Baldinger, Samuel H.

Enriquez, Alan D.

John, Roy

Kumar, Saurabh

Sobieszczyk, Piotr S.

Stevenson, William G.

Elsevier - Publisher Connector 

Options for ventricular tachycardia ablation after double valve replacement 

Samuel H. Baldinger

Saurabh Kumar

Alan D. Enriquez

Piotr S. Sobieszczyk

Roy John

William G. Stevenson

Crossref

HeartRhythm Case Reports

Options for ventricular tachycardia ablation after double valve replacement

Baldinger, Samuel Hannes

Bern Open Repository and Information System (BORIS)

source: https://doi.org/10.7892/boris.83900 | downloaded: 13.3.2017Options for ventricular tachycardia ablation afterdouble valve replacementSamuel H. Baldinger, MD, Saurabh Kumar, MD, PhD, Alan D. Enriquez, MD, Piotr S. Sobieszczyk, MD,Roy John, MD, PhD, FHRS, William G. Stevenson, MD, FHRSFrom the Cardiac Arrhythmia Center, Cardiovascular Division, Brigham and Women’s Hospital, Boston, Massachusetts.IntroductionTranscoronary ethanol ablation (TCEA) for ventriculartachycardia (VT) is a treatment option for selected patientswhen endocardial and epicardial ablation have failed. Wepresent a case of successful TCEA for treatment of nearlyincessant VT in a patient in whom access to the left ventricle(LV) was impeded because of prosthetic double valvereplacement.Case reportA 52-year-old man was referred for treatment of recurrentsustained monomorphic VT with variable cycle lengths(CLs) of 360 to 480 ms (125–166 bpm) causing recurrentimplantable cardioverter-deﬁbrillator (ICD) shocks despiteincreasing doses of amiodarone. He had rheumatic heartdisease and had undergone mitral and aortic valve replace-ments with mechanical St. Jude prostheses as well astricuspid valve repair 14 years previously. Two years aftersurgery, he had an embolic lateral wall myocardial infarctionand subsequently developed recurrent episodes of heartfailure, ﬂuctuating renal dysfunction, and monomorphicVT for which an ICD was implanted. In the past year, VTepisodes increased despite therapy with amiodarone at dosesof up to 600 mg daily. The patient was admitted for nearlyincessant slow VT with a CL of 430 ms, right bundle branchblock-like conﬁguration in lead V1, and rightward frontalplane axis, consistent with an origin in the lateral LV scar.His left ventricular ejection fraction was 20%, with LV end-diastolic diameter of 7.3 cm. Serum creatinine was 1.07 mg/dL.KEYWORDS Ventricular tachycardia; Catheter ablation; Transcoronary etha-nol ablation; Double valve replacement; Epicardial ablationABBREVIATIONS CL ¼ cycle length; ICD ¼ implantable cardioverter-defibrillator; LV ¼ left ventricle; RF ¼ radiofrequency; RV ¼ rightventricle; TCEA ¼ transcoronary ethanol ablation; VT ¼ ventriculartachycardia (Heart Rhythm Case Reports 2015;1:163–166)Dr. Baldinger received educational grants from the University Hospitalof Bern, Switzerland, and the Swiss Foundation for Pacemakers andElectrophysiology. Dr. Stevenson is co-holder of a patent for needle ablationthat is consigned to Brigham and Women’s Hospital. Address reprintrequests and correspondence: Dr. Samuel H. Baldinger, Brigham andWomen’s Hospital, 75 Francis Street, Boston, MA 02115. E-mail address:sbaldinger1@partners.org.2214-0271 B 2015 Heart Rhythm Society. Published by Elsevier Inc. This is an o(http://creativecommons.org/licenses/by-nc-nd/4.0/).A sestamibi rest myocardial perfusion single-photon emis-sion computerized tomographic study showed a severelydilated LV with a large region of myocardial scar in thedistribution of the distal left circumﬂex coronary artery(Figure 1). Although he had a small paravalvular leak aroundthe aortic valve, hemodynamic function was deemed sat-isfactory and not warranting repeat surgery. Warfarin washeld, and the patient was started on intravenous heparin. Hewas subsequently taken to the electrophysiology laboratory.Programmed ventricular stimulation from the right ven-tricular (RV) apex with the patient under general anesthesiainduced 3 different morphologies of sustained monomorphicVT (VT1–VT3), all