Faculty Bibliography

Background: Left atrial posterior wall (LAPW) isolation is associated with favorable outcomes for catheter ablation of persistent atrial fibrillation (AF) in several studies. Reported techniques for LAPW isolation include ablation at the periphery without ablation within the LAPW, and high density ablation of all sites of electrical activity within the LAPW. The proportion of LA isolated by the lesion set in various reports also varies greatly. The optimal technique to achieve LAPW isolation is not clear.
Objective(s): To assess impact of ablation lesion density within the LAPW and dimensions of LAPW isolation region on arrhythmia recurrence in catheter ablation of persistent AF.
Method(s): LAPW lesion density, and LAPW isolation surface area relative to total LA surface area were calculated using electroanatomic maps of 110 consecutive patients undergoing LAPW isolation for persistent AF (CARTO 3, Biosense Webster, Inc.) LAPW isolation lesion sets were created at the discretion of 5 experienced operators after LA voltage mapping. LAPW and PV entrance block and exit block were confirmed. Arrhythmia recurrence at one year was assessed by the Kaplan-Meier method.
Result(s): LAPW lesion density ranged from 0% - 99%. Proportion of LA surface area isolated ranged from 35% - 75%. There was no significant difference in arrhythmia-free survival by quartile of LAPW ablation density (81% vs. 68% vs. 85% vs. 78%, p=0.8), or by quartile of LA surface area proportion isolated (85% vs. 75% vs. 79% vs. 74%, p=0.3). Voltage map guided LAPW isolation resulted in no significant difference in incidence of recurrent arrhythmia by quartile of total LA surface area (81% vs. 78% vs. 78% vs. 74%, p=0.5).
Conclusion(s): Neither the density of ablation within the LAPW nor the dimensions of the isolated region predicted arrhythmia-free survival LAPW isolation for catheter ablation of persistent AF. Voltage map guided LAPW isolation resulted in similar ablation efficacy regardless of LA size.
Copyright

Background: Cardiomyocytes are dependent on inward sodium currents for rapid phase 0 depolarization to initiate normal excitation-contraction coupling. In cardiovascular diseases where inward sodium currents are decreased, such as Brugada syndrome, calcium currents are thought to safeguard against conduction failure. Consequently, it has been suggested that combined sodium and calcium channel blockade may be more effective in unmasking Brugada syndrome. Fibroblast growth factor homologous factor 2 (FHF2) binds to sodium channels and modulates their function. Loss of FHF2 reduces inward sodium currents secondary to accelerated rates of both closed-state and open-state sodium channel inactivation. As a result, FHF2 KO mice are susceptible to conduction disturbances at elevated temperatures, with electrocardiogram tracings appearing similar to those seen in Brugada syndrome.

Background: Left ventricular outflow tract (LVOT) obstruction is associated with adverse outcomes in hypertrophic cardiomyopathy (HCM). AV sequential pacing has not demonstrated benefit for patients with medication-refractory LVOT obstruction in prospective, randomized clinical trials, although these trials did not include transthoracic echocardiogram (TTE) guided optimization or concomitant pharmacotherapy with disopyramide.
Objective(s): To evaluate efficacy of a standardized TTE guided AV optimization protocol for patients with persistent LVOT obstruction despite AV sequential pacing for reduction in LVOT gradient.
Method(s): Outcomes of 20 consecutive HCM patients with medication refractory LVOT gradients who were not surgical candidates and underwent AV sequential pacing from 8/2014 to 6/2017 were analyzed. ECG guided AV intervals were determined by the implanting cardiac electrophysiologist at the time of implant. Patients with incomplete response to initial settings underwent Doppler TTE guided AV optimization.
Result(s): All patients received maximally tolerated disopyramide and beta or calcium channel blockade. Following initial implant, 8 of 20 (40%) of patients had complete elimination of LVOT gradient with, and 12 of 20 (60%) had incomplete response and underwent TTE guided optimization. Compared to initial ECG guided programming, the TTE optimized sensed AV delays were shorter in all patients (mean reduction 51 +/- 48ms). Following TTE guided AV optimization, 9 of 12 patients had elimination of LVOT gradient, and 3 of 12 patients had 82.6 +/- 5.2% reduction in LVOT gradient. Patients undergoing TTE optimization had significant reduction in NYHA heart failure class (1.0 +/- 0 vs. 2.2 +/- 0.7, p=0.004).
Conclusion(s): TTE guided AV optimization shows promise as a means of improving outcomes in patients with incomplete response to medical therapy including disopyramide and AV sequential pacing for reduction of LVOT gradient in HCM.
Copyright

