Billinger, Michael

Cook, Stephane

Hess, Otto M.

Togni, Mario

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EDITORIALSeptal myectomy: cut, coil, or boil?Mario Togni, Michael Billinger, Stephane Cook, and Otto M. Hess*Swiss Cardiovascular Center, University Hospital Inselspital, Freiburgstrasse, CH-3010 Berne, SwitzerlandThis editorial refers to ‘Non-surgical septal myocardialreduction by coil embolization for hypertrophic obstruc-tive cardiomyopathy: early and 6 months follow-up’ byE. Durand et al.,† on page 348Hypertrophic cardiomyopathy (HOCM) is characterized by asym-metric septal hypertrophy with outflow tract obstruction inapproximately one-third of patients. However, recent studiessuggest that obstruction may be present in up to 70% of patientswith enhanced sympathetic activation under exercise conditions.1Clinical features are dyspnoea on exertion, angina pectoris, andatrial and ventricular arrhythmias, which mainly are due to diastolicdysfunction, whereas syncope and presyncope often are due tooutflow tract obstruction and represent an ominous sign of ventri-cular arrhythmias and sudden cardiac death.The treatment strategy is 3-fold: (i) medical therapy for targetingdiastolic dysfunction; (ii) myectomy (interventional or surgical) forrelief of obstruction; and (iii) implantable defibrillators for preven-tion of sudden cardiac death.2For decades, the gold standard for septal myectomy has beensurgical treatment, with excellent short- and long-term results.3In 1995, a new interventional technique (alcohol ablation ofthe septum) was put forward for percutaneous treatment ofHOCM.4 In their study, Durand and co-workers5 propose a newtechnique for septal ablation of the myocardium, namely coilingof septal branches. One to five coils were deployed into the firstor second septal branch of the left anterior descending artery in20 patients with HOCM, thereby inducing septal ischaemia withmyocardial necrosis and a consecutive creatine kinase (CK) riseof 386 U/L. As a result, the pressure gradient decreased signifi-cantly from 80 to 35 mmHg at the 6 months follow-up examin-ation. Clinical symptoms and exercise capacity improved, asreflected by a significant increase in peak oxygen consumption(from 14.8+ 4.5 to 18.5+ 4.5 ml/kg/min) and a prolongation ofexercise duration (from 7.1+3.5 to 9.0+3.8 min). The pro-cedure was well tolerated, and no AV blocks were observed.However, in one patient, septal perforation occurred, which wassurgically treated; however, the patient died postoperatively.Other complications were not reported, and the authors claimfrom this series that in contrast to alcohol ablation or surgicalmyectomy, no AV blocks occur with coil embolization. Nevertheless,they suggest that larger studies, ideally employing a randomizedcomparison between coil embolization and alcohol septal ablation,are warranted.The authors are to be congratulated for these results and thisnew technique. A major limitation of alcohol ablation is, indeed,an AV block, which occurs in 27% of all patients (transient);10% need pacemaker implantation (Table 1). However, previousdata suggest that infarct size is larger with alcohol ablation (10–15 g) compared with 3 g with coil embolization. This finding is par-alleled by a larger CK rise with alcohol ablation (1038 U/L) whencompared with coil embolization (386 U/L). Alcohol appears topenetrate more deeply into the septal region and induces alarger area of necrosis, whereas coil embolization leads primarilyto ischaemia and only secondarily to necrosis. However, in somerare cases, alcohol dissipation (spill over) to non-target myocardialareas (right ventricle or apex of the left ventricle) may occur.In Durand et al.’s pilot study, a quarter of the patients had unsuc-cessful treatment with a resting