of which had a shorter CL than thedocumented VTs (Figure 2). None were bundle branchreentry, and all appeared remote from the RV apex andbasal septum, where the His-bundle catheter was located.Mechanical prosthetic aortic and mitral valves precludedeither a retrograde aortic or transseptal approach to the LVendocardium. Epicardial access was attempted using asubxiphoid percutaneous approach as described by Sosaet al,1 and the pericardial space was entered beneath the RV.There was no signiﬁcant pericardial bleeding or evidence ofinadvertent ventricular puncture. However, pericardial adhe-sions from prior cardiac surgery limited catheter mapping tothe apical aspect of the LV. An electroanatomic voltage mapof the accessible epicardial surface was created using amapping system (CARTO 3, Biosense Webster, DiamondBar, CA) and a 3.5-mm irrigated-tip ablation catheter. Anextensive area of low bipolar voltage (o1.5 mV) consistentwith scar was present in the inferolateral LV apex extendingto the accessible mid-LV, consistent with perfusion imaging(Figures 1 and 3). With pacing there was no left phrenicnerve capture in the area. Monomorphic VT4 with CL of 410ms, right bundle branch block-like conﬁguration in lead V1,and right inferior frontal plane axis was induced with burstpacing from the ablation catheter (Figure 2). It terminatedspontaneously. Substrate modiﬁcation of the scar was thenperformed targeting regions of slow conduction evident aslate or fractionated potentials or stimulus-to-QRS delays440 ms during pace-mapping.2 Radiofrequency (RF) abla-tion was performed with power of 30–50 W aiming for aminimum impedance drop of 10 Ω at each site in an attemptpen access article under the CC BY-NC-ND licensehttp://dx.doi.org/10.1016/j.hrcr.2015.02.007Figure 2 Three fast ventricular tachycardia (VT) morphologies differentfrom the documented VT were induced from the right ventricular (RV) apex(VT1–VT3). Another 3 VTs with different morphologies consistent withorigin in the lateral scar area, all with right bundle block-like morphology inlead V1 and right frontal plane axis, were induced by pacing in the epicardialscar area (VT5–VT6). VT6 was induced after the ﬁrst transcoronary ethanolablation (TCEA) and remained inducible.KEY TEACHING POINTS After double valve replacement, an initialepicardial approach to radiofrequency ablation fortreatment of ventricular tachycardia (VT) can beconsidered when VT morphology is not suggestiveof a septal origin. However, percutaneousepicardial access often is limited in patients withprior cardiac surgery. Options for left ventricular (LV) access after doublevalve replacement include direct percutaneous LVpuncture, percutaneous interventricular septalpuncture, and open chest surgical ablation. Transcoronary ethanol ablation can provideeffective treatment of recurrent VT for selectedpatients when access to the LV endocardium andepicardium is impeded.Heart Rhythm Case Reports, Vol 1, No 4, July 2015164to render the region electrically unexcitable to pacing (10mA and 2-ms pulse width). During pace-mapping within thescar, sustained monomorphic VT5 with a cycle length of 510ms, right bundle branch block-like conﬁguration in lead V1,and right superior frontal plane axis was induced (Figure 2).It was initially hemodynamically tolerated, allowing activa-tion and entrainment mapping. Earliest activation (10 mspresystolic) was noted in the most posterior portion of theaccessible scar. However, activation was early over a broadarea. Entrainment mapping in that region produced con-cealed fusion with a postpacing interval of 25 ms (Figure 3).The VT did not terminate despite multiple RF applicationsup to 120 seconds in duration. The epicardial unipolarvoltage map also showed extensive low unipolar voltage(Figure 2).3 These ﬁndings suggested either an endocardialFigure 1 Tc-99m sestamibi rest myocardial perfusion single-photon emission colarge region of myocardial scar in the distribution of the distal left circumﬂex coronlarge inferolateral area