center between 2009 and 2022 were included. Patients who presented with a first episode of tolerated VT and w a LVEF≥35% were offered catheter ablation (CA) as first-line therapy. Patients were categorized according to (1) LVEF, (2) clinical presentation (hemodynamically tolerated/non-tolerated VT) and (3) acute ablation outcome. According to the institutional protocol, ICD was offered to all patients after ablation, but was subject to shared decision making, explaining the available evidence supporting ICDs for the different categories. Results Eighty-six ICM patients without ICD underwent ablation for VT. Mean age was 69±9 years and 72 (84%) were men, mean LVEF was 41±9% and 34 patients (28%) were using anti-arrhythmic drugs (AAD). The median VT cycle length (VTCL) at presentation was 323ms [300 – 375] and VT was tolerated in 58 (67%) patients (median tolerated VTCL 325ms [300 – 371]). In 66 (77%) patients, the LVEF was ≥35% of which 51 had well-tolerated VT. Of these 51 patients, 37 (73%) were rendered non-inducible after ablation and in 14 patients non-clinical VTs remained inducible (median remaining VTCL 238ms [203-288]). In 5/37 non-inducible and in 11/14 inducible patients, an ICD was implanted. Of the 35 patients who had LVEF&amp;lt;35% and/or non-tolerated VTs, 7 refused ICD implantation. (Figure 1) During a median follow-up of 35 [22 – 53] months, 10 patients (12%) had VT-recurrence and one patient with an ICD had SCD. Mortality was 22%. In the 37 patients with LVEF≥35%, tolerated VT and non-inducibility post procedure, no SCD or VT-recurrence was observed. Also, in this group no patient was using AAD for VT at last follow-up. In the 14 remaining patients with LVEF≥35% and tolerated VT who were still inducible after ablation, no SCD occurred but VT recurred in 29% (median VTCL 303ms [200-374]) with AAD-use for VT in 29%. Conclusion This study supports that ICM patients without prior ICD and LVEF≥35% who present with hemodynamically well-tolerated VT and are non-inducible after ablation have an excellent prognosis. Successful CA without ICD implantation seems to be safe in these selected patients.

Optimisation of decrementing evoked potential mapping for functional substrate identification in ischaemic ventricular tachycardia ablation

Abstract Funding Acknowledgements Type of funding sources: None. Background Decrement evoked potential (DeEP) mapping has been shown to identify the functional substrate critical to the Ventricular Tachycardia (VT) circuit with a higher specificity than late potential mapping.[1] However, there is limited data on methodological optimisation of this technique which could identify more relevant regions of conduction delay and functional block that occurs during clinical VT by activating the substrate at coupling intervals closer to the VT cycle length (CL). Purpose The goal of this study was to investigate a range of short coupled extra-stimuli and decrement thresholds to improve DeEP mapping target identification in patients with ischaemic cardiomyopathy. Methods Thirteen patients (70±12 years) underwent VT ablation. Mapping was performed with the Advisor HD Grid multipolar catheter. Maps were generated using omnipolar electrograms (EGMs). DeEP mapping was performed using 3 different extra-stimuli (S2) sequentially in each case: (1) 400 ms (DeEP-400); (2) VT cycle length (VTCL); (3) ventricular effective refractory period (VERP) + 20 ms. For each of the DeEP-400, DeEP-VTCL and DeEP-VERP maps, the definition of a DeEP was altered from the standard 10 ms decrement to multiple thresholds of 10 ms to 50 ms in 10 ms increments (figure 1). DeEP maps were compared to the VT exit site identified with VT activation maps. All patients underwent DeEP-400 focused ablation. Results All patients had 1 clinical VT (VTCL = 353 ± 48 ms; VERP + 20 ms = 300 ± 20 ms). Mean left ventricular ejection fraction was 30 ± 12 %. Sensitivity and specificity analyses (figure 2) show the optimal threshold for defining a DeEP is with an EGM prolongation of ≥ 20 ms for the DeEP-400 (sens. 77%, spec. 79%, ROC AUC 0.84), DeEP-VTCL (sens. 77%, spec. 79%, ROC AUC 0.83) and DeEP-VERP (sens. 69%, spec. 74%, ROC AUC 0.76) maps. Proportional to total mapped area, the DeEP-400 map area was significantly smaller than DeEP-VERP map area (19.0 ± 7.6 % vs 26.4 ± 14.3%; p=0.02). Delivering the S2 at the conventional VERP + 20 ms using a 10 ms decrement definition yielded a sensitivity of 84.6% and a specificity of 62.0% with a target ablation area of 33.9 cm2. With the optimised protocol of delivering the S2 at 400 ms using a 20 ms decrement definition, the sensitivity remains high at 76.9% with an improved specificity of 79.0%, thus reducing the ablation target area by 50% to 16.8 cm2. 92% patients were free of any VT after DeEP-400 guided ablation at 6-month median follow-up. Conclusion In this prospective, mechanistic study utilising omnipolar technology to explore a range of S2 extra-stimuli and decrement thresholds, DeEPs were optimally defined by a conduction delay of ≥ 20 ms with an S2 extra-stimulus coupling interval of 400 ms or VTCL to more accurately localise the VT exit site. This optimised DeEP mapping protocol further refines identification of the critical myocardial sites involved in the initiation and maintenance of VT.

