Very High Power Short Duration Ablation: It Takes Two to Make a Thing Go Right? Samuel D. Maidman, M.D. & Chirag R. Barbhaiya, M.D.From the Leon H. Charney Division of Cardiology, NYU Grossman School of Medicine, NYU Langone Health, New York, New York, USA

Dear Editor, We read with great interest the article recently published in Journal of Cardiovascular Electrophysiology, “Left atrial appendage dimension predicts elevated brain natriuretic peptide in nonvalvular atrial fibrillation” by Cook JA. et al. 1 The authors have studied the relation between Brain natriuretic peptide (BNP) elevations and left atrial appendage measurements in patients who referred for left atrial appendage (LAA) occlusion in patients with nonvalvular atrial fibrillation (AF). BNP release is largely from the ventricles and it is also dynamically dependent on myocardial stretch and fluid volume status. However, it seems difficult to prove that BNP levels are directly related to the LAA measurements. Correlating BNP elevation only with left atrial or LAA measurements means ignoring left ventricular strain. Considering that these patients were referred for LAA occlusion and had a high CHA 2DS 2-VASc score, and not taking heart failure with preserved ejection fraction into account may lead to errors in interpreting the results. Moreover, it should be evaluated that the left atrial appendage may undergo remodeling or enlargement as a result of the left ventricular end-diastolic pressure increase. In this case, although the study is valuable, remains a cross-sectional study and a snapshot of the correlation of BNP and LAA. Second, it should be disclosed whether patients have paroxysmal or chronic AF and how long the patient has had AF. A relationship was established between LAA dimensions and BNP in the study, it is essential that the duration of AF should be considered and subgroup analyses should be evaluated if possible, since AF has a significant effect on BNP release. We appreciate this study and believe that a more detailed evaluation including left ventricular evaluation and prospectively monitored LAA and BNP would yield more realistic results. In addition, we think that it would be useful to evaluate midregional pro-A-type natriuretic (MR-proANP) in LAA studies, which is specific to the left atrial enlargement and similar physiology to BNP. 2

A 65 year-old with history of prior ablations for regular narrow QRS short- RP tachycardia presented with recurrence of palpitations. An electrophysiological study showed long VA tachycardia with concentric atrial activation with a left ventricular origin extrastimulus delivered during His refractoriness, advancing the next ‘A’. A HRVPB can only reset an ORT if it ‘pulls in’ the local V at the ventricular insertion of an accessory pathway. As showcased in this case, erudite analysis of the pattern of perturbation of local ventricular electrograms is of paramount significance when interpreting responses to this maneuver. This concept when fortified with a heightened index of clinical suspicion for mitral annular block, anatomical knowledge of the pattern of LA-CS muscular connections, and pathway orientation, led to accurate electrophysiological diagnosis and management.

In this issue of the Journal, Kushnir, et al. provide a report of temporal trends in first time ablation at a large academic medical center over a 10 year period. This editorial provides commentary on the report.

Response to “Delay in AF ablation costs lives”Andrew J. Sessions BS1, Heidi T. May, PhD, MSPH2, Brian G. Crandall, MD2, John D. Day, MD3, Michael J. Cutler DO, PhD2, Christopher A. Groh MD4, Leenapong Navaravong MD4, Ravi Ranjan MD, PhD4, Benjamin A. Steinberg MD, MHS4, T. Jared Bunch, MD4Corresponding Author: Dr. T. Jared BunchUniversity of Utah School of Medicine, Salt Lake City, Utah, USADepartment of Cardiology, Intermountain Heart Institute, Intermountain Medical Center, Salt Lake City, Utah, USASt. Marks Hospital, Salt Lake City, UtahDepartment of Internal Medicine, Division of Cardiology, University Hospital, Salt Lake City, Utah, USAAddress for correspondence: T. Jared Bunch, M.D.University of Utah School of Medicine Division of Cardiology, Department of Internal Medicine 50 N Medical Drive Salt Lake City, Utah 84132 Phone: 801-585-7676Short Title: Impact of delays in catheter ablationFunding : None

A document by E. Heist. Click on the document to view its contents.

Acknowledgements: On behalf of the Steering Committee of the Medical Device Innovation Consortium Initiative on Early Feasibility Studies in Cardiac Electrophysiology

Safety and Effect on Length of Stay of Intravenous Sotalol Initiation for Arrhythmia ManagementDiane H. Rizkallah, BS; Marwan M. Refaat, MDDivision of Cardiology, Department of Internal Medicine, American University of Beirut Medical Center, Beirut, LebanonRunning Title: Safety and Effect on LOS of IV SotalolWords: 598 (excluding the title page and references)Keywords: Heart Diseases, Cardiovascular Diseases, Cardiac Arrhythmias, Safety, Length of StayFunding: NoneDisclosures: NoneCorresponding Author:Marwan M. Refaat, MD, FACC, FAHA, FHRS, FRCPTenured Professor of MedicineTenured Professor of Biochemistry and Molecular GeneticsVan Dyck Medical Educator and Director of the Cardiovascular Fellowship ProgramDepartment of Internal Medicine, Cardiovascular Medicine/Cardiac ElectrophysiologyAmerican University of Beirut Faculty of Medicine and Medical CenterPO Box 11-0236, Riad El-Solh 1107 2020- Beirut, LebanonUS Address: 3 Dag Hammarskjold Plaza, 8th Floor, New York, NY 10017, USAOffice: +961-1-350000/+961-1-374374 Extension 5353 or Extension 5366 (Direct)Email: mr48@aub.edu.lbSotalol is a class III antiarrhythmic drug with beta-adrenergic blocking activity, used to manage both supraventricular and ventricular arrhythmias. It is available in both oral and intravenous formulations[1]. The FDA approved intravenous Sotalol in March 2020. Sotalol is known to cause QTc prolongation with serum sotalol concentration linearly correlating with QTc length regardless of the route of administration [2,3], with women being at higher risk than men[4]. QTc interval prolongation is one of many parameters that is associated with cardiovascular mortality [5]. QTc prolongation may lead to polymorphic ventricular tachycardia/Torsade de Pointes which is a potentially lethal condition that is acquired from medications or due to an underlying channelopathy predisposing to sudden cardiac arrest[6]. Additional adverse effects of sotalol may include hypotension, bradycardia and AV block[7,8]. Nevertheless, since its approval, IV sotalol has been successfully and safely used in both adult and pediatric patient populations for the management of arrhythmias in acute and chronic settings [9,10,11,12]. Initiation of sotalol therapy with PO loading requires 5 successive oral doses over a 3-day hospital stay for monitoring, at an estimated cost of $2931.55 per day [13]. In 2020, a protocol for IV loading of sotalol was developed using data modeling. This protocol was hypothesized to allow a significant reduction in the length of hospitalization, and thus in the incurred costs[14]. However, there has not been any large-scale implementation of this protocol, nor any comparison of its safety profile and efficacy to that of the traditional oral loading protocol.This study by Liu et al. is a nonrandomized clinical trial in which 29 patients underwent IV sotalol loading. They were compared by chart review to 20 patients who underwent PO sotalol loading in the same timeframe. The indication for sotalol initiation in both cases was for primary atrial or ventricular arrhythmias. The study’s main aim was to assess the safety profile of IV sotalol loading while comparing the length of hospitalization to that required for PO sotalol loading. The same exclusion and inclusion criteria were applied to both groups. Notably, patients with significantly depressed LVEF and creatinine clearance were excluded. The study revealed that safety outcomes were similar in both groups but that IV sotalol loading led to significantly shorter hospital stays. It also found that QT or QTc in patients receiving IV sotalol was similar at the conclusion of the one-hour infusion to that at discharge.These findings support the use of IV loading for sotalol initiation, as they suggest it requires shorter hospital stays than PO loading with similar safety profiles. As shorter hospital stays translate into lower patient days, lower costs, and these results suggest IV sotalol loading is more cost-efficient than its oral counterpart. They also suggest that the maximal increase in QT or QTc length following sotalol initiation is attained by the end of IV loading, thus indicating that patients may be discharged within less than 24 hours of drug initiation.While this study offered valuable insight, its design had significant limitations. Firstly, this was not a randomized clinical trial. A comparison of baseline characteristics between the two populations studied revealed a significantly higher proportion of females in the oral group, which may have inherently skewed outcomes related to QT and QTc length.Secondly, the sample size was small, with no long-term follow-up. Lastly, patients with significantly depressed GFR or LVEF, particularly prone to developing adverse effects with sotalol use, were excluded from the study. Randomized clinical trials examining the short-term and long-term safety of IV sotalol loading and the optimal length of hospitalization are needed, and such efforts are already underway.References:Batul, S. A., & Gopinathannair, R. (2017). Intravenous Sotalol - Reintroducing a Forgotten Agent to the Electrophysiology Therapeutic Arsenal. Journal of atrial fibrillation , 9 (5), 1499. https://doi.org/10.4022/jafib.1499Somberg, J. C., Preston, R. A., Ranade, V., & Molnar, J. (2010). QT prolongation and serum sotalol concentration are highly correlated following intravenous and oral sotalol. Cardiology , 116 (3), 219–225. https://doi.org/10.1159/000316050Barbey, J. T., Sale, M. E., Woosley, R. L., Shi, J., Melikian, A. P., & Hinderling, P. H. (1999). Pharmacokinetic, pharmacodynamic, and safety evaluation of an accelerated dose titration regimen of sotalol in healthy middle-aged subjects. Clinical pharmacology and therapeutics , 66 (1), 91–99. https://doi.org/10.1016/S0009-9236(99)70058-5Somberg, J. C., Preston, R. A., Ranade, V., Cvetanovic, I., & Molnar, J. (2012). Gender differences in cardiac repolarization following intravenous sotalol administration. Journal of cardiovascular pharmacology and therapeutics , 17 (1), 86–92. https://doi.org/10.1177/1074248411406505Al-Kindi SG, Refaat M, Jayyousi A, Asaad N, Al Suwaidi J, Abi Khalil C. Red Cell Distribution Width is Associated with All-Cause and Cardiovascular Mortality in Patients with Diabetes. Biomed Res Int 2017; 2017: 5843702Refaat MM, Hotait M, Tseng ZH: Utility of the Exercise Electrocardiogram Testing in Sudden Cardiac Death Risk Stratification.Ann Noninvasive Electrocardiol 2014; 19(4): 311-318.Marill, K. A., & Runge, T. (2001). Meta-analysis of the Risk of Torsades de Pointes in patients treated with intravenous racemic sotalol. Academic emergency medicine,  8 (2), 117–124. https://doi.org/10.1111/j.1553-2712.2001.tb01275.xMacNeil, D. J., Davies, R. O., & Deitchman, D. (1993). Clinical safety profile of sotalol in the treatment of arrhythmias. The American journal of cardiology , 72 (4), 44A–50A. https://doi.org/10.1016/0002-9149(93)90024-7Malloy-Walton, L. E., Von Bergen, N. H., Balaji, S., Fischbach, P. S., Garnreiter, J. M., Asaki, S. Y., Moak, J. P., Ochoa, L. A., Chang, P. M., Nguyen, H. H., Patel, A. R., Kirk, C., Sherman, A. K., Avari Silva, J. N., & Saul, J. P. (2022). IV Sotalol Use in Pediatric and Congenital Heart Patients: A Multicenter Registry Study. Journal of the American Heart Association , 11 (9), e024375. https://doi.org/10.1161/JAHA.121.024375Borquez, A. A., Aljohani, O. A., Williams, M. R., & Perry, J. C. (2020). Intravenous Sotalol in the Young: Safe and Effective Treatment With Standardized Protocols. JACC. Clinical electrophysiology , 6 (4), 425–432. https://doi.org/10.1016/j.jacep.2019.11.019Kerin, N. Z., & Jacob, S. (2011). The efficacy of sotalol in preventing postoperative atrial fibrillation: a meta-analysis. The American journal of medicine , 124 (9), 875.e1–875.e8759. https://doi.org/10.1016/j.amjmed.2011.04.025Milan, D. J., Saul, J. P., Somberg, J. C., & Molnar, J. (2017). Efficacy of Intravenous and Oral Sotalol in Pharmacologic Conversion of Atrial Fibrillation: A Systematic Review and Meta-Analysis. Cardiology , 136 (1), 52–60. https://doi.org/10.1159/000447237Varela, D. L., Burnham, T. S., T May, H., L Bair, T., Steinberg, B. A., B Muhlestein, J., L Anderson, J., U Knowlton, K., & Jared Bunch, T. (2022). Economics and outcomes of sotalol in-patient dosing approaches in patients with atrial fibrillation. Journal of cardiovascular electrophysiology , 33 (3), 333–342. https://doi.org/10.1111/jce.15342Somberg, J. C., Vinks, A. A., Dong, M., & Molnar, J. (2020). Model-Informed Development of Sotalol Loading and Dose Escalation Employing an Intravenous Infusion. Cardiology research , 11 (5), 294–304. https://doi.org/10.14740/cr1143