of low bipolar voltageo1.5 mV (middle panel) and unipoINF ¼ inferior; LAT ¼ lateral; Uni ¼ unipolar voltage.or intramural VT origin with a broad epicardial breakout.However, lack of accessibility to the endocardial LVprompted a detailed bedside interdisciplinary discussionamong electrophysiologists, interventional cardiologists,and cardiac surgeons about the next approach. Coronaryangiography was performed with the ablation cathetermputerized tomographic study showing a severely dilated left ventricle with aary artery (left panels). The epicardial voltage map (left lateral view) shows alar voltageo8.3 mV (right panel). ANT ¼ anterior; Bi ¼ bipolar voltage;Figure 3 Entrainment mapping from the ablation catheter positioned in the inferolateral epicardial scar, where transcoronary ethanol ablation wassubsequently performed, showing concealed fusion with a postpacing interval of 25 ms. Abl ¼ ablation catheter; dist ¼ distal; prox ¼ proximal.165Baldinger et al Options for VT Ablation After Double Valve Replacementpositioned in the inferolateral LV scar at the site of earliestactivation and shortest postpacing intervals consistent withthe VT exit (Figure 4). Distal branches of a marginal branchappeared to be supplying the scar (Online SupplementaryMaterial, Cine 1). The decision was made to perform TCEA.An angioplasty balloon was inserted into 1 of the marginalbranches over the wire. The patient’s ongoing VT terminatedas soon as contrast was injected into the branch. The balloonwas positioned proximal to a bifurcation and inﬂated withcontrast to occlude the vessel. Ethanol 3 mL was theninjected down the vessel over several minutes. The balloonremained inﬂated for 10 minutes (Online SupplementaryMaterial, Cine 2). Repeat angiography showed successfulocclusion of the targeted marginal branch (Online Supple-mentary Material, Cine 3). Ventricular stimulation wasrepeated from the epicardial LV. The previous VTs wereno longer inducible. However, another morphology of VT(VT6) was induced (Figure 2). Therefore, a second smallmarginal branch inferior to the previous vessel was cannu-lated and injected with ethanol after balloon occlusion. VT6remained inducible, however, and no further ablation wasperformed.During follow-up, the patient remained free of VT. Hisdevice was subsequently upgraded to provide AV syn-chrony and biventricular pacing, with subsequent re-explo-ration for atrial lead dislodgment. He had no furtherICD shocks or documented VT, but he died 2 monthslater from complications of sepsis, possibly related to deviceinfection.Figure 4 Overlay of coronary angiography and epicardial voltage mapshowing distal branches of a marginal branch (arrows) supplying theinferolateral area where the ablation catheter is located.DiscussionCatheter ablation of VT originating from the LV endocar-dium typically is performed using an atrial transseptal orretrograde aortic approach. However, neither approach isfeasible in the setting of mechanical aortic and mitral valvesgiven the high risk of catheter entrapment. When VTmorphology is not suggestive of a septal VT, an initialepicardial approach for RF ablation can be considered. In ourexperience, percutaneous epicardial access in patients withprior cardiac surgery is successful in only about 30% ofpatients.4 Tschabrunn et al5 reported obtaining access thatwas limited but allowed for ablation in 8 patients with priorsurgery for valvular heart disease. As in our case, extensivemapping was limited by adhesions. A surgical subxiphoidapproach that allows blunt dissection of adhesions underdirect vision has been performed successfully and offers analternative.6In our case, epicardial ablation abolished some of theinducible VTs, but others remained likely because ofintramural, endocardial, or epicardial substrate that was outof reach beneath adhesions. Hsieh et al7 reported 2 cases inwhich direct percutaneous LV puncture and catheter ablationwere used effectively to treat scar-related VT in patients withprosthetic aortic and mitral