EDITORIAL COMMENT
Myectomy or Alcohol Septal Ablation
Surgery and Percutaneous Intervention Go Another Round*
Alan W. Heldman, MD ,*,
Katherine C. Wu, MD, FACC,
Theodore P. Abraham, MD, FACC and
Duke E. Cameron, MD
Division of Cardiology, Johns Hopkins Hypertrophic Cardiomyopathy Center, Baltimore, Maryland
Division of Cardiac Surgery, Johns Hopkins Hypertrophic Cardiomyopathy Center, Baltimore, Maryland.
* Reprint requests and correspondence: Dr. Alan W. Heldman, The Johns Hopkins Hypertrophic Cardiomyopathy Center, Carnegie 565, 600 North Wolfe Street, Baltimore, Maryland 21287. (Email: aheldman{at}jhmi.edu).
Since the development of alcohol septal ablation by Sigwart (1) and its increasing adoption, the treatment of symptomatic hypertrophic obstructive cardiomyopathy (HOCM) with myectomy versus alcohol septal ablation has generated a passion of debate and disagreement not often seen. Of course one contributor to the intensity of this controversy is that myectomy is done by surgeons, and ablation by interventional cardiologists: debaters accustomed to disagreeing over the best approach to coronary revascularization and other issues (2) such as valvular heart disease and the repair of septal defects. However, participants in the HOCM debate have substantial arguments to fuel their passion, and one important point of contention is the risk of late arrhythmic events occurring after alcohol ablation. Indeed, guidelines offered by the American College of Cardiology and the European Society of Cardiology (3) have noted with caution the enthusiastic adoption of alcohol septal ablation, which now outnumbers myectomy. Septal ablation, the argument goes, produces a myocardial scar in patients who already have an arrhythmogenic myocardial substrate, whereas myectomy does not.
It is worth noting that electrophysiology studies (4,5) after septal ablation have not indicated an increased arrhythmogenic substrate, but cases of ventricular tachycardia (6,7) and sudden death (8) occurring after septal ablation have been reported. The specter of re-entrant arrhythmias arising from the septal ablation scar is certainly a plausible concern. Arrhythmia and sudden cardiac death complicate hypertrophic cardiomyopathy with or without intervention. For patients with clinical markers of risk (9) for ventricular arrhythmias, an implanted defibrillator effectively reduces the risk (10).
An important contribution to the debate is the report of Valeti et al. (11) in this issue of the Journal. The investigators performed cardiac magnetic resonance imaging (CMR) before and after myectomy (n = 24) or alcohol septal ablation (n = 24). The findings in and of themselves are not surprising: with surgical myectomy, a discrete segment of resection was identified, with minimal to no CMR evidence of myocardial necrosis, whereas with alcohol ablation, delayed hyperenhancement denoting myocardial infarction was always seen. This was described as "a large transmural infarction, located more inferiorly in the basal septum than myectomy and usually extending into the right ventricular side of the septum at mid-ventricular level" (11).
The pattern of infarction seen by CMR after ablation makes sense if we imagine the effects of infusing alcohol into a septal branch of the proximal left coronary: the distribution of injury ought to conform to the more or less wedge-shaped distribution of the coronary branch. A wave front of profound microvascular obstruction results, with infarction of most of the tissue within this zone. We previously reported this phenomenon with serial CMR studies after alcohol septal ablation (12).
Both septal ablation and myectomy relieve left ventricular outflow tract (LVOT) obstruction. In the study in this issue of the Journal, as in other nonrandomized comparisons (13), myectomy patients were 12 to 13 years younger than septal ablation patients. Because of the very different ages at presentation for treatment, one must wonder whether the genotype-phenotype mix differs between the 2 groups. In comparing the 2 techniques, age, comorbidities, and genotype will affect outcomes. Other comparisons of surgical myectomy and alcohol septal ablation not controlled for age have indicated similar effects on the outflow tract gradient and on symptoms (14), but have indicated greater gains in maximal oxygen consumption during exercise testing (15) with myectomy. In 1 age-matched comparison (16), efficacy (including exercise capacity) was not different between the 2 groups, and in that comparison, septal ablation resulted in more heart block, whereas myectomy was associated with more aortic regurgitation. Without a randomized study, it is difficult to assign efficacy differences to the treatments themselves, but it is abundantly clear that the site and extent of myocardial change differ substantially between the 2 treatments. One need only to look at the electrocardiograms after treatment to see a difference.