PO-05-031 CATHETER ABLATION AS FIRST LINE TREATMENT IN PATIENTS WITH ISCHEMIC CARDIOMYOPATHY, TOLERATED VENTRICULAR TACHYCARDIA AND LEFT VENTRICULAR EJECTION FRACTION ≥35%: LONG TERM OUTCOMES

Patients with ischemic cardiomyopathy (ICM) and ventricular tachycardia (VT) are at risk for sudden cardiac death (SCD). Prior studies have suggested that patients with well-tolerated VTs and preserved/moderately reduced left ventricular ejection fraction (LVEF) and successful VT ablation may not benefit from cardioverter defibrillator implantation (ICD). Current guidelines indicate that in selected patients catheter ablation should be considered instead of ICD. This study aims to analyze arrythmia outcomes of ICM patients referred for VT ablation without prior ICD implantation according to LVEF, tolerance of VT and ablation outcome. ICM patients without prior ICD implantation undergoing VT ablation in a single center between 2009 and 2022 were included. Patients who presented with tolerated VT and who had a LVEF≥35% were offered catheter ablation (CA) as first-line therapy. Patients were categorized according to (1) LVEF, (2) hemodynamical tolerance of VT, and (3) acute ablation outcome. According to the institutional protocol, ICD was offered to all patients after ablation. Eighty-six patients (mean age 69±9 years, 84% male, mean LVEF 41±9%) underwent VT ablation. The median presenting VT cycle length (VTCL) was 323ms [300 – 375] and was tolerated in 67% (tolerated VTCL 325ms [300 – 371]). In 66 patients, the LVEF was ≥35%, of which 51 had well-tolerated VT. Of these 51 patients, 37 (73%) were rendered non-inducible and in 14 patients non-clinical VTs remained inducible (median VTCL 238ms [203-288]). In 5/37 non-inducible and in 11/14 inducible patients, an ICD was implanted. Of the 35 patients who had LVEF<35% and/or non-tolerated VTs, 7 refused ICD implantation. During a median follow-up of 35 [22 – 53] months, 10 patients (12%) had VT-recurrence and one patient with an ICD had SCD. Overall mortality was 22%. In the 37 patients with LVEF≥35%, tolerated VT and non-inducibility post procedure, no SCD or VT-recurrence was observed. Also, in this group no patient was using AAD for VT at last follow-up. In the 14 remaining patients with LVEF≥35% and tolerated VT who were inducible after ablation, no SCD occurred but VT recurred in 29% (median VTCL 303ms [200-374]). This study supports that ICM patients without prior ICD and LVEF≥35% with hemodynamically well-tolerated VT and are non-inducible after ablation have an excellent prognosis. Successful catheter ablation without ICD implantation seems to be safe in these selected patients.