Background: Increased catheter stability during AF ablation is associated with higher ablation success rates. Rapid cardiac pacing and high frequency jet ventilation (HFJV) have both been independently shown to improve catheter stability. Simultaneous modulation of cardiac and respiratory motion has not been previously studied.
Objective(s): To study the effects of modulating heart rate and respiratory rate simultaneously on catheter stability.
Method(s): Forty paroxysmal AF patients were randomized to four study conditions. Ablation lesions were created at 15 prespecified locations. Twenty patients received atrial pacing (500 msec) during the first half of each lesion; twenty patients were paced during the second half of each lesion. Within each group, half received HFJV and half received standard ventilation. Contact force (CF) variability, defined as CF standard deviation, was compared between study groups.
Result(s): Compared to sinus rhythm and standard ventilation, rapid pacing (5.45 g vs. 5.86 g; p=0.006) and HFJV (5.10 g; p=0.003) each significantly reduced mean CF standard deviation. Simultaneous pacing and HFJV produced even greater reduction of mean CF standard deviation (4.29 g; p<0.001) (Figure). Pacing and HFJV alone had similar effects on mean CF variability (p=0.2).
Conclusion(s): Rapid pacing and HFJV synergistically improve catheter stability during AF ablation. Simultaneous pacing with HFJV further optimizes catheter stability over pacing or HFJV alone and may improve ablation outcomes. [Figure presented]
Copyright

Background: Despite the increased prevalence of atrial fibrillation (AF) in hypertrophic cardiomyopathy (HCM), the efficacy of radiofrequency ablation (RFA) has been characterized over limited follow-up intervals (~1 year). Several large meta-analyses note that patients with HCM have substantially higher rates of arrhythmia recurrence after RFA, compared to patients without HCM. The implication of confirmed HCM mutations on ablation efficacy has similarly only been assessed in small-scale studies.
Objective(s): To assess arrhythmia recurrence after RFA in patients with HCM and paroxysmal AF (PAAF) or persistent AF (PEAF) as well as its relation to their genetic background and LVOT gradient.
Method(s): Arrhythmia recurrence after RFA was assessed in 66 HCM patients and compared to 343 patients without HCM. AF recurrence was defined as AF on EKG or >30s of AF on ICD/pacemaker interrogation or on monitoring devices after a 3-month blanking period. Kaplan-Meier analysis was performed to compare arrhythmia recurrence rate and timing.
Result(s): The EF of HCM patients was higher than that of the non-HCM patients in both the PAAF and PEAF groups (65.5 and 63.0% vs 61.4 and 53.3%, respectively, p<0.001); within the HCM group, the clinical characteristics of the genetically (+) HCM group (n=14) did not differ from those of the genetically (-) group (n=12). Arrhythmia recurrence at 1 year in PAAF and PEAF was not significantly different between HCM and non-HCM patients (18% vs 11%, p=0.2, and 33% vs 26%, p=1), nor was mean time to arrhythmia recurrence (PAAF 193+/-48 vs 181+/-59 days, p=0.8, and PEAF 175+/-58 vs 168+/-20 days, p=0.6). Recurrence rates over the entire follow-up period of the HCM patients were 54 and 85% in the PAAF and PEAF groups (1076+/-187 and 1050+/- 201 days of follow-up), respectively. Amongst HCM patients with LVOT gradients >70mmHg (PAAF, n = 8, and PEAF, n = 3) longer-term rates of arrhythmia recurrence were similar at 88% and 67% (p=0.9).
Conclusion(s): Arrhythmia recurrence at 1 year following AF ablation in HCM patients is similar to that of non-HCM AF patients regardless of the type of AF. Absolute rates of atrial arrhythmia recurrence in HCM patients at >3 years post ablation are considerable. Confirmed HCM mutations and severe LVOT gradients do not modify the outcome of AF ablation.
Copyright

OBJECTIVES/OBJECTIVE:This study sought to determine whether a radiation safety time-out reduces radiation exposure in electrophysiology procedures. BACKGROUND:Time-outs are integral to improving quality and safety. The authors hypothesized that a radiation safety time-out would reduce radiation exposure levels for patients and the health care team members. METHODS:The study was performed at the New York University Langone Health Electrophysiology Lab. Baseline data were collected for 6 months prior to the time-out. On implementation of the time-out, data were collected prospectively with analyses to be performed every 3 months. The primary endpoint was dose area product. The secondary endpoints included reference point dose, fluoroscopy time, use of additional shielding, and use of alternative imaging such as intracardiac and intravascular ultrasound. RESULTS:, representing a 21% reduction (p = 0.007). The median reference point dose prior to time-out was 163 mGy, and during the time-out was 122 mGy (p = 0.011). The use of sterile disposable protective shields and ultrasound imaging for access increased significantly during the time-out. CONCLUSIONS:A radiation safety time-out significantly reduces radiation exposure in electrophysiology procedures. Electrophysiology laboratories, as well as other areas of cardiovascular medicine using fluoroscopy, should strongly consider the use of radiation safety time-outs to reduce radiation exposure and improve safety.

