Alcohol Septal Ablation: What Have We Learned From Multicenter Versus Single-Center Experience, and Aggregate Versus Individualized Outcomes?

Srihari S. Naidu, MD

Srihari S. Naidu, MD

Developed over 20 years ago, alcohol septal ablation no longer qualifies as a novel procedure with opaque risks. Indeed, by some estimation, it is performed more frequently than surgical myectomy in the United States, and by far more frequently in the remainder of the world, despite 2011 American Heart Association/American College of Cardiology guidelines promoting surgical myectomy as the gold standard.1 The reasons behind this apparent paradox in favor of the percutaneous approach are multifactorial and include large observational experiences indicating similar safety and efficacy both short and long-term, less morbidity and recuperation, diminishing pacemaker-dependency rates to the single digits, strong physician and patient preference for a minimally invasive option with reduced length of stay and earlier return to work, relatively less availability and generalizability of surgical myectomy, an aging population with serious comorbidities and debilitation, and both religious and spiritual beliefs in a large portion of the world against open procedures. Consistent with this international trend and accumulated data, more recent 2014 guidelines from the European Society of Cardiology (ESC) support both alcohol septal ablation and surgical myectomy equally as class-1 indications, with surgery preferred only in those who require concomitant surgical interventions, such as valve replacement.2

Much of this exuberance and international support, however, is predicated on the ability of alcohol septal ablation to mirror the results of surgical myectomy. And, in large observational multicenter experiences, this is indeed the case. Both procedures result in improvement in New York Heart Association class by at least one grade in 80%-90% of patients, and marked reductions in gradients to <10-20 mm Hg, somewhat better with surgery but clearly sufficient and non-obstructive with alcohol septal ablation. Thus, both provide robust clinical and hemodynamic benefits, a marker of comprehensively successful procedures that should stand the test of time. More recent data also confirm <1% procedural mortality for both surgery and alcohol septal ablation in large single-center experience, <1%-2% procedural mortality for both in multiple large multicenter studies (both within the United States and in Europe), and no long-term survival difference between the two, approaching 75%-80% at 8-10 years when controlled for age and gender.3-5 Taken together with the updated ESC guidelines, it is not surprising that alcohol septal ablation procedures may be on the rise, and that future United States guideline iterations may consider elevating the corresponding recommendation similarly.

In the current issue of the Journal of Invasive Cardiology, however, the study by Cooper et al asks a useful question: “Does reporting of aggregate outcomes hide less-favorable results experienced by a substantial proportion of patients?”6 In their single-center, single-operator experience, roughly 80 patients underwent alcohol septal ablation over 12 years (~6-7 procedures per year). Indications for therapy were consistent with currently published criteria, and their technique evolved during this time frame toward current standards of myocardial contrast echocardiography guidance and lower aliquots of ethanol. They then followed patients for early and late complications, including pacemaker placement, as well as the frequency of clinical success, hemodynamic success, both or neither at long-term follow-up. Compartmentalized in this fashion, they found that only 66% of patients achieved both clinical and hemodynamic success, hardly reassuring, and resulting in their above question. But, as with all things, the devil is in the details and a closer examination of the data sheds necessary light on the findings.

First, let us examine the procedural outcome. The operator performed 6-7 procedures per year, below the 10 per year recommended by competency statements.7 Nonetheless, knowing the field well and this particular center, I am confident that the operator was as experienced or more than most performing this relatively rare procedure. However, despite this, there was a very high failure rate. In total, 27% of patients required repeat procedures, compared with 5% in established multicenter series, including the 10-fold larger North American registry.3 And whereas most of these 5% only required one repeat procedure, several patients in the current series required three procedures and 1 patient required a fourth encounter. This large recurrence rate is unheard of, and suggests less than optimal preprocedure planning, localization of the site of septal contact, identification of septal perforators (some of which are small and unappealing at first glance), or intraprocedural hemodynamic evaluation (patients who are sedated, for example, may have false indications of success). The high pacemaker rate of 18% is also inconsistent with current literature and the improvement in the second half of their experience remains significantly higher than expected.3 Thus, to the authors’ question, one might rebut: “Does reporting of individual operator and center outcomes adequately portray procedural safety and efficacy when generalized to the wider population of centers, operators, and patients?” To this, I would answer with a resounding “no,” and indeed this is the linchpin concept that drives the hierarchy of accepted clinical evidence favoring multicenter randomized controlled trials and meta-analyses of multicenter observational experience over multicenter observational experience, single-center observational experience, single-operator experience, and on down to case series and case reports.

Second, even if one were to assume that the procedural planning, skill, and technique were ideal, do the data portray a less than stellar procedure or a less than ideal patient population? To wit, 66% of patients achieved both clinical and hemodynamic success, but another 18% achieved hemodynamic success without clinical improvement. Possibilities here include remaining residual limiting cardiac dysfunction, such as profound diastolic dysfunction or irreversible pulmonary hypertension, or the distinct possibility that cardiac disease was not the limiting factor in the patient’s clinical condition. Indeed, current United States guidelines favor alcohol septal ablation for those at prohibitive surgical risk, and this has encroached also into patients in whom it is unclear whether the cardiac disease, specifically the outflow tract obstruction itself, is limiting the patient. These include the morbidly obese, the ancient, those with severe arthritis, and other severe comorbidities such as profound lung disease, the latter found in one-half of the non-responders in the current series. In my own patient population, where patients often seek out the Winthrop HCM Center due to our expertise in alcohol septal ablation, my average patient undergoing the procedure is in their mid-60s, with several well into their 80s, and a sizable portion have severe comorbidities such as lung disease or severe pulmonary hypertension. Such patients are not surgical candidates, and alcohol septal ablation becomes the only viable option to remove obstruction and improve any secondary phenomena, such as diastolic dysfunction or pulmonary hypertension. But, at the end of the day, if the obstruction is not the limiting component of their syndrome, alcohol septal ablation will provide hemodynamic benefit but not clinical benefit. As the current authors suggest, VO2 testing might provide some discerning ability in the future, but is not an exact science. Taken together, if you add the 18% to the 66%, over 80% of patients in the current series achieved the type of hemodynamic success that would be expected to provide symptom relief, and this is consistent with the large alcohol septal ablation and surgical myectomy experiences in patients who are otherwise healthy. 