PO-04-186 ASSESSING PROXIMITY TO THE VENTRICULAR TACHYCARDIA CIRCUIT EARLY IN THE PACING TRAIN: NUMBER NEEDED TO RESET

When ventricular tachycardia (VT) continues after entrainment the post pacing interval (PPI) can be used to assess proximity to the circuit. It is not known if the initial beats of a pacing train can be used to assess reentry circuit proximity, which could be useful when pacing terminates or alters VT. We hypothesized that the number of stimuli with local electrogram(EGM) capture needed to reset (NNR) VT may provide an indication of proximity to the reentry circuit as has been shown in atrial flutter. During stable scar-related VT, pacing trains 10 – 40ms faster than the VT cycle length with the first stimulus synchronized to a ventricular electrogram were delivered. We included sites with stable VT cycle length(TCL) and without perturbation of VT post pacing to allow comparison with the PPI-TCL. Of 102 trains at 92 sites in 28 VTs in 17 patients the first capturing stimulus was earlier than 30 ms in prematurity relative to local activation, such that NNR could be artificially short. NNR was analyzed in the remaining 23 trains at 21sites in 10 VTs (457ms +/- 85ms CL). The PPI-TCL ranged from 0-100ms and the NNR ranged from 1-6. PPI-TCL was correlated with NNR (r=0.67, p=0.006) (figure). When the first or second stimulus reset VT (NNR = 1 or 2) the PPI-TCL was < 30ms and 3-6 with a PPI-TCL of >30ms. The NNR provides an indication to the proximity to the circuit with NNR <2 indicating a PPI-TCL of <30ms that can potentially be applied if pacing terminates VT. Application of NNR requires attention to synchronization of the pacing train that is not straight forward in areas of fractionated electrograms.

PO-05-082 ANTITACHYCARDIA PACING IS MORE EFFECTIVE WHEN DELIVERED TO THE LEFT BUNDLE BRANCH COMPARED TO THE RIGHT VENTRICLE IN A CANINE ISCHEMIC VENTRICULAR TACHYCARDIA MODEL

Implantable cardioverter-defibrillators (ICDs) can terminate ventricular tachycardia (VT) with Antitachycardia pacing (ATP) delivered to a right ventricular (RV) pacing lead, thereby avoiding painful and damaging high-energy shocks. However, ATP efficacy is limited for fast VT, and ATP can accelerate VT or convert VT to ventricular fibrillation (VF). Physiological pacing delivered to the left bundle branch (LBB) has emerged as a clinically relevant target to minimize ventricular dyssynchrony and pacing-induced heart failure. ATP efficacy and safety delivered to the LBB are yet to be investigated. Evaluate the therapeutic efficacy and safety of ATP delivered to an LBB lead compared to ATP delivered to a conventional RV lead. In 6 anesthetized dogs, pacing leads from two ICDs (CobaltTM XT DR, Medtronic, Inc) were implanted at the RV apex (6947 Sprint Quattro SecureTM, Medtronic, Inc) and the LBB (3830 SelectSecureTM, Medtronic, Inc). A lateral thoracotomy procedure was performed, and a two-hour lateral anterior descending artery ischemia-reperfusion injury was caused. The thoracotomy was closed and on post-infarct day 4, dogs were anesthetized, and sustained VT episodes were induced by programmed electrical stimulation. ATP (up to 5 trains of 8 pulses at approximately 88% of the VT cycle length) was delivered to either the LBB or RV pacing site in a randomized fashion. The success rate of ATP in terminating the VT episodes and the rate of VT acceleration and degeneration into VF from both pacing locations were evaluated. In our canine ischemic VT model, VT was induced 80 times, with a mean VT cycle length of 178±35 ms. ATP was delivered and tested for each episode. For ATP delivered to the RV, the success rate for terminating VT was 54%. The success rate for terminating VT for ATP delivered to the LBB was 73% (Fig. A, p < 0.05). ATP resulted in VT acceleration for 10% and 5% of ATP attempts delivered to the RV and LV, respectively (Fig. B, p = Not Significant, NS). Degeneration to VF occurred for 5% of all ATP attempts delivered to the RV, and there was no such incident for ATP delivered to the LBB (Fig. B). Higher efficacy and lower incidence of VT acceleration were observed with ATP delivered to LBB compared to ATP delivered to the RV in this canine ischemic VT model. Improved performance of ATP delivered to LBB compared to RV provides additional incentive for expanded use of LBB leads for pacing and therapy delivery.