Background: Deficits in myocardial conduction velocity (CV) are associated with ventricular arrhythmias and conduction block. Abnormal organization and expression of cardiac sodium channel NaV1.5 and gap junction protein Cx43, key determinants of myocardial CV, are known features of arrhythmogenic heart disease. We previously identified fibroblast growth factor homologous factor 2 (FHF2) as a modulator of CV through its effects on NaV1.5. The aim of this study was to investigate whether modulating junctional conductance synergizes with loss of FHF2 to create conduction reserve deficits and susceptibility for arrhythmias. Method(s): ECGs were acquired to characterize conduction intervals of 2-3 month old wildtype (WT), cardiomyocyte-specific Cx43 heterozygous (Cx43 cHet), FHF2 KO, and FHF2 KO/Cx43 cHet mice. ECGs were then acquired with increasing doses of a gap junction channel blocker, carbenoxolone (CBX). Result(s): WT, Cx43 cHet, and FHF2 KO mice had normal conduction while FHF2 KO/Cx43 cHet mice showed ventricular conduction slowing at baseline. FHF2 KO and FHF2 KO/Cx43 cHet mice showed ventricular conduction slowing with CBX in a dose dependent fashion. Lethal conduction slowing was observed in FHF2 KO/Cx43 cHet mice given 120mg/kg CBX. Conclusion(s): These results identify a key role for FHF2 in maintaining myocardial conduction reserve which protects against stressors that depress junctional conductance (aging, pharmacologic blockade, genetic deficiency) and subsequent arrhythmias. [Figure presented]2019 American College of Cardiology Foundation. All rights reserved

PURPOSE/OBJECTIVE:Elimination of pace-capture along pulmonary vein isolation (PVI) lesion sets reduces atrial fibrillation (AF) recurrence in catheter ablation of paroxysmal AF. Pacing from the RF ablation electrode during RF application is prevented within the CARTO electroanatomic mapping system (Biosense Webster, Inc.) due to theoretical safety considerations. We evaluated a method of pacing the distal ablation electrode during RF application in the CARTO system, thus avoiding repeated activation and inactivation of the pacing channel and facilitating immediate recognition of pace-capture loss. We investigated the safety, feasibility, and utility of simultaneous pace-ablate (SPA) during AF ablation with the CARTO-3 system and a contact-force sensing RF ablation catheter. METHODS:Safety of feasibility of SPA was evaluated in 250 patients undergoing first-time AF ablation. Frequency and regional distribution of pace-capture following PVI was evaluated in a cohort of 50 consecutive patients undergoing catheter ablation of paroxysmal AF. RESULTS:SPA was successfully performed in all 250 patients without adverse event. At least one pace-capture site was noted in 22 of 50 PAF patients (44%), and pace-capture following PVI was most common at anterior and superior left atrial sites. There were 2.0 ± 3.3 RF applications during pacing via the distal ablation electrode per patient, and all lesions sets were successfully rendered unexcitable. CONCLUSIONS:Pace-capture along the completed PVI lesion set remains common despite utilization of contact-force sensing RF ablation catheters and automated lesion annotation. Simultaneous pace-ablate in AF ablation using the CARTO system may be safely used to render atrial lesion sets unexcitable.

Rapid impulse propagation is a defining attribute of the pectinated atrial myocardium and His-Purkinje system (HPS) that safeguards against atrial and ventricular arrhythmias, conduction block, and myocardial dyssynchrony. The complex transcriptional circuitry that dictates rapid conduction remains incompletely understood. Here, we demonstrate that ETV1 (ER81)-dependent gene networks dictate the unique electrophysiological characteristics of atrial and His-Purkinje myocytes. Cardiomyocyte-specific deletion of ETV1 results in cardiac conduction abnormalities, decreased expression of rapid conduction genes (Nkx2-5, Gja5, and Scn5a), HPS hypoplasia, and ventricularization of the unique sodium channel properties that define Purkinje and atrial myocytes in the adult heart. Forced expression of ETV1 in postnatal ventricular myocytes (VMs) reveals that ETV1 promotes a HPS gene signature while diminishing ventricular and nodal gene networks. Remarkably, ETV1 induction in human induced pluripotent stem cell-derived cardiomyocytes increases rapid conduction gene expression and inward sodium currents, converting them towards a HPS phenotype. Our data identify a cardiomyocyte-autonomous, ETV1-dependent pathway that is responsible for specification of rapid conduction zones in the heart and demonstrate that ETV1 is sufficient to promote a HPS transcriptional and functional program upon VMs.