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• W2591992007 abstract "HomeCirculationVol. 135, No. 9The Sound of Silence Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBThe Sound of SilenceHow Much Noise Should We Make About Postablation Silent Strokes? Paul C. Zei, MD, PhD and Nirali Vora, MD Paul C. ZeiPaul C. Zei From Department of Medicine, Cardiac Electrophysiology (P.C.Z.), and Department of Neurology, Stroke Service, Stanford University, CA (N.V.). Search for more papers by this author and Nirali VoraNirali Vora From Department of Medicine, Cardiac Electrophysiology (P.C.Z.), and Department of Neurology, Stroke Service, Stanford University, CA (N.V.). Search for more papers by this author Originally published28 Feb 2017https://doi.org/10.1161/CIRCULATIONAHA.117.026982Circulation. 2017;135:878–880Article, see p 867Catheter ablation has become an essential therapeutic option for the treatment of ventricular arrhythmias. For premature ventricular complex (PVC)/ventricular tachycardia (VT) ablation in structurally normal hearts, recently reported success rates are as high as 80% for right ventricular outflow tract ablation, and 60% to 100% for left-sided ablation.1 Procedural safety and efficacy have improved with better understanding of surface ECG predictors of PVC origin location, refined electroanatomic mapping techniques, evermore precise electroanatomic activation maps to localize PVC origins, automated techniques to quantify the fidelity of pace-mapping surface QRS morphologies, improved ablation technology, and intracardiac ultrasound.1 Although these advancements might lead us to believe we have entered a golden age for interventional electrophysiology, we as electrophysiologists and cardiologists need to continue our vigilance for serious complications arising from these invasive procedures.In this issue of Circulation, Whitman et al2 evaluate the incidence of subclinical brain emboli in a small series of patients with structurally normal hearts undergoing endocardial catheter ablation for PVCs and VT. Electrophysiologists frequently map and ablate in the left ventricular (LV) endocardial and aortic root spaces,1,3,4 with an assumption that, with proper intravenous systemic anticoagulation, the risk of systemic embolization phenomenon is acceptably low. In addition, with transseptal procedures, the risk of air or thrombus entry to the systemic circulation via the transseptal sheath is minimized through continuous saline flush through the long sheaths, or by retracting the sheath back to the right atrium. More recently, with the near-universal adoption of open-irrigated catheters, it is assumed that the risks of catheter char, coagulum, or thrombus are mitigated, although there are few clinical data to support this claim.It turns out that we know very little about whether any of these measures are truly effective in minimizing systemic embolization. Reported systemic embolization complications are low for LV1,3,4 and for left atrial catheter ablation procedures,5 but may be underestimated because the events were based only on clinical symptoms. Silent MRI-confirmed central nervous system embolic events have a reported incidence as high as 38% in left atrial catheter ablation,5–8 22% for aortic valve–crossing procedures, and 10% for routine coronary angiography.9,10 The mechanisms for emboli postulated in these cases are heterogeneous, and it is not clear how these data apply to patients undergoing LV PVC/VT ablation who do not have the same risk factors. With atrial fibrillation ablation, factors including left atrial appendage stasis, a significantly larger area of endocardial tissue ablated, and increased underlying stroke risk differentiate it from LV PVC/VT ablation. Patients undergoing cardiac catheterization typically have significant comorbidities and increased stroke risk attributable to atherosclerotic risk.For the patient population evaluated in this article, ie, those with no or minimal underlying structural heart disease and fewer stroke risk factors undergoing ablation for PVCs or VT, reported overt clinical neurological event rates are very low or absent.1,3,4 Whitman et al are the first to evaluate the incidence of subclinical brain embolization in this population, finding MRI evidence in 7 of 12 (58%) patients undergoing left-sided ablation. As expected, the 6 control patients undergoing right-sided ablation had no subclinical or clinical emboli; pulmonary embolism rates were not evaluated. All but one of the patients undergoing LV ablation had access to the LV obtained via a retrograde aortic approach.This central result of this study is both surprising and alarming. Could electrophysiologists be unknowingly causing subclinical emboli unacceptably often, while believing we are reliably avoiding clinically significant events?The higher than expected incidence of emboli may in part be explained by improved detection through better neuroimaging techniques such as the stronger 3T magnet in comparison with the 1.5T magnet used in prior studies.5–10 If this possible underestimation of events is indeed alarming to the reader, it should be emphasized that the clinical significance of these emboli remains uncertain. Silent brain infarcts are those diagnosed incidentally on neuroimaging but not associated with any overt acute clinical symptoms. The majority are punctate subcortical lesions, often associated with small-vessel ischemia, although a small percentage may be cortically based, typically from cardioembolism. Population-based studies associate unprovoked silent infarcts with increased risk of symptomatic stroke, but, because of limited data, the current guidelines recommend screening and management of traditional cerebrovascular risk factors as is done for primary, rather than secondary, stroke prevention.11 When the silent infarct is provoked from a cardiac procedure, we are even less certain if there is a true risk of future recurrence that would warrant any postprocedural pharmacological intervention. Regardless of the cause, there is also controversy whether there are irreversible neurocognitive sequelae of these covert infarcts, or if they are truly silent and self-resolving.12 Longer-term data are needed to better characterize the clinical significance of these “silent” emboli, and cognitive testing should increasingly be included as a functional outcome measure in electrophysiology and stroke studies.Perhaps an analogous scenario is the dreaded risk of atrioesophageal fistula resulting from atrial fibrillation ablation. For this complication, we understand the event rate to be low, yet a surprisingly high incidence of subclinical esophageal injury is seen when we look for it.13 Similarly, this provocative article suggests that with LV ablation, we are possibly seeing very few clinical events despite a high incidence of subclinical events; and, most distressing, we have a poor understanding of the pathophysiology of these embolic events.The immediate question raised by this study is, what are the underlying mechanism(s) for the embolization phenomenon observed? The basic hypothesis is that procedural endothelial injury caused by ablation unleashes the coagulation cascade, leading to localized thrombus.14 Additional contributors may include air embolism via infusion from open irrigated catheters, intracardiac thrombus, catheter-based thrombus, or atheroemboli, particularly from aortic arch scraping.5–12 Interestingly, in this study, the majority of retrograde aortic procedures were associated with emboli, whereas the single reported transseptal procedure had no emboli. It is clear that with a single transseptal case, it is impossible to draw useful conclusions, but the emboli with a retrograde aortic approach might result from mechanical trauma to aortic arch atheroma.In this study, the authors attempted to evaluate at least some of these potential embolic sources. Clinical history and femoral arteriograms demonstrated a low likelihood of peripheral artery disease; however, there was no systematic evaluation for aortic atheroma for which this population had moderate risk. The reported neuroimaging was not consistent with “watershed” hypoperfusion that may be seen periprocedurally. The pattern of multifocal punctate embolic cortical and subcortical ischemia favors a nonspecific cardioembolic source. A detailed tracking of periprocedural systemic anticoagulation was performed, demonstrating adequate anticoagulation, at least to the standards of common practice. There were no reports of abnormal ablation parameters, including evidence of steam pops or excessive impedance changes. However, none of the above observations can definitively exclude any specific source of embolization.So where do we go from here? Validation of this article’s findings in larger populations is needed. We need to clarify the etiology of these emboli, which will influence preventative targets. One may consider the use of periprocedural microemboli detection with transcranial Doppler to characterize exactly when they begin to occur and if they are truly spared in the transseptal approach. Once the likely source(s) have been identified, we need to determine whether these silent emboli have any important long-term sequelae, and whether interventions to limit these phenomena are necessary and effective. It is not clear, for example, that the authors’ intervention of initiating aspirin postprocedure is useful, because there does not seem to be a high recurrence risk. Collaboration with vascular neurology colleagues will be a critical part of future investigation and therapies.This study population is one of the healthier groups among those undergoing endocardial catheter ablation for LV arrhythmias. One might postulate that patients with underlying structural heart disease and other risk factors for stroke may be at even higher risk of embolic phenomena; that population certainly warrants evaluation. As our field moves toward permissiveness in obtaining MRIs in patients with implanted devices,15 there should be fewer barriers to similarly evaluating these additional patient populations, where the prevalence of in situ implantable cardiac defibrillators is much higher. However, including functional/clinical outcomes will be necessary to interpret the significance of these radiographic outcomes.When it comes to the potential risk of embolic complications, the stakes are