Pulmonary Vein Isolation-induced Vagal Nerve Injury and Gastric Motility DisordersBachir Lakkiss, MD; Marwan M. Refaat, MDDivision of Cardiology, Department of Internal Medicine, American University of Beirut Medical Center, Beirut, LebanonRunning Title: PVI-induced vagal nerve injury and gastric motility disordersWords: 665 (excluding the title page and references)Keywords: Heart Diseases, Cardiovascular Diseases, Cardiac Arrhythmias, Atrial Fibrillation, Catheter Ablation, Pulmonary Vein IsolationFunding: NoneDisclosures: NoneCorresponding Author:Marwan M. Refaat, MD, FACC, FAHA, FHRS, FRCPTenured Professor of MedicineTenured Professor of Biochemistry and Molecular GeneticsVan Dyck Medical Educator and Director of the Cardiovascular Fellowship ProgramDepartment of Internal Medicine, Cardiovascular Medicine/Cardiac ElectrophysiologyAmerican University of Beirut Faculty of Medicine and Medical CenterPO Box 11-0236, Riad El-Solh 1107 2020- Beirut, LebanonUS Address: 3 Dag Hammarskjold Plaza, 8th Floor, New York, NY 10017, USAOffice: +961-1-350000/+961-1-374374 Extension 5353 or Extension 5366 (Direct)Email: mr48@aub.edu.lbAtrial fibrillation (AF) is the most prevalent heart rhythm abnormality worldwide. An estimated three to six million people in the United States have AF. It is expected that this number is likely to double by 2050, making AF a significant public health burden. (1) AF is a leading cause of stroke and thromboembolism and is associated with a reduced quality of life. (2) Furthermore, it is linked to an increased mortality in both men and women, with an OR for death of 1.5 in men and 1.9 in women. (3) Medical expenditures for AF are significant, ranging from an annual cost of $1,632 to $21,099, with acute care accounting for the largest cost component in addition to anticoagulation therapy, which accounted for almost one-third of these costs. (4) The four pillars of AF management include rhythm control, rate control, stroke prevention and risk factor management. (5, 6) While antiarrhythmic drugs are used in some patients for AF rhythm control, AF ablation using pulmonary vein isolation (PVI) is regarded as the major modality for rhythm control. (6)The vagal nerve provides most of the parasympathetic innervation to the abdominal organs, including the stomach, esophagus, and a significant portion of the intestines. It serves a major role in the regulation of gastric and esophageal motility, in addition to maintaining lower esophageal sphincter tone. (7-9) Due to the relatively close vicinity of the vagal nerve plexus located on the anterior surface of the esophagus and the left atrial posterior wall, the thermal energy utilized during ablation can result in uncommon but potentially fatal complications such as esophageal perforation and atrial-esophageal fistula formation. (10-12) In addition, radiofrequency ablation for AF is associated with non-fatal complications such as an increased risk of gastric motility disorders and acid reflux. (13, 14)In the current issue of the Journal of Cardiovascular Electrophysiology, Meininghaus et al. recruited 85 patients to assess the incidence of ablation-induced vagal nerve injury (VNI) using both cryoballoon and radiofrequency ablation. Although many cases of VNI induced by PVI have been documented previously, this is one of the first studies to utilize electrophysiologic measurements of gastric motility (EGG) using cutaneous electrodes to record the electrical activity of the stomach two days