I applaud the authors for their work, however, mainly because their question needed to be raised. Practically speaking, surgical myectomy is not an option for everyone, whereas alcohol septal ablation oftentimes is. And, I will be the first to state that this is a dangerous statement to make. Indeed, anatomically, the very opposite is true. Surgical myectomy can address all anatomic derangements, including abnormal membranes, redundancy of the mitral leaflets, asymmetric severe hypertrophy, or abnormal papillary muscles (size, thickness, location, or insertion). In contrast, anatomically, alcohol septal ablation is limited, only able to tackle asymmetric hypertrophy in the absence of other significant derangements. Yet, clinically, surgical myectomy is not for everyone – those too old or sick for surgery or the recuperation required will not be offered open-heart surgery, and rightly so. This leads to a potential overutilization of alcohol septal ablation in patients who will not benefit – those with significant anatomic derangements that will sustain obstructive physiology even if the basal hypertrophy regresses, and those with other clinical conditions that are the truly limiting factors. In such patients, there is a hemodynamic improvement, but not a clinical one.

So where do we go from here? To me, the more important part of this study is the final discussion regarding improvements to alcohol septal ablation that will make it more appropriate, generalizable, safe, and efficacious. First and foremost, we must not deviate from the strict indications and contraindications to the procedure. Anatomic criteria are paramount, and if there is low likelihood of hemodynamic success, then this should be relayed to the referring physician and patient, and alcohol septal ablation not pursued unless all are willing to take a less than optimal outcome. Surgical myectomy should be preferred in these settings if the patient is a surgical candidate. Second, we must do a better job of ascertaining the limiting problem. Is it severe coronary disease, pulmonary disease, arthritis, overall debilitation and poor nutrition, or morbid obesity, for example, instead of the obstructive physiology? Further, at the extremes of age, patients may have suffered a lifetime of chronic low-output state and congestive heart failure, with relief of obstruction being too little or too late. Surgical myectomy would of course not be contemplated in such high-risk patients, but the minimally-invasive alcohol septal ablation might be. The distinct possibility of hemodynamic success without clinical success must be both considered and accepted in such patients.

Finally, as the authors correctly suggest, there are technical limitations of the procedure that require ongoing research. We need to identify appropriate anatomy better, we need to identify and engage the optimal septal artery better, we need to target the left ventricular side of the septum better, and we need to develop ways of modifying and optimizing our results, such as with improved hemodynamic intraprocedure endpoints, or complementary or alternative procedures such as Mitraclip, microspheres, or endocardial radiofrequency ablation.5 In addition, we have to make sure that patients are sent to centers of high volume with documented short-term and long-term success, consistent with current guidelines and competency statements.1,2 Such centers will maintain <1%-2% procedural mortality and <10% new pacemaker rate, perform a minimum of 8-10 alcohol septal ablations per year, and operate as one component of a comprehensive, multidisciplinary HCM center devoted to these patients.7 To this end, even existing HCM centers will benefit from procedural training courses, such as the one I initiated in 2014 and conduct annually at Beaumont Medical Center. Such training courses that dive into the indications, contraindications, anatomic pitfalls, technical optimization, follow-up care, and long-term options to treat recurrence are sorely needed and should be embraced by those both early and late in their procedural expertise, thereby reducing practice variation in case selection and technique, and resultant variation in outcomes.


  1. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy. Circulation. 2011;124(24):2761-2796. Epub 2011 Nov 8.
  2. Elliott PM, Anastasakis A, Borger MA, et al. 2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy. Eur Heart J. 2014;35(39):2733-2779.Epub 2014 Aug 29.
  3. Nagueh SF, Groves BM, Schwartz L, et al. Alcohol septal ablation for the treatment of hypertrophic obstructive cardiomyopathy. A multicenter North American registry. J Am Coll Cardiol. 2011;58(22):2322-2328.
  4. Steggerda RC, Damman K, Balt JC, Liebregts M, ten Berg JM, van den Berg MP. Periprocedural complications and long-term outcome after alcohol septal ablation versus surgical myectomy in hypertrophic obstructive cardiomyopathy. JACC Cardiovasc Interv. 2014;7(11):1227-1234.
  5. Sorajja P, Ommen SR, Holmes DR Jr, et al. Survival after alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Circulation. 2012;126(20):2374-2380.
  6. Cooper RM, Shahzad A, McShane J, Stables RH. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: safe and apparently efficacious but does reporting of aggregate outcomes hide less-favorable results, experienced by a substantial proportion of patients? J Invasive Cardiol 2015;27(5):xxz-xzz.
  7. Harold J, Bass T, Bashore TM, et al. ACCF/AHA/SCAI 2013 update of the clinical competence statement on coronary artery interventional procedures. J Am Coll Cardiol. 2013;62(4):357-396.


From the Hypertrophic Cardiomyopathy Treatment Center, Division of Cardiology, Winthrop University Hospital, Mineola, New York.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Address for correspondence: Srihari S. Naidu, MD, FACC, FSCAI, FAHA, Director, HCM Treatment Center, Winthrop University Hospital Mineola, NY 11501. Email