gradient .50 mmHg at 6 months.This reflects the learning curve, as stated by the authors, or indi-cates the less aggressive nature of the technique. Alcohol ablationhas been reported to be successful in 90–95% of all patients.As an alternative, radiofrequency ablation has been rec-ommended for reduction of septal hypertrophy in children withHOCM, because alcohol ablation in this patient group is stronglydiscouraged due to the induction of potential arrhythmias.6 Fromreviewing the literature and comparing alcohol ablation with coilembolization (Table 1), there are clear differences in the releaseof CK and the decrease in outflow tract gradient, suggesting alarger infarct with alcohol ablation than with coil embolization.The absence of AV block with coil embolization could be explainedby the smaller infarct size and the modest decrease in pressuregradient.Interestingly enough, a Polish group7 performing coil emboliza-tion in patients with HOCM reported a transient AV block in43% of patients (Table 1). Thus, Durand’s study may represent ahighly selected group that does not show AV block during coilembolization. Larger samples may answer this question.Only a randomized trial will allow for a fair comparison of thetwo techniques. A contraindication for alcohol ablation (and anThe opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.* Corresponding author. Tel: þ41 31 632 9653, Fax: þ41 31 632 4771. Email: otto.hess@insel.ch† doi:10.1093/eurheartj/ehm632Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.European Heart Journal (2008) 29, 296–298doi:10.1093/eurheartj/ehm561indication for coil embolization) may represent pre-existing leftbundle branch block (LBBB). A complete AV block may occur inthese patients when alcohol ablation induces right bundle branchblock (RBBB) in up to 50% of patients. Amiodarone treatment isanother contraindication due to associated AV conduction pro-longation. A third contraindication to alcohol ablation is the pre-existing AV block I or II (Figure 1).In summary, coil embolization represents a new and promisingmethod for reducing septal hypertrophy in patients with HOCM.The first results suggest a lower risk for the occurrence of AVblock during septal ablation, but haemodynamic success may belimited, with less reduction in outflow tract gradient.Conflict of interest: none declared.References1. Maron MS, Olivotto I, Zenovich AG, Link MS, Pandian NG,Kuvin JT, Nistri S, Cecchi F, Udelson JE, Maron BJ. Hypertrophiccardiomyopathy is predominantly a disease of left ventricularoutflow tract obstruction. Circulation 2006;114:2232–2239.2. Maron BJ, Spirito P, Shen WK, Haas TS, Formisano F, Link MS,Epstein AE, Almquist AK, Daubert JP, Lawrenz T, Boriani G,Estes NA 3rd, Favale S, Piccininno M, Winters SL, Santini M,Betocchi S, Arribas F, Sherrid MV, Buja G, Semsarian C,Bruzzi P. Implantable cardioverter–defibrillators and preventionof sudden cardiac death in hypertrophic cardiomyopathy. JAMA2007;298:405–412.3. Schoendube FA, Klues HG, Reith S, Flachskampf FA, Hanrath P,Messmer BJ. Long-term clinical and echocardiographic follow-upafter surgical correction of hypertrophic obstructive cardiomyopa-thy with extended myectomy and reconstruction of the subvalvu-lar mitral apparatus. Circulation 1995;92(Suppl):II122–127.4. Sigwart U. Non-surgical myocardial reduction for hypertrophicobstructive cardiomyopathy. Lancet 1995;346:211–214.5. Durand E, Mousseaux E, Coste P, Pillie`re R, Dubourg O,Trinquart L, Chatellier G, Hage`ge A, Desnos M, Lafont A. Non-surgical septal myocardial reduction by coil embolization forhypertrophic obstructive cardiomoypathy: early and 6 monthsfollow-up. Eur Heart J 2008;29:348–355. doi:10.1093/eurheartj/ehm632.6. Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn HJ,Seidman CE, Shah PM, Spencer WH 3rd, Spirito P, Ten Cate FJ,Wigle ED, Task Force on Clinical Expert Consensus Documents.American College of Cardiology; Committee for Practice Guide-lines. European Society of Cardiology. American College of Cardi-ology/European Society of Cardiology clinical expert consensusdocument on hypertrophic cardiomyopathy. A report of theAmerican College of Cardiology Foundation Task Force on Clini-cal Expert Consensus Documents and the European Society ofFigure 1 Treatment recommendations in HCOM (adults).. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Table 1 A comparison of alcohol ablation and coil embolizationAuthor Year nAV blockPM Death (cardiac) Peak CK (U/L)LVOTG resting (mmHg)Transient Permanent Before AfterAlcohol ablationChang8 2003 224 N/A 14% – – 1335 62 20Osterne9 2003 18 44% 11% 11% 5.5% – 68 3.8Chang10 2004 173 16% – – – 1387 58 19Gietzen11 2004 146 N/A 11% 25% 2.5% 508 52 14Talreja12 2004 58 N/A 12% 12% – – 72 11Faber13 2005 242 N/A 10% 10% 1.2% 483 57 25Fernandes14 2005 130 N/A 13% 13% 1.5% 1676 74 4Streit15 2007 24 21% 13% 13% 0% 931 38 13Total or mean 1015 27% 12% 14% 2% 1038 60 17Coil embolizationIacob7 2004 7 43% 0% 0% 0% N/A 72 34Durand5 2007 28 0% 0% 0% 4% 386 80 35Total or mean 35 9% 0% 0% 3% 386 78 35N/A, not available; PM, pacemaker, CK, creatine kinase; LVOTG, left ventricular outflow tract gradient.Septal myectomy: cut, coil, or boil? 297Cardiology Committee for Practice Guidelines. J Am Coll Cardiol2003;42:1687–1713.7. Iacob M, Pinte F, Tintoiu I, Cotuna L, Caroescu M, Popa A,Cristian G, Goleanu V, Greere V, Moscaliuc I, Neagoe G,Crisan P, Garjeu A, Chiriac L, Bolohan R, Murgu V, Lobont B,Filip S, Roates J, Hila G, Postolea E. Microcoil embolisation forablation of septal hypertrophy in hypertrophic obstructive cardio-myopathy. Kardiol Pol 2004;61:350–355.8. Chang SM, Nagueh SF, Spencer WH 3rd, Lakkis NM. Completeheart block: determinants and clinical impact in patients withhypertrophic obstructive cardiomyopathy undergoing non-surgical septal reduction therapy. J Am Coll Cardiol 2003;42:296–300.9. Osterne EC, Seixas TN, Paulo Filho W, Osterne EM, Gomes OM.Percutaneous transluminal septal alcoholization for the treatmentof refractory hypertrophic obstructive cardiomyopathy: initialexperience in the Federal District. Arq Bras Cardiol 2003;80:359–378.10. Chang SM, Lakkis NM, Franklin J, Spencer WH 3rd, Nagueh SF.Predictors of outcome after alcohol septal ablation therapy inpatients with hypertrophic obstructive cardiomyopathy. Circulation2004;109:824–827.11. Gietzen FH, Leuner CJ, Obergassel L, Strunk-Mueller C, Kuhn H.Transcoronary ablation of septal hypertrophy for hypertrophicobstructive cardiomyopathy: feasibility, clinical benefit, andshort term results in elderly patients. Heart 2004;90:638–644.12. Talreja DR, Nishimura RA, Edwards WD, Valeti US, Ommen SR,Tajik AJ, Dearani JA, Schaff HV, HolmesDR Jr. Alcohol septal ablationversus surgical septal myectomy: comparison of effects on atrio-ventricular conduction tissue. J Am Coll Cardiol 2004;44:2329–2332.13. Faber L, Seggewiss H, Gietzen FH, Kuhn H, Boekstegers P,Neuhaus L, Seipel L, Horstkotte D. Catheter-based septal ablationfor symptomatic hypertrophic obstructive cardiomyopathy:follow-up results of the TASH-registry of the German CardiacSociety. Z Kardiol 2005;94:516–523.14. Fernandes VL, Nagueh SF, Wang W, Roberts R, Spencer WH 3rd.A prospective follow-up of alcohol septal ablation for symptomatichypertrophic obstructive cardiomyopathy—the Baylor experience(1996–2002). Clin Cardiol 2005;28:124–130.15. Streit S, Walpoth N, Windecker S, Meier B, Hess OM. Is alcoholablation of the septum associated with recurrent tachyarrhthy-mias. Swiss Med Wkly 2007; in press.Mario Togni et al.298

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