high, particularly in patients whose indication for the procedure is to relieve symptoms. A central nervous system event could be a catastrophic complication. This article should serve as a wake-up call to our field, perhaps a reminder that we cardiologists and electrophysiologists need to continue our vigilance for risks of significant harm to our patients from invasive procedures. We as a field need to collaborate with our vascular neurology colleagues to determine whether these “silent” emboli are a clinically important phenomena requiring intervention, or whether we are simply making too much noise about a problem that can remain silent.DisclosuresDr Zei received research support from Biosense Webster, Inc., and was a consultant to St Jude Medical/Abbot Medical. Dr Vora has no disclosures.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Circulation is available at http://circ.ahajournals.org.Correspondence to: Paul C. Zei, MD, PhD, Cardiac Electrophysiology, Stanford University, 300 Pasteur Drive, H2146, Stanford, CA 94305. E-mail [email protected]References1. Tanawuttiwat T, Nazarian S, Calkins H. The role of catheter ablation in the management of ventricular tachycardia.Eur Heart J. 2016; 37:594–609. doi: 10.1093/eurheartj/ehv421.CrossrefMedlineGoogle Scholar2. Whitman IR, Gladstone RA, Badhwar N, Hsia HH, Lee BK, Josephson SA, Meisel KM, Dillon WP, Hess CP, Gerstenfeld EP, Marcus GM. Brain emboli after left ventricular endocardial ablation.Circulation. 2017: 135;867–877. doi: 10.1161/CIRCULATIONAHA.116.025546.LinkGoogle Scholar3. Yamada T, Litovsky SH, Kay GN. The left ventricular ostium: an anatomic concept relevant to idiopathic ventricular arrhythmias.Circ Arrhythm Electrophysiol. 2008; 1:396–404. doi: 10.1161/CIRCEP.108.795948.LinkGoogle Scholar4. Bogun F, Crawford T, Reich S, Koelling TM, Armstrong W, Good E, Jongnarangsin K, Marine JE, Chugh A, Pelosi F, Oral H, Morady F. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention.Heart Rhythm. 2007; 4:863–867. doi: 10.1016/j.hrthm.2007.03.003.CrossrefMedlineGoogle Scholar5. Scherr D, Sharma K, Dalal D, Spragg D, Chilukuri K, Cheng A, Dong J, Henrikson CA, Nazarian S, Berger RD, Calkins H, Marine JE. Incidence and predictors of periprocedural cerebrovascular accident in patients undergoing catheter ablation of atrial fibrillation.J Cardiovasc Electrophysiol. 2009; 20:1357–1363. doi: 10.1111/j.1540-8167.2009.01540.x.CrossrefMedlineGoogle Scholar6. Deneke T, Shin DI, Balta O, Bünz K, Fassbender F, Mügge A, Anders H, Horlitz M, Päsler M, Karthikapallil S, Arentz T, Beyer D, Bansmann M. Postablation asymptomatic cerebral lesions: long-term follow-up using magnetic resonance imaging.Heart Rhythm. 2011; 8:1705–1711. doi: 10.1016/j.hrthm.2011.06.030.CrossrefMedlineGoogle Scholar7. 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Prevention of Stroke in Patients With Silent Cerebrovascular Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association.Stroke. 2017; 48:e44–e71. doi: 10.1161/STR.0000000000000116.LinkGoogle Scholar12. von Bary C, Deneke T, Arentz T, Schade A, Lehrmann H, Eissnert C, Schwab-Malek S, Fredersdorf S, Ücer E, Baldaranov D, Wendl C, Schlachetzki F. Silent cerebral events as a result of left atrial catheter ablation do not cause neuropsychological sequelae–a MRI-controlled multicenter study.J Interv Card Electrophysiol. 2015; 43:217–226. doi: 10.1007/s10840-015-0004-6.CrossrefMedlineGoogle Scholar13. Nakagawa H, Seres KA, Jackman WM. Limitations of esophageal temperature-monitoring to prevent esophageal injury during atrial fibrillation ablation.Circ Arrhythm Electrophysiol. 2008; 1:150–152. doi: 10.1161/CIRCEP.108.805366.LinkGoogle Scholar14. Haines D. Biophysics of radiofrequency lesion formation., Huang SKS, Miller J, Catheter Ablation of Cardiac Arrhythmias. 3rd ed. Philadelphia, PA:Elsevier Saunders; 2014:3–21.Google Scholar15. Nazarian S, Beinart R, Halperin HR. Magnetic resonance imaging and implantable devices.Circ Arrhythm Electrophysiol. 2013; 6:419–428. doi: 10.1161/CIRCEP.113.000116.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Fakess S, O’Loughlin M and Tolat A (2022) Left ventricular thrombus following radiofrequency ventricular tachycardia ablation, HeartRhythm Case Reports, 10.1016/j.hrcr.2022.03.013, 8:6, (441-444), Online publication date: 1-Jun-2022. Romero J and Goldhaber S (2022) Uninterrupted Oral Anticoagulation During Catheter Ablation of Ventricular Tachycardia, JACC: Clinical Electrophysiology, 10.1016/j.jacep.2022.04.007, 8:6, (749-753), Online publication date: 1-Jun-2022. Piechocki K and Kozanecki M (2021) Hydration in thermo-responsive oligoether methacrylate hydrogels studied by FT-IR spectroscopy, Polymer, 10.1016/j.polymer.2021.123638, 223, (123638), Online publication date: 1-May-2021. February 28, 2017Vol 135, Issue 9 Advertisement Article InformationMetrics © 2016 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.117.026982PMID: 28242639 Originally publishedFebruary 28, 2017 Keywordsventricular premature complexestachycardia, ventricularstrokeablationPDF download Advertisement SubjectsArrhythmiasCatheter Ablation and Implantable Cardioverter-Defibrillator" @default.
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