valves. Hemorrhage into the leftpleural space occurred in the ﬁrst case and was prevented inthe second by using a minithoracotomy and pursestring tiesto control bleeding from the LV puncture site. Vaseghi et al8reported successful percutaneous interventricular septalpuncture to gain access to the LV endocardium for VTablation in a patient with dual mechanical valve replacement.Open chest surgical ablation is also an option but was notHeart Rhythm Case Reports, Vol 1, No 4, July 2015166selected in our patient because of his comorbidities andabsence of need for surgical revision of his valves.9TCEA is an option for selected patients when endocardialand epicardial ablation have failed.10 It can provide effectivetermination of VT storm and reduce the number of arrhyth-mic episodes.11 Our patient was challenging because routineendocardial LV access was not possible, epicardial accesswas hampered by adhesions from prior cardiac surgery, andcomorbidities increased the risks of surgical cryoablation andtransventricular access. The case demonstrates the feasibilityof TCEA for treatment of VT when access to the LVendocardium and epicardium is impeded.AppendixSupplementary dataSupplementary material cited in this article is availableonline at http://dx.doi.org/10.1016/j.hrcr.2015.02.007.References1. Sosa E, Scanavacca M, d'Avila A, Oliveira F, Ramires JA. Nonsurgicaltransthoracic epicardial catheter ablation to treat recurrent ventricular tachycardiaoccurring late after myocardial infarction. J Am Coll Cardiol 2000;35:1442–1449.2. Stevenson WG, Sager PT, Natterson PD, Saxon LA, Middlekauff HR, Wiener I.Relation of pace mapping QRS conﬁguration and conduction delay to ventriculartachycardia reentry circuits in human infarct scars. J Am Coll Cardiol 1995;26:481–488.3. Tokuda M, Tedrow UB, Inada K, Reichlin T, Michaud GF, John RM, EpsteinLM, Stevenson WG. Direct comparison of adjacent endocardial and epicardialelectrograms: implications for substrate mapping. J Am Heart Assoc 2013;2:e000215.4. Sarkozy A, Tokuda M, Tedrow UB, Sieria J, Michaud GF, Couper GS, John R,Stevenson WG. Epicardial ablation of ventricular tachycardia in ischemic heartdisease. Circ Arrhythm Electrophysiol 2013;6:1115–1122.5. Tschabrunn CM, Haqqani HM, Cooper JM, Dixit S, Garcia FC, Gerstenfeld EP,Callans DJ, Zado ES, Marchlinski FE. Percutaneous epicardial ventriculartachycardia ablation after noncoronary cardiac surgery or pericarditis. HeartRhythm 2013;10:165–169.6. Soejima K, Couper G, Cooper JM, Sapp JL, Epstein LM, Stevenson WG.Subxiphoid surgical approach for epicardial catheter-based mapping and ablationin patients with prior cardiac surgery or difﬁcult pericardial access. Circulation2004;110:1197–1201.7. Hsieh CH, Thomas SP, Ross DL. Direct transthoracic access to the left ventriclefor catheter ablation of ventricular tachycardia. Circ Arrhythm Electrophysiol2010;3:178–185.8. Vaseghi M, Macias C, Tung R, Shivkumar K. Percutaneous interventricularseptal access in a patient with aortic and mitral mechanical valves: a noveltechnique for catheter ablation of ventricular tachycardia. Heart Rhythm 2013;10:1069–1073.9. Anter E, Hutchinson MD, Deo R, et al. Surgical ablation of refractory ventriculartachycardia in patients with nonischemic cardiomyopathy. Circ ArrhythmElectrophysiol 2011;4:494–500.10. Sacher F, Sobieszczyk P, Tedrow U, Eisenhauer AC, Field ME, Selwyn A,Raymond JM, Koplan B, Epstein LM, Stevenson WG. Transcoronary ethanolventricular tachycardia ablation in the modern electrophysiology era. HeartRhythm 2008;5:62–68.11. Tokuda M, Sobieszczyk P, Eisenhauer AC, Kojodjojo P, Inada K, Koplan BA,Michaud GF, John RM, Epstein LM, Sacher F, Stevenson WG, Tedrow UB.Transcoronary ethanol ablation for recurrent ventricular tachycardia after failedcatheter ablation: an update. Circ Arrhythm Electrophysiol 2011;4:889–896.

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Options for ventricular tachycardia ablation after double valve replacement

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