Reply
Deborah H. Kwon, MD,
Samir R. Kapadia, MD,
E. Murat Tuzcu, MD,
Harry M. Lever, MD,
Milind Y. Desai, MD*
We thank Drs. Parakh and Bhargava for their interest in our paper (1). Their letter highlights the long-standing controversy regarding alcohol septal ablation (ASA) versus surgical myectomy for optimal management of patients with hypertrophic obstructive cardiomyopathy (HOCM). We feel that the concerns raised by Drs. Parakh and Bhargava are a bit presumptuous. The mean amount of alcohol injected, even by 1997 to 2000 standards for our study population (1), was very low and the operators were extremely judicious in its use (mean volume: 2.65 ± 0.81 cc). The pacemaker implantation rate is high, although our study shows similar incidence to studies from a comparable U.S. center (2). The likely reason for high pacemaker rate could be the possibility that these patients were relatively older, with more conduction abnormalities at baseline (12 of 55 patients had either left or right bundle branch block). Also, the assumption on the part of Drs. Parakh and Bhargava that we subjected all surgical "rejects" indiscriminately to ASA, irrespective of septal perforator anatomy, is wrong. All the alcohol injections were targeted to the contact point of the mitral valve to the septum, using echocardiographic (including contrast) guidance. The success rate of the procedure proves that the procedure was performed appropriately (1).
As a high-volume practice, we do feel strongly that the choice of procedural treatment of HOCM should be made after thorough multimodality imaging evaluation of the actual cause of dynamic outflow tract obstruction. According to some estimates, up to 20% of patients have persistent symptoms due to left ventricular outflow tract (LVOT) obstruction following ASA, which is likely due to suboptimal procedural result (3–5). A recent study demonstrated that patients undergoing ASA usually end up with a basal inferoseptal (as opposed to the preferred anteroseptal) infarction, as compared with patients who undergo myectomy (6). That study also demonstrated that myