Travis Richardson

and 1 more

High Density Pace-Mapping for Scar-related Ventricular Tachycardia AblationTravis D. Richardson MD and William G. Stevenson MD.1 Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN, USARunning Title: High Density Pace MappingCorresponding Author:Travis D. Richardson, MDDivision of Cardiovascular MedicineVanderbilt University Medical Center1211 Medical Center DrNashville, TN 37232USAEmail: travis.d.richardson@vumc.orgWord Count: 2,225Conflicts of Interest :Dr. Stevenson has received speaking Honoria from: Boston Scientific, Medtronic, Abbott, Johnson and Johnson, and Biotronik; he is co-holder of a patent for irrigated needle ablation that is consigned to Brigham and Women’s Hospital.Dr. Richardson has received research funding from Medtronic Inc, Abbott Inc and served as a consultant for Philips Inc and Johnson and Johnson.This work did not receive any funding.Despite advances in medical and interventional therapies, ventricular tachycardia (VT) due to reentrant activity within complex regions of myocardial scar remains a common late complication of myocardial infarction.1 While implantable defibrillators (ICD) may prevent sudden death, ICD shocks are painful and impact quality of life2. Catheter ablation reduces the likelihood of ICD therapies and it’s role early in the course of disease is expanding3–5. However, several factors limit the success and safety of catheter ablation procedures. Scar-related reentry circuits can be large with a critical isthmus shared by multiple loops. Ablation of the isthmus is associated with a low risk of recurrence of that VT6,7. The critical isthmus can be identified during VT by detailed activation mapping and entrainment. However, prolonged mapping during VT is often not feasible or desired. Patients undergoing VT ablation often have severe systolic heart failure as well as other comorbid conditions. VT is often not hemodynamically tolerated and even when tolerated, prolonged time in VT may lead to decompensation. Strategies to limit initiation and mapping of VT may improve procedural safety8. Methods to guide ablation based on characterization of the sinus rhythm substrate alone have generally shown good results9. A number of approaches have been applied, including ablation over the entire low voltage area (scar homogenization)10. While this is often successful, areas of scar can be quite extensive, and undoubtedly this technique leads to ablation of more areas than absolutely necessary for success. This approach is also more effective if epicardial ablation is routinely included, which has the potential to increase procedural risk. A strategy to focus on the critical regions, particularly when a clinically relevant VT is known, remains a reasonable first step in the procedure. A variety of electrogram markers of critical regions have been described including late potentials, potentials that display variable coupling to surrounding tissue during programmed stimulation11 , and areas of slow conduction identified by high density mapping 12,13. While these are likely to increase the specificity of ablation targets compared to electrogram voltage alone, they are also seen at bystander areas14.Pace-mapping during sinus rhythm is useful to help identify the general location of focal arrhythmia sources,15 and can also be used in scar related reentry.16,17 At the reentry circuit exit region the paced QRS morphology often resembles the VT QRS, and this will also occur at sites proximal to the exit provided that the stimulated wavefront follows the reentry path to the exit. A stimulus – QRS > 40 ms is also consistent with slow conduction away from the pacing site, that can be a marker for reentry substrate17.In this issue of the Journal of Cardiovascular Electrophysiology,Guenancia et al. review their technique of using high density pace mapping to guide VT ablation18. Their method takes advantage of software available in electroanatomic mapping systems that assigns a measure of correlation between two different QRS morphologies; in this case the VT and the paced QRS morphology.19 A pacing correlation map is generated by pacing multiple sites within the ventricle and color coding the algorithmically derived score for display at each point on the anatomic map. Sites near the exit from the reentry circuit isthmus, typically along the border of a scar, will display good correlation with induced VT. As one moves along the isthmus deeper into the low voltage scar the S-QRS prolongs due to the conduction time between the pacing site and the exit region. If the isthmus is anatomically defined, such that it is present during VT and sinus rhythm, the QRS morphology remains similar to the VT as long as the paced wavefront follows the isthmus out to the exit. Moving to the entrance or adjacent sites outside the isthmus can produce an abrupt transition to a markedly different paced QRS because the wavefront can propagate away without following the path of the isthmus.20 Thus, the pace-map correlation maps can outline the location of a reentry circuit isthmus during sinus rhythm, as they illustrate.Their method can also help identify cases in which the critical isthmus is not located on the surface being mapped. When the VT circuit is epicardial or intramural, the earliest endocardial activation may appear focal. Similarly, the pace-map correlation maps may reveal a concentric or focal pattern of matching, potentially allowing recognition of this situation without the need for activation mapping during VT.We agree with the fundamental principles described, and feel this technique can be a helpful substrate mapping approach. There are several caveats. Evaluation to clarify its specificity and sensitivity is limited. The authors report that in their unpublished experience an abrupt transition is seen in the majority of post-infarct cases, they have also published a series of 10 post-infarct patients undergoing VT ablation during which the pacing correlation maps visually matched VT activation maps.21This technique is likely to be effective in cases where the VT isthmus is confined to the ventricular surface being mapped. Pacing can capture deep to the endocardium depending on current strength.22 Whether this technique can detect intramural isthmuses and whether deep tissue that can be captured with pacing can also be ablated from the pacing site is not clear.It is important to point out that very good correlations with VT can be observed pacing in an outer loop immediately adjacent to the exit where one would not anticipate RF ablation delivery would be effective. If a focal pattern is seen on both the endocardial and epicardial surfaces very little can be inferred about the VT circuit; the site with better correlation would be expected to be closer to the exit. In this setting entrainment during a brief episode of induced VT with assessment of the post-pacing interval can potentially clarify the proximity to the reentry circuit.During VT, areas of functional conduction block may be present that are absent during sinus rhythm. Functional block can also occur remote from the reentry isthmus and alter activation wavefronts during VT changing the QRS morphology. Theoretically it is then possible to have poor correlation between the VT and paced QRS at its exit. In animal models of post-infarction VT exit regions have been shown to harbor very slow areas of conduction which could be prone to altering total ventricular activation during VT.23.We would caution against generalizing these techniques to patients with dilated cardiomyopathies where confluent regions of low voltage scar are absent. Diffuse interstitial fibrosis may play a greater role in some of these VT circuit and anatomically fixed isthmus sites are less likely to be present.Further study is needed before utilizing this technique when anatomical structures within the ventricle are involved in the VT circuit. Structures such as the moderator band may by definition have multiple exits and varied QRS morphologies24, and papillary muscles may display large areas of similar paced morphology25, potentially distorting pacing correlation maps.This technique is unlikely to correctly characterize VT circuits that involve a portion of the cardiac conduction system as occurs in some scar-related VTs and in bundle-branch reentry.26 These circuits may demonstrate a focal pattern at the left or right ventricular apical septum on pacing correlation maps due to the long, insulated nature of the reentrant circuit itself, and ablation at the exit site is very unlikely to be effective.This strategy of high density pace mapping adds to the available substrate mapping methods for guiding VT ablation while limiting VT induction. This strategy does not rely on electrogram interpretation, making it of particular interest in regions of very low voltage. Indeed, when utilizing larger recording electrodes, such as an ablation catheter, pacing will often reveal the presence of excitable tissue where a local electrogram is not always apparent. In post-infarct ventricular tachycardia circuits with a well-defined scar and a short anatomically bounded isthmus, pacing correlation maps are likely to be revealing. More study is warranted to further assess this method in relation to other substrate mapping methods, in complex substrate with intramural components, and in other disease substrates. It is useful to have multiple tools in the tool box. More studies are needed to further define which tools work best for which substrate.References:1. Stevenson WG: Ventricular Tachycardia After Myocardial Infarction: From Arrhythmia Surgery to Catheter Ablation. J Cardiovasc Electrophysiol 1995; 6:942–950.2. Moss AJ, Schuger C, Beck CA, et al.: Reduction in inappropriate therapy and mortality through ICD programming. N Engl J Med 2012; 367:2275–2283.3. Sapp JL, Wells GA, Parkash R, et al.: Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs. N Engl J Med 2016; 375:111–121.4. Cronin EM, Bogun FM, Maury P, et al.: 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias: Executive summary. Heart Rhythm 2020; 17:e155–e205.5. Della Bella P, Baratto F, Vergara P, et al.: Does Timing of Ventricular Tachycardia Ablation Affect Prognosis in Patients With an Implantable Cardioverter Defibrillator? Results From the Multicenter Randomized PARTITA Trial. Circulation 2022; .6. Hadjis A, Frontera A, Limite LR, et al.: Complete Electroanatomic Imaging of the Diastolic Pathway Is Associated With Improved Freedom From Ventricular Tachycardia Recurrence. Circ Arrhythm Electrophysiol 2020; 13:e008651.7. Tokuda M, Kojodjojo P, Tung S, et al.: Characteristics of Clinical and Induced Ventricular Tachycardia Throughout Multiple Ablation Procedures. J Cardiovasc Electrophysiol 2016; 27:88–94.8. Yu R, Ma S, Tung R, et al.: Catheter ablation of scar-based ventricular tachycardia: Relationship of procedure duration to outcomes and hospital mortality. Heart Rhythm 2015; 12:86–94.9. Irie T, Yu R, Bradfield JS, et al.: Relationship between sinus rhythm late activation zones and critical sites for scar-related ventricular tachycardia: systematic analysis of isochronal late activation mapping. Circ Arrhythm Electrophysiol 2015; 8:390–399.10. Di Biase L, Santangeli P, Burkhardt DJ, et al.: Endo-Epicardial Homogenization of the Scar Versus Limited Substrate Ablation for the Treatment of Electrical Storms in Patients With Ischemic Cardiomyopathy. J Am Coll Cardiol 2012; 60:132–141.11. de Riva M, Naruse Y, Ebert M, et al.: Targeting the Hidden Substrate Unmasked by Right Ventricular Extrastimulation Improves Ventricular Tachycardia Ablation Outcome After Myocardial Infarction. JACC Clin Electrophysiol 2018; 4:316–327.12. Anter E, Neuzil P, Reddy VY, et al.: Ablation of Reentry-Vulnerable Zones Determined by Left Ventricular Activation From Multiple Directions: A Novel Approach for Ventricular Tachycardia Ablation: A Multicenter Study (PHYSIO-VT). Circ Arrhythm Electrophysiol 2020; 13:e008625.13. Tung R: Substrate Mapping in Ventricular Arrhythmias. Card Electrophysiol Clin 2019; 11:657–663.14. Nayyar S, Wilson L, Ganesan AN, et al.: High-density mapping of ventricular scar: a comparison of ventricular tachycardia (VT) supporting channels with channels that do not support VT. Circ Arrhythm Electrophysiol 2014; 7:90–98.15. Bennett R, Campbell T, Kotake Y, et al.: Catheter ablation of idiopathic outflow tract ventricular arrhythmias with low intraprocedural burden guided by pace mapping. Heart Rhythm O2 2021; 2:355–364.16. Brunckhorst CB, Delacretaz E, Soejima K, Maisel WH, Friedman PL, Stevenson WG: Identification of the ventricular tachycardia isthmus after infarction by pace mapping. Circulation 2004; 110:652–659.17. Stevenson WG, Sager PT, Natterson PD, Saxon LA, Middlekauff HR, Wiener I: Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars. J Am Coll Cardiol 1995; 26:481–488.18. Guenancia C, Supple GE, Sellal J-M, et al.: How to use pace mapping for ventricular tachycardia ablation in post-infarct patients. J Cardiovasc Electrophysiol .19. de Chillou C, Sellal J-M, Magnin-Poull I: Pace Mapping to Localize the Critical Isthmus of Ventricular Tachycardia. Card Electrophysiol Clin 2017; 9:71–80.20. Hanaki Y, Komatsu Y, Nogami A, et al.: Combined endo- and epicardial pace-mapping to localize ventricular tachycardia isthmus in ischaemic and non-ischaemic cardiomyopathy. Eur Eur Pacing Arrhythm Card Electrophysiol J Work Groups Card Pacing Arrhythm Card Cell Electrophysiol Eur Soc Cardiol 2022; 24:587–597.21. de Chillou C, Groben L, Magnin-Poull I, et al.: Localizing the critical isthmus of postinfarct ventricular tachycardia: the value of pace-mapping during sinus rhythm. Heart Rhythm 2014; 11:175–181.22. Itoh T, Yamada T: Excellent Pace Maps Recorded from Two Remote Sites Inside and Outside the Scar in a Patient with Ischemic VT: What Is the Mechanism? Pacing Clin Electrophysiol 2017; 40:72–74.23. Anter E, Tschabrunn CM, Buxton AE, Josephson ME: High-Resolution Mapping of Postinfarction Reentrant Ventricular Tachycardia: Electrophysiological Characterization of the Circuit. Circulation 2016; 134:314–327.24. Jiang C-X, Long D-Y, Li M-M, et al.: Evidence of 2 conduction exits of the moderator band: Findings from activation and pace mapping study. Heart Rhythm 2020; 17:1856–1863.25. Itoh T, Yamada T: Usefulness of pace mapping in catheter ablation of left ventricular papillary muscle ventricular arrhythmias with a preferential conduction. J Cardiovasc Electrophysiol 2018; 29:889–899.26. Bogun F, Good E, Reich S, et al.: Role of Purkinje fibers in post-infarction ventricular tachycardia. J Am Coll Cardiol 2006; 48:2500–2507.

Asad Aboud

and 8 more

Introduction Programmed electrical stimulation is an essential part of VT ablation procedures but VT is not always inducible, usually for reasons that are not clear. We sought to review pacing site-specific failure of programmed electrical stimulation (PES) to induce scar-related ventricular tachycardia (VT). Methods A series of patients in whom aggressive programmed stimulation from traditional RV pacing sites failed to induce VT, but VT was easily inducible from a non-traditional site are reviewed. Computer simulations in a simple 2-dimensional model of reentry were performed. Results Six patients who had no inducible sustained VT from the RV apex/outflow tract with at least 3 extrastimuli, but relatively easily induced VT from the LV, basal RV, epicardium, or atrium are described. In 5 of these patients, the site that induced VT was closer to the likely reentry circuit region based on mapping and ablation. Computer simulations illustrated that the spatial relation between the pacing site and the entrance and exits of a reentry isthmus can determine the ease of initiation of reentry by determining the time available for recovery of excitability at the initial region of block. Conclusions The site of PES has a marked effect on inducibility of VT in some patients such that PES from the RV apex and outflow regions will fail to expose clinically relevant VTs. The frequency with which this occurs is not certain. Stimulation from alternative sites is a reasonable consideration in selected patients.

Jason Cook

and 1 more

Leadless Pacing with Mechanical Atrial Sensing and Variable AV ConductionJason Cook, MDTravis D. Richardson, MDFrom Vanderbilt University Medical Center. Nashville, TennesseeCorresponding author:Travis D. Richardson, MDAssistant Professor Cardiac ElectrophysiologyVanderbilt Heart and Vascular Institute1215 21st Ave S. Nashville, TNMedical Center East, South Tower, Suite 5209ph (615) 936-7537fax (615) 936-5064travis.d.richardson@vanderbilt.eduWord Count:1331Disclosures: The authors report no relevant financial disclosures.Funding: NoneThe MicraTM leadless transcatheter pacing system (Medtronic Inc., Mounds View, MN) has been shown to be an effective alternative to transvenous pacing with excellent implantation success rates and durable long-term performance.1–3 The first generation device provided single chamber right ventricular pacing with rate responsiveness enabled by a 3-axis accelerometer.Recently, the MARVEL 2 study (Micra Atrial tRacking using a Ventricular accELerometer 2) reported the ability of software enhancements to allow a leadless pacemaker to deliver single chamber atrioventricular (AV) synchronized pacing.4 In contrast to dual-chamber transvenous pacemakers which sense atrial electrograms, the MARVEL 2 algorithm adjudicates atrial events using mechanically sensed atrial activity from the 3-axis accelerometer. During initial programming, the relative timing of mechanical events to the ventricular electrogram allows for identification of A3 (passive ventricular filling) and A4 (atrial contraction). Atrial-sensed events are then defined by the A4 signal, and tracking may occur. MARVEL 2 reported VDD pacing was achieved at rest in an impressive 89.2% of patients.The Micra AVTM system’s unique programming includes three basic pacing modes: VDD, VVI and VDIR (Figure 1). Additionally, two mode switch algorithms are available and by default programmed on: the AV conduction mode switch and the activity mode switch. Unlike mode switch algorithms in dual chamber pacing systems, which are intended to avoid inappropriate tracking of atrial arrhythmias, these algorithms are intended to 1) minimize ventricular pacing, and 2) to improve rate support during patient activity respectively.When the AV conduction mode switch algorithm is enabled, the device periodically switches from VDD to VVI at 40 bpm to allow for intrinsic AV conduction. If ventricular sensing occurs above a rate of 40 bpm, in order to reduce right ventricular pacing, VVI 40 programming will continue regardless of the programmed lower rate limit. However, if two of any window of four beats are paced at VVI 40, the device reverts to VDD. Thereafter, reassessments of AV conduction are performed at increasing intervals starting at 2 minutes until either AV conduction is detected or 8 hours is reached at which point subsequent testing occurs at regular 8 hour intervals.The activity mode switch algorithm utilizes the sensor indicated rate in an attempt to ensure adequate ventricular rate support during patient activity regardless of AV conduction. The sensor in the MicraTM is always running. If at any time 1) the sensor indicated rate is above the device programmed ADL rate, and 2) the current ventricular rate is >20 BPM below the sensor rate, the activity mode switch will change the device to VDIR mode with heart rates determined by the sensor. This switch may occur from either the VDD mode or VVI in the setting of AV conduction. The device will revert to VDD mode when the sensor rate drops below the ADL rate.With the added functionality of atrial sensing and the incorporation of the MARVEL 2 algorithms described above, in this issue of the Journal of Cardiovascular Electrophysiology, Garweg et al. examined the pacing behavior of the Micra AVTM in the presence of variable AV conduction, atrial arrhythmias, sinus bradycardia (< 40 bpm), sinus arrhythmia, and periods of atrial and ventricular ectopy (Reference). During the data collection period in MARVEL 2, ECG, electrogram, accelerometer waveforms, and device marker data were obtained; this was collected either after initial implant and follow-up or, for patients with previously placed devices, during a single encounter. The average monitoring period was 153 minutes. The study included 73 patients with normal sinus node function and varying degrees of AV block.While the number of patients with variable AV conduction was small (5), the investigators found that the rhythm checks allowed for appropriate mode adjustments during the study period. During periods of AV block, as expected, 99.9% ventricular pacing was observed while during 1:1 AV conduction only 0.2% pacing was observed. Ventricular pacing was monitored in patients with 1:1 AV conduction using conventional VVI pacing and MARVEL 2 programming. MARVEL 2 programming using the AV conduction mode switch algorithm resulted in a reduction in ventricular pacing from 22.8% to 0.2% (n=18). Reducing the burden of ventricular pacing is an important enhancement to the system with the potential to minimize pacing-induced cardiomyopathy.5One potential pitfall of atrial sensing addressed by this study is tracking of atrial arrhythmias. While the sample size was small (n=7), tracking of atrial fibrillation resulting in pacing at the upper tracking rate was not observed in any of the patients. In one patient with atrial flutter, intermittent atrial tracking did occur but did not result in tachycardia. In contrast to atrial rate based mode switching used in conventional dual-chamber pacemakers, the behavior of the MARVEL 2 algorithm during atrial fibrillation is dictated by the sensed ventricular rate. With the AV conduction mode switch enabled, if the ventricular rate is above 40 bpm, the pacing mode will be VVI at 40 bpm. If rates are less than 40 bpm, the pacing mode will be VDD. In the context of atrial fibrillation, reduced atrial contractility results in lack of mechanical sensing, and pacing at the lower rate is observed. In this small sample size, atrial arrhythmias did not result in device tracking resulting in tachycardia. Further investigation in a larger number of patients is warranted to better characterize these findings and to assess pacing behavior during more organized atrial arrhythmias which could result in mechanical sensing (atrial tachycardia and atrial flutter, for example).While the MARVEL 2 programming seems to perform well in the setting of atrial fibrillation or intermittent complete AV block, there are some potential pitfalls. AV conduction mode switch behavior is based on sensed ventricular rates with a threshold of 40 bpm; this cutoff is not currently programmable. Any ventricular sensed rhythm with a rate greater than 40 bpm will result in the device continuing at VVI 40. For example, in a patient with sinus rhythm at 90 bpm and 2:1 AV conduction, the device would not track the atrium and pace at 90 bpm, but rather remain VVI 40 because the ventricular sensed rate is above 40 bpm. The same would be observed in patients with junctional or ventricular escape rhythms >40 bpm. In this sense, pacing could be inappropriately inhibited during a potentially hemodynamically significant rhythm. For this reason, in our opinion, the AV conduction mode switch algorithm should be disabled in the majority of patients with AV block as this physiology is dynamic and sudden loss of rate support can have deleterious consequences. While the activity mode switch algorithm may address some of these concerns real world data are needed for validation.There is no question that the functionality and indications for leadless pacemakers will continue to expand. In current guidelines, which predate the development of the Micra AVTM, single chamber ventricular pacing is only recommended in patients with AV block and permanent atrial fibrillation, a low burden of anticipated pacing, or substantial comorbidities.6 Given the potential for lower complication rates compared with transvenous systems, Micra AV may be a superior option in some patients with complete heart block and preserved ventricular function. However, with the advent of conduction system pacing, the decreased risks of a leadless system have to be balanced with the relative risk of long term right ventricular pacing. Although the results will need to be validated with larger, longer-term studies, which are underway (Clinical trials.gov NCT04245345), these data indicate that Micra AVTM is likely to perform well in the setting of atrial arrhythmias. In patients with variable AV conduction, there are certainly pitfalls to the AV conduction mode switch algorithm, many of which could be avoided by the ability to program the mode switch VVI rate. While leadless pacing is often considered in patients with multiple comorbidities at high risk of complications from a transvenous system, we may be on the cusp of a dramatic paradigm shift. The technological developments and success of leadless pacing to date prompt the question of when, and not if, leadless dual chamber pacing and potentially even cardiac resynchronization will be available.References:1. Reynolds D, Duray GZ, Omar R, et al. A Leadless Intracardiac Transcatheter Pacing System. https://doi.org/10.1056/NEJMoa1511643. doi:10.1056/NEJMoa15116432. El-Chami MF, Al-Samadi F, Clementy N, et al. Updated performance of the Micra transcatheter pacemaker in the real-world setting: A comparison to the investigational study and a transvenous historical control. Heart Rhythm . 2018;15(12):1800-1807. doi:10.1016/j.hrthm.2018.08.0053. Duray GZ, Ritter P, El-Chami M, et al. Long-term performance of a transcatheter pacing system: 12-Month results from the Micra Transcatheter Pacing Study. Heart Rhythm . 2017;14(5):702-709. doi:10.1016/j.hrthm.2017.01.0354. Steinwender C, Khelae SK, Garweg C, et al. Atrioventricular Synchronous Pacing Using a Leadless Ventricular Pacemaker: Results From the MARVEL 2 Study. JACC Clin Electrophysiol . 2020;6(1):94-106. doi:10.1016/j.jacep.2019.10.0175. Merchant FM, Mittal S. Pacing induced cardiomyopathy. J Cardiovasc Electrophysiol . 2020;31(1):286-292. doi:10.1111/jce.142776. Kusumoto Fred M., Schoenfeld Mark H., Barrett Coletta, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation . 2019;140(8):e382-e482. doi:10.1161/CIR.0000000000000628

oluwaseun adeola

and 3 more

Pulmonary vein isolation (PVI) is the cornerstone of catheter ablation for atrial fibrillation (AF) However AF recurrence after a single ablation procedure is common and often attributed to ineffective lesion delivery during PVI. In this issue of the Journal of Cardiovascular Electrophysiology, Chen et al reported their experience with 122 patients who underwent an ablation index-high power (AI-HP) strategy RF ablation for AF using 50W power, targeting AI values of 550 on the anterior left atrium (LA), 400 on the posterior wall and inter-lesion distance (ILD) 6mm. They achieved 1st pass PVI in 96.7% of cases, mean RF time was 11.5min and total procedure time was only 55.8min. All patients had 72h-Holter monitor and trans-telephonic follow up. They reported 89.4% arrhythmia free survival among patients with paroxysmal AF and 80.4% among patients with persistent AF at 15-month follow up. Sixty (49%) patients had luminal esophageal temperature (LET) >390C out of which 3 (2.5%) had asymptomatic endoscopic esophageal erosions/erythema. Four (3%) patients had clinically apparent steam pops during ablation with no adverse clinical sequela. While AI-HP guided RF ablation may be an attractive strategy for PVI that likely reduces procedure times and probably has comparable efficacy to conventional ablation settings, its safety requires further evaluation. Feedback from the ablated tissue may need to be incorporated into optimized ablation energy parameters to further improve outcomes.