Idiopathic Outflow Tract Ventricular Arrhythmia Ablation

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 9, No. 9Idiopathic Outflow Tract Ventricular Arrhythmia Ablation Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBIdiopathic Outflow Tract Ventricular Arrhythmia AblationAre We Ablating Too Much or Too Little? Pasquale Santangeli, MD, PhD and David J. Callans, MD Pasquale SantangeliPasquale Santangeli From the Cardiovascular Division, Hospital of the University of Pennsylvania, Philadelphia. and David J. CallansDavid J. Callans From the Cardiovascular Division, Hospital of the University of Pennsylvania, Philadelphia. Originally published13 Sep 2016https://doi.org/10.1161/CIRCEP.116.004537Circulation: Arrhythmia and Electrophysiology. 2016;9:e004537Outflow tract ventricular arrhythmias (OT-VAs) in the setting of an apparently normal heart are a common and perplexing clinical entity. The traditional belief that these arrhythmias have an entirely benign prognosis and excellent response to therapy with antiarrhythmic drugs and catheter ablation has been challenged by recent evidences reporting the presence of localized concealed cardiomyopathic substrates in many of these patients1,2 and large epidemiological studies showing an independent longitudinal association between VAs and the risk of heart failure and death,3 together with the disappointing results of randomized trials testing VA suppression with antiarrhythmic drug therapy and long-term catheter ablation outcome data from experienced centers reporting a recurrence rate of ≤30%.4,5 Although there are patients with no arrhythmia-related symptoms and normal left ventricular function who do not derive benefit from VA suppression regardless of the VA burden, achievement of durable VA suppression represents a relevant therapeutic end point to improve quality of life when arrhythmia-related symptoms are present4 or to reverse left ventricular systolic dysfunction in patients with VA-induced cardiomyopathy.6See Article by Yamada et alCatheter ablation remains the most important therapeutic option to eliminate OT-VAs.5 However, the complex 3-dimensional anatomic relationships between different adjacent structures in the right and left ventricular OTs pose substantial difficulties to mapping and ablation of VAs arising from this region.7–9 The reasons underlying ablation failure are multifactorial and include lack of accurate localization because of minimal ectopy available to map,10 safety concerns with ablation at the target site(s),7,11 recurrence of different VAs,4 and inability to access critical sites for mapping or ablation.7,12–14 In this regard, currently available mapping tools allow direct mapping and ablation of endocardial structures (ie, endocardial right or left OTs), coronary or pulmonic cusp region,15,16 or the epicardium via either a direct percutaneous approach or via the coronary venous system.7,9Intramural sites cannot be accessed for detailed mapping and ablation, and a definite determination of the site of origin of intramural VAs or of the best accessible adjacent anatomic site to deliver ablation (and the optimal ablation approach) are major challenges.12–14,17 In select instances, direct intramural recording from a small caliber multipolar catheter or from partially insulated unipolar recording/pacing wires advanced to a septal perforator branch of the anterior interventricular vein has been shown to identify intramural VAs.12 However, even these techniques are highly dependent on the specific anatomic location of the septal perforator branch—which is variable—18 and, more importantly, provide access to only one specific intramural site (ie, the upper septum), whereas intramural VAs can arise also from other sites that cannot be directly recorded.Clinical studies on intramural VAs have used a combination of criteria to define this type of arrhythmias which include the following: (1) lack of pacemap match from accessible endocardial and epicardial sites together with suboptimal activation and similarly early at multiple adjacent endo-epicardial sites, (2) improvement of pacemap match with dual-site pace mapping at the earliest accessible breakthrough sites, (3) earliest activation within a septal perforator branch with pacemap match, (4) requirement for radiofrequency application from multiple adjacent sites to effectively eliminate the arrhythmia (Table).12,14,17 Using the latter definition, in this issue of Circulation: Arrhythmia and Electrophysiology, Yamada et al14 describe their institutional experience with left ventricular outflow tract VAs arising from intramural foci. The study comes from a respected group of investigators and provides substantial incremental clinical value for the management of intramural VAs. Out of a consecutive series of 82 patients, the authors identified 18 (22%) intramural VA cases that required either sequential or simultaneous unipolar radiofrequency ablation from both the endocardium and epicardium to successfully eliminate the arrhythmia. The differences between intramural VAs eliminated with sequential versus simultaneous ablation have been already reported by the same authors in a separate study.20 Of note, both 12-lead ECG features and mapping results of intramural VAs did not differ significantly from those classified as endocardial, that is, VAs successfully targeted from the endocardium only; similarly, the authors reported a great degree of overlap in ECG and mapping findings between intramural VAs successfully eliminated with sequential ablation compared with those undergoing simultaneous ablation.20 The most striking differences were observed between endocardial/intramural VAs and epicardial VAs, which is in line with previous reports.7,20,21 In particular, epicardial VAs presented higher R wave amplitude ratio in leads III/II and Q wave amplitude ratio in leads aVL/aVR, higher maximum deflection index, and overall longer electrogram-to-QRS at the earliest site. These findings are particularly useful to decide when to access the coronary venous system for mapping and ablation in the individual patients. For instance, an endocardial pace map at the site of earliest activation displaying a smaller R-wave amplitude ratio in leads III/II or Q-wave amplitude ratio in aVL/aVR compared with the clinical VA may prompt for coronary venous instrumentation for further mapping. On the contrary, the lack of peculiar signature signs distinguishing intramural VAs from endocardial VAs supports the concept that current mapping approaches are unable to correctly identify the true site of origin of OT-VAs and that a distinction between the site of origin and the site of successful ablation must be made. For instance, it is possible that some VAs classified by Yamada et alas endocardial (or also epicardial) had, indeed, an intramural site of origin despite the fact that successful ablation could be delivered from an adjacent endocardial (or epicardial) site. In this regard, information on the time to VA suppression and regional wall thickness that could be indexed as distance between the endocardium and the epicardium on the 3-dimensional mapping system may have provided important clues on why some patients responded better to endocardial or epicardial ablation only compared with those who required sequential or simultaneous ablation from multiple sites. We have previously shown that successful ablation of OT-VAs from an adjacent vantage point can be achieved when the anatomic distance from the selected site of origin is <13.5 mm.22 The possible benefit of ablation from anatomically adjacent structures such as the coronary cusp region or the most leftward aspect of the septal right ventricular OT was not evaluated in this study. Finally, whether intramural VAs could be effectively targeted with more prolonged lesion delivery at the single earliest endocardial or epicardial site was not evaluated. Per study protocol, radiofrequency lesions were delivered for 10 seconds and extended to ≤30 to 60 seconds only in case of VA suppression during the initial 10 seconds. In our experience, complete suppression of VAs from an adjacent vantage point may require up to 3- to 5-min lesions. In rare instances, in case of unsuccessful ablation with sequential prolonged unipolar ablation at the earliest site and anatomically adjacent regions, we also have adopted the simultaneous unipolar ablation approach described by Yamada et al20 with good results. We have preferred this approach over bipolar energy application23 to guarantee adequate energy delivery at both catheter tip electrodes when positioned in regions with impedance mismatch (like the coronary venous system or the left ventricle/right ventricle endocardium) or whenever there is catheter contact mismatch. On the contrary, bipolar ablation may offer the advantage of some degree of directionality of energy application between the 2 catheter tips, which is not possible with simultaneous unipolar ablation. In particular, the latter requires precise positioning of the ablation catheters at anatomically opposite sites, and currently available mapping systems do not allow for simultaneous magnetic navigation and visualization of 2 ablation catheters.Table. Summary of Studies Evaluating Catheter Ablation of Idiopathic Intramural VasAuthorYearNo. of PatientsDefinitionFollow-Up, MoVT-Free SurvivalYokokawa et al1220127Earliest activation in the SPB of the AIV, matching pacemap (≥10/12 leads)11±571%Chen et al1920142Earliest activation in the SPB of the AIV24100%Yamada et al20201514The local ventricular activation <−10 ms on both the Endo and Epi sides.The earliest local ventricular activation <−20 ms on either the Endo or Epi side.Unsuccessful ablation at the site of the earliest local ventricular activation or best pace map and successful sequential or simultaneous ablation at the sites directly opposite40*100%Yamada et al14201618Unsuccessful ablation at the site of the earliest local ventricular activation or best pace map and successful sequential or simultaneous ablation at the sites directly opposite51*100%Yokokawa et al17201618Absence of a matching pace map (<10/12 matching leads) when pacing at the site of earliest ventricular activation in adjacent anatomic areas.Earliest activation in the SPB of the AIV20±1667%Yokokawa et al13201610Absence of a matching pace map (<10/12 matching leads) when pacing at the site of earliest ventricular activation in adjacent anatomic areas.Earliest activation in the SPB of the AIV6±570%AIV indicates anterior interventricular vein; Endo, endocardial; Epi, epicardial; and SPB, septal perforator branch.*Median follow-up.Yamada et al14 should be congratulated for their important report. Intramural VAs may in fact be more common than previously thought, with a prevalence of more than 1 every 5 patients with left ventricular OT-VAs. The solution proposed by the authors to tackle these challenging arrhythmias is clearly to ablate more. In most situations where we continue to struggle in electrophysiology (VT in the setting of structural heart disease and long-lasting persistent atrial fibrillation), it is our sincere hope that what we really need is to understand more. Whether similar success may be achieved with less or more focused ablation can be answered only by further studies trying to delineate better methods to map and precisely localize the true site of origin of intramural VAs.Nonetheless, we feel strongly that, despite the difficulty encountered in individual cases, ablation is underutilized in the treatment of patients who have need for therapy (important symptoms or to relieve premature ventricular complex–related cardiomyopathy). We remain confused at how often patients are ignored, falsely reassured that their severe symptoms are meaningless once structural heart disease has been excluded. In addition, the electrophysiology community is passionate for ablation treatment of premature ventricular complex–related myopathy, given the high likelihood of restoring left ventricular function to normal or nearly so. We do not think that the technical difficulties that we face in intramural VT syndromes is the feature that is keeping so many patients from receiving treatment that would meaningfully improve their lives.DisclosuresNone.FootnotesThe opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.Correspondence to David J. Callans, MD, Cardiovascular Division, Department of Medicine, Hospital of the University of Pennsylvania, 9 Founders Pavilion – Cardiology, 3400 Spruce St, Philadelphia, PA 19104. E-mail [email protected]References1. 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Chung F, Vicera J, Lin Y, Chang S, Lo L, Hu Y, Lin C, Tuan T, Chao T, Liao J, Chang T, Salim S, Liu C, Chuang C, Chen C, Chin C, Wu C, Chou C and Chen S (2019) Clinical efficacy of open‐irrigated electrode cooled with half‐normal saline for initially failed radiofrequency ablation of idiopathic outflow tract ventricular arrhythmias, Journal of Cardiovascular Electrophysiology, 10.1111/jce.14057, 30:9, (1508-1516), Online publication date: 1-Sep-2019. September 2016Vol 9, Issue 9 Advertisement Article InformationMetrics © 2016 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.116.004537PMID: 27625171 Originally publishedSeptember 13, 2016 KeywordsEditorialsprognosisheart failureventricular tachycardiaendocardiumcatheter ablationPDF download Advertisement SubjectsArrhythmiasCatheter Ablation and Implantable Cardioverter-Defibrillator