Myectomy is performed through aortotomy while on cardiopulmonary bypass, with resection of septal myocardium to create a channel expanding the LVOT. The experienced Mayo surgeons relieved the LVOT obstruction in all cases; no patient required a permanent pacemaker, and 1 patient had a stroke 2 weeks after the operation. Left bundle branch block is a frequent consequence of myectomy. In contrast, right bundle branch block is a frequent consequence of septal ablation (17), and complete heart block occurs in some cases. Septal ablation is performed by administering ethanol via a small inflated and occlusive angioplasty balloon into 1 or more of the coronary branches supplying the septum (18). Variability (19) in the location, size, and distribution of the first septal branch of the left anterior descending coronary artery adds a dimension of complexity to this procedure; septal infarction by ethanol may be transmural or may preferentially affect the right or left endocardial surfaces of the septum. Before injecting alcohol, the distribution of the selected branch can be studied with echocardiography, while an echocardiographic contrast agent is instilled through the balloon, allowing confirmation that the region to be infarcted is indeed the part of the septum that causes the left ventricular outflow tract obstruction. This technique also avoids injecting alcohol into a septal branch supplying other parts of the heart, either directly or via collaterals.
Some septal ablation patients had residual obstruction, and it is an important finding that most of these had nontransmural infarction of the right ventricular side of the septum, sparing the more proximal basal septum. In theory, echocardiography with contrast instillation into the selected branch should show the distribution of the target vessel. One wonders why, in some cases, was the goal of infarcting the basal septum not achieved? For the cardiologist seeking perfect results with alcohol septal ablation, these failures may be instructive. A number of "failure modes" of contrast echo-guided septal ablation can be postulated: - 1 The branch or branches injected with alcohol did not actually supply the most basal septum, although echocardiography suggested otherwise. Blame echo "blooming" artifact, or inadequate contrast border definition and spatial resolution.
- 2 Echocardiography showed sparing of the basal septum by the contrast instillation, but alcohol injection was performed anyway. It may have been impossible to identify a branch supplying that territory. In our experience, frequently an accessory septal branch (from the left main coronary, high intermediate branch, or diagonal branch) supplies the basal left side of the septum, and concerted efforts to find and cannulate this branch are rewarded by successful ablation of the basal septal bulge. Although it may be tempting to ablate the largest or easiest septal branch of the LAD, sometimes these arteries supply the right ventricular side of the septum (20) or other distant parts of the heart (21,22).
- 3 Echocardiography correctly showed contrast distribution to the basal septum, but alcohol injection in the selected branch was ineffective at treating that particular myocardial segment. Perhaps the different viscosities of echocardiographic contrast versus absolute ethanol explain the difference in localization. Other percutaneous approaches to septal ablation have been tried, including arterial embolization with foam particles (23) and coils (24); should we consider using a more viscous alcohol gel?
How large an infarct should we create? One study (25) suggested that a larger risk area defined by contrast echocardiography predicts a greater risk of heart block and other complications and that a smaller risk area predicts fewer complications without sacrificing efficacy at relieving obstruction. On the other hand, a study (26) of predictors of treatment failure with septal ablation found that higher baseline gradient, fewer septal branches injected, lower peak creatine kinase, and smaller risk area by contrast echocardiogram (and higher residual gradient in the catheterization laboratory) all predicted incomplete relief of obstruction. A small randomized study comparing low (1 to 2 ml) and higher (2 to 4 ml) doses of ethanol found no safety nor efficacy differences (27). Because continued regression of LV hypertrophy, including in the septum, has been shown after septal ablation (28), most experienced cardiologists have adopted an approach to alcohol septal ablation relying heavily on contrast echocardiography guidance for selection of the most suitable branch and saturation of the target myocardium with a low dose of slowly infused alcohol.
How should a prudent practitioner (or concerned patient) choose a therapy today, in the absence of randomized comparisons of myectomy with alcohol septal ablation? Both are effective in most cases (29); crossovers and repeat procedures do occur with either. Both have low but finite risk, and if there is any difference in procedural mortality between the 2 approaches, it is small. For old and very old patients (30), the less invasive approach may be safer; mortality in surgical series has been reported in the range of 1.5% (31) to 3.2% (32) and was associated with age and female gender. Mortality in series of patients having alcohol septal ablation was 1.2% (33) or 1.3% (34).
The specter of the arrhythmogenic scar deserves further consideration. Until we have improved arrhythmia risk detection tools, a cautious approach considers clinical risk factors for ventricular arrhythmias and sudden cardiac death; when these risk factors are present, defibrillator implantation after septal ablation certainly is reasonable. Speculation that myectomy spares the need for a defibrillator is intriguing, but when the stakes are so high, the value of insurance (in the form of a defibrillator) is hard to dismiss, no matter which other treatment has been applied.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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Catheter interventional treatment for hypertrophic obstructive cardiomyopathyAcute and long-term results after transcoronary ablation of septal hypertrophy (TASH). Eur Heart J 1999;20:1342-1354.[Abstract/Free Full Text] 5. Lawrenz T, Obergassel L, Lieder F, et al. Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk patients with hypertrophic obstructive cardiomyopathy Pace Pacing Clin Electrophysiol 2005;28:295-300.[CrossRef][Medline] 6. Boltwood Jr. CM, Chien W, Ports T. Ventricular tachycardia complicating alcohol septal ablation N Engl J Med 2004;351:1914-1915.[Free Full Text] 7. Simon RD, Crawford 3rd FA, Spencer 3rd WH, Gold MR. Sustained ventricular tachycardia following alcohol septal ablation for hypertrophic obstructive cardiomyopathy Pacing Clin Electrophysiol 2005;28:1354-1356.[CrossRef][Medline] 8. Batalis NI, Harley RA, Collins KA. 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Microvascular obstruction after nonsurgical septal reduction for the treatment of hypertrophic cardiomyopathy Circulation 2001;104:1868. 13. Ralph-Edwards A, Woo A, McCrindle BW, et al. Hypertrophic obstructive cardiomyopathy: comparison of outcomes after myectomy or alcohol ablation adjusted by propensity score J Thorac Cardiovasc Surg 2005;129:351-358.[Abstract/Free Full Text] 14. Qin JX, Shiota T, Lever HM, et al. Outcome of patients with hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation and septal myectomy surgery J Am Coll Cardiol 2001;38:1994-2000.[Abstract/Free Full Text] 15. Firoozi S, Elliott PM, Sharma S, et al. Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathyA comparison of clinical, haemodynamic and exercise outcomes. Eur Heart J 2002;23:1617-1624.[Abstract/Free Full Text] 16. Nagueh SF, Ommen SR, Lakkis NM, et al. 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Usefulness of selective myocardial contrast echocardiography in percutaneous transluminal septal myocardial ablation: a case report Jpn Circ J 2001;65:842-844.[CrossRef][Medline] 21. Faber L, Seggewiss H, Ziemssen P, Gleichmann U. Intraprocedural myocardial contrast echocardiography as a routine procedure in percutaneous transluminal septal myocardial ablation: detection of threatening myocardial necrosis distant from the septal target area Cathet Cardiovasc Interv 1999;47:462-466.[CrossRef][Web of Science][Medline] 22. Alfonso F, Isla LP, Seggewiss H. Contrast echocardiography during alcohol septal ablation: friend or foe? Heart 2005;91:e18.[Free Full Text] 23. Gross CM, Schulz-Menger J, Kramer J, et al. Percutaneous transluminal septal artery ablation using polyvinyl alcohol foam particles for septal hypertrophy in patients with hypertrophic obstructive cardiomyopathy: acute and 3-year outcomes J Endovasc Ther 2004;11:705-711.[CrossRef][Web of Science][Medline] 24. Lafont A, Durand E, Brasselet C, Mousseaux E, Hagege A, Desnos M. Percutaneous transluminal septal coil embolisation as an alternative to alcohol septal ablation for hypertrophic obstructive cardiomyopathy Heart 2005;91:92.[Free Full Text] 25. Monakier D, Woo A, Puri T, et al. Usefulness of myocardial contrast echocardiographic quantification of risk area for predicting postprocedural complications in patients undergoing septal ethanol ablation for obstructive hypertrophic cardiomyopathy Am J Cardiol 2004;94:1515-1522.[CrossRef][Web of Science][Medline] 26. Chang SM, Lakkis NM, Franklin J, Spencer 3rd WH, Nagueh SF. Predictors of outcome after alcohol septal ablation therapy in patients with hypertrophic obstructive cardiomyopathy Circulation 2004;109:824-827Epub 2004 Feb 16. 27. Veselka J, Prochazkova S, Duchonova R, et al. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: lower alcohol dose reduces size of infarction and has comparable hemodynamic and clinical outcome Catheter Cardiovasc Interv 2004;63:231-235.[CrossRef][Web of Science][Medline] 28. van Dockum WG, Beek AM, ten Cate FJ, et al. Early onset and progression of left ventricular remodeling after alcohol septal ablation in hypertrophic obstructive cardiomyopathy Circulation 2005;111:2503-2508Epub 2005 May 2. 29. Faber L, Seggewiss H, Gietzen FH, et al. Catheter-based septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: follow-up results of the TASH-registry of the German Cardiac Society Z Kardiol 2005;94:516-523.[CrossRef][Web of Science][Medline] 30. Lee CH, Ng W, Chow WH. Ethanol septal ablation for hypertrophic obstructive cardiomyopathy in a very old patient Age Ageing 2001;30:351-353.[Abstract/Free Full Text] 31. Woo A, Williams WG, Choi R, et al. Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy Circulation 2005;111:2033-2041. 32. Robbins RC, Stinson EB. Long-term results of left ventricular myotomy and myectomy for obstructive hypertrophic cardiomyopathy J Thorac Cardiovasc Surg 1996;111:586-594.[Abstract/Free Full Text] 33. Kuhn H, Seggewiss H, Gietzen FH, Boekstegers P, Neuhaus L, Seipel L. Catheter-based therapy for hypertrophic obstructive cardiomyopathyFirst in-hospital outcome analysis of the German TASH Registry. Z Kardiol 2004;93:23-31.[CrossRef][Web of Science][Medline] 34. Faber L, Seggewiss H, Welge D, et al. Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience Eur J Echocardiogr 2004;5:347-355.
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