prior to and two days after the procedure. (15-17) Moreover, the authors have used endoscopy to detect lesions such as erosions, ulcers, and perforations in the esophagus one week prior to and within two days of the procedure.The findings from this study add to our understanding of one of the complications of PVI in patients with AF (13, 14). One of the key outcomes the researchers observed was the perceived direct link between VNI and preexisting esophageal vulnerability. The authors have found that patients who had preexisting esophagitis had an elevated risk of developing VNI. In addition, the authors identified that in patients in whom EGG showed VNI, the elevated risk of ablation-induced endoscopic pathology was present in the post-procedure endoscopy. Furthermore, another significant finding was the detection of VNI on EGG in approximately one-third of PVI patients, irrespective of energy source, whether high power short duration, or moderate power moderate duration. These findings did not corroborate other studies, which showed that titration of the duration of the ablation energy could prevent VNI in patients undergoing AF ablation. (18)Overall, the authors should be commended for their tremendous efforts in attempting to understand the intricate pathophysiology and the association of esophageal lesions, atrial-esophageal fistula formation, and vagal nerve injury following PVI using EGG. Certainly, the results of this study have tremendous clinical implications. EGG could have a very important role in the prevention of atrial-esophageal fistula formation in the future. The article had a few limitations, mainly that the results were from a single-center study. Further studies incorporating additional patients from different medical centers should be conducted to better understand the complex pathophysiology of vagal nerve injury and gastric motility disorders following PVI. Advances in esophageal protection technologies will help in decreasing esophageal lesions during PVI. (19-20)References1. Miyasaka Y, Barnes ME, Gersh BJ, Cha SS, Bailey KR, Abhayaratna WP, et al. Secular Trends in Incidence of Atrial Fibrillation in Olmsted County, Minnesota, 1980 to 2000, and Implications on the Projections for Future Prevalence. Circulation. 2006;114(2):119-25. doi: doi:10.1161/CIRCULATIONAHA.105.595140.2. Jalloul Y, Refaat MM. IL-6 Rapidly Induces Reversible Atrial Electrical Remodeling by Downregulation of Cardiac Connexins. J Am Heart Assoc. 2019;8(16):e013638. Epub 2019/08/20. doi: 10.1161/jaha.119.013638. PubMed PMID: 31423871; PubMed Central PMCID: PMCPMC6759896.3. Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998;98(10):946-52. Epub 1998/09/16. doi: 10.1161/01.cir.98.10.946. PubMed PMID: 9737513.4. Wodchis WP, Bhatia RS, Leblanc K, Meshkat N, Morra D. A review of the cost of atrial fibrillation. Value Health. 2012;15(2):240-8. Epub 2012/03/22. doi: 10.1016/j.jval.2011.09.009. PubMed PMID: 22433754.5. Lakkis B, Refaat MM. Is esophageal temperature management needed during cryoballoon ablation for atrial fibrillation? Journal of Cardiovascular Electrophysiology. 2022;33(12):2567-8. doi: https://doi.org/10.1111/jce.15725.6. Chung MK, Refaat M, Shen W-K, Kutyifa V, Cha Y-M, Di Biase L, et al. Atrial Fibrillation: JACC Council Perspectives. Journal of the American College of Cardiology. 2020;75(14):1689-713. doi: https://doi.org/10.1016/j.jacc.2020.02.025.7. Richards WG, Sugarbaker DJ. Neuronal control of esophageal function. Chest Surg Clin N Am. 1995;5(1):157-71. Epub 1995/02/01. PubMed PMID: 7743145.8. Hsu M, Safadi AO, Lui F. Physiology, Stomach. StatPearls. Treasure Island (FL): StatPearls PublishingCopyright © 2022, StatPearls Publishing LLC.; 2022.9. Goyal RK, Chaudhury A. Physiology of normal esophageal motility. J Clin Gastroenterol. 2008;42(5):610-9. Epub 2008/03/28. doi: 10.1097/MCG.0b013e31816b444d. PubMed PMID: 18364578; PubMed Central PMCID: PMCPMC2728598.10. Kapur S, Barbhaiya C, Deneke T, Michaud GF. Esophageal Injury and Atrioesophageal Fistula Caused by Ablation for Atrial Fibrillation. Circulation. 2017;136(13):1247-55. doi: doi:10.1161/CIRCULATIONAHA.117.025827.11. D’Avila A, Ptaszek LM, Yu PB, Walker JD, Wright C, Noseworthy PA, et al. Images in cardiovascular medicine. Left atrial-esophageal fistula after pulmonary vein isolation: a cautionary tale. Circulation. 2007;115(17):e432-3. Epub 2007/05/02. doi: 10.1161/circulationaha.106.680181. PubMed PMID: 17470703.12. Sánchez-Quintana D, Cabrera JA, Climent V, Farré J, Mendonça MCd, Ho SY. Anatomic Relations Between the Esophagus and Left Atrium and Relevance for Ablation of Atrial Fibrillation. Circulation. 2005;112(10):1400-5. doi: doi:10.1161/CIRCULATIONAHA.105.551291.13. Shah D, Dumonceau J-M, Burri H, Sunthorn H, Schroft A, Gentil-Baron P, et al. Acute Pyloric Spasm and Gastric Hypomotility: An Extracardiac Adverse Effect of Percutaneous Radiofrequency Ablation for Atrial Fibrillation. Journal of the American College of Cardiology. 2005;46(2):327-30. doi: https://doi.org/10.1016/j.jacc.2005.04.030.14. Park S-Y, Camilleri M, Packer D, Monahan K. Upper gastrointestinal complications following ablation therapy for atrial fibrillation. Neurogastroenterology & Motility. 2017;29(11):e13109. doi: https://doi.org/10.1111/nmo.13109.15. Choi SW, Kang SH, Kwon OS, Park HW, Lee S, Koo BS, et al. A case of severe gastroparesis: indigestion and weight loss after catheter ablation of atrial fibrillation. Pacing Clin Electrophysiol. 2012;35(3):e59-61. Epub 2010/10/05. doi: 10.1111/j.1540-8159.2010.02912.x. PubMed PMID: 20883511.16. Lakkireddy D, Reddy YM, Atkins D, Rajasingh J, Kanmanthareddy A, Olyaee M, et al. Effect of atrial fibrillation ablation on gastric motility: the atrial fibrillation gut study. Circ Arrhythm Electrophysiol. 2015;8(3):531-6. Epub 2015/03/17. doi: 10.1161/circep.114.002508. PubMed PMID: 25772541.17. Kuwahara T, Takahashi A, Takahashi Y, Kobori A, Miyazaki S, Takei A, et al. Clinical characteristics and management of periesophageal vagal nerve injury complicating left atrial ablation of atrial fibrillation: lessons from eleven cases. J Cardiovasc Electrophysiol. 2013;24(8):847-51. Epub 2013/04/05. doi: 10.1111/jce.12130. PubMed PMID: 23551640.18. KUWAHARA T, TAKAHASHI A, KOBORI A, MIYAZAKI S, TAKAHASHI Y, TAKEI A, et al. Safe and Effective Ablation of Atrial Fibrillation: Importance of Esophageal Temperature Monitoring to Avoid Periesophageal Nerve Injury as a Complication of Pulmonary Vein Isolation. Journal of Cardiovascular Electrophysiology. 2009;20(1):1-6. doi: https://doi.org/10.1111/j.1540-8167.2008.01280.x.19. D’Avila A, Ptaszek LM, Yu PB, Walker JD, Wright C, Noseworthy PA, Myers A, Refaat M, Ruskin JN: Left Atrial-Esophageal Fistula After Pulmonary Vein Isolation. Circulation May 2007; 115(17): e432-3.20. El Moheb MN, Refaat MM. Protecting the Esophagus During Catheter Ablation: Evaluation of a Novel Vacuum Suction-Based Retractor. J Cardiovasc Electrophysiol Jul 2020; 31 (7): 1670-1671.

Editorial

Ventricular tachycardia is a major cause of sudden death. Several pharmacological and device-based therapies in recent years have delayed the progression of heart failure and have improved survival. A new study reveals a significant increase in age-adjusted mortality from ventricular tachycardia over the past 13 years, with higher mortality in men, black Americans and patients from the Southern United States. These findings reinforce the previous observations made on the influence of age, gender, ethnicity and geography on cardiovascular outcomes. The use of ICD 10 codes to ascertain cause of death limits differentiation between ventricular tachycardia as the true underlying mechanism leading to death and the presence of ventricular tachycardia in patients dying from other causes. While the insights gained from the report on contemporary ventricular tachycardia related mortality in the general population with cardiovascular disease is hypothesis generating, further studies are needed to delineate ventricular tachycardia as a proximate cause of death from an association.

I am not sure this editorial comment deserves an abstract. Plesae advise.

Left anterior descending (LAD) coronary arterial injury is an underappreciated and rare consequence of ablation in the right ventricular outflow tract (RVOT). The authors present five cases of acute or subacute LAD injury after RVOT ablation. Most patients had fairly extensive ablation and two had coincident cardiac perforation. The patients reported also had a strikingly similar ECG morphology of their spontaneous ventricular arrhythmias. The authors’ report serves an important cautionary tale regarding ablation of intramural septal VAs.

Predictive Modeling of Lead Durability, An Important Step ForwardGeorge H. Crossley MD, FHRS, FACCVanderbilt Heart and Vascular Institute, Nashville, TN; and Cardiovascular Diseases Section, Vanderbilt University School of MedicineRWI: Dr. Crossley consults for Medtronic, Boston Scientific, and Phillips.Running Title: Lead Durability AnalysisWord Count: 893

Radiofrequency (RF) ablation for the treatment of atrial fibrillation has gained widespread acceptance since the concept was introduced by Haissaguerre et al a quarter of a century ago. High power short duration ablation has been widely adopted in the management of atrial fibrillation. Evidence for combining lesion size index and high power short duration ablation is lacking. In this issue of the journal, Cai et al evaluated the combination of HPSD with LSI with a focus on long-term efficacy.

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Catheter ablation of atrial fibrillation (AF) in patients with heart failure associated with a reduced EF (HFrEF) was associated with a significantly lower rate of a composite endpoint of death from any cause or hospitalization for worsening heart failure (HF) than medical therapy in the CASTLE-AF trial. In patients with HF and also with a preserved EF (HFpEF), AF is known to be associated with increased mortality. Although the particular benefit in patients with an EF >35% may suggest the need for prospective randomized control trial data in patients with HF to assess the role of ablation as a first-line therapy as Sessions AJ, et al. stated, we believe at present that 1) whether there is structural heart disease detected by cardiac images and 2) whether the left atrial voltage is generally low, should be assessed “before ablation” in each patient with HF to achieve a successful ablation.

Introduction: Pulmonary vein isolation (PVI) using radiofrequency (RF) and cryoballoon (Cryo) ablation are standard approaches for rhythm control of symptomatic atrial fibrillation. Both strategies involve scar formation of the left atrium (LA). There have been few studies investigating the differences in residual fibrosis and scar formation in patients undergoing RF and Cryo using cardiac magnetic resonance imaging (CMR).     Methods: The current study is a sub-analysis of the control arm of the Delayed-Enhancement MRI Determinant of Successful Catheter Ablation of Atrial Fibrillation study (DECAAF II). The study was a multicenter, randomized, controlled, single blinded trial that evaluated atrial arrhythmia recurrence (AAR) between PVI alone and PVI plus CMR atrial fibrosis guided ablation. Pre-ablation CMR and 3–6-month post ablation CMR were obtained to assess baseline LA fibrosis and scar formation respectively.     Results: Of the 843 patients randomized in the DECAAF II trial, we analyzed the 408 patients in the primary analysis control arm that received standard PVI. Five patients received combined RF and Cryo ablations so were excluded from this sub-analysis. Of the 403 patients analyzed, 345 underwent RF and 58 Cryo. The average procedure duration was 146 minutes for RF and 103 minutes for Cryo (p = 0.001). The rate of AAR at ~15 months occurred in 151 (43.8%) patients in the RF group and 28 (48.3%) patients in the Cryo group (p = 0.62). On 3-month post CMR the RF arm had significantly more covered fibrosis (3.6% vs. 3.0%, p = 0.04) and scar (8.8% vs. 6.4%, p = 0.001) compared to Cryo. Patients with ≥ 6.5% LA scar on 3-month post CMR had less AAR independent of ablation technique (RF p = 0.009, Cryo p = 0.02). Cryo caused a greater percentage of right and left pulmonary vein (PV) scar (p = 0.04, p = 0.02) and less non-PV scar (p = 0.009) compared to RF. On Cox regression Cryo patients free of AAR had a greater percentage of left PV scar (p = 0.01) and less non-PV scar (p = 0.004) compared to RF free of AAR.     Conclusion: In this sub-analysis of the control arm of the DECAAF II trial, there was no significant difference in the rate of AAR in patients undergoing PVI alone between RF vs. Cryo. Post ablation LA scar ≥ 6.5% predicted freedom from AAR, independent of ablation technique. Cryo formed a greater percentage of PV scar and less non-PV scar compared to RF, which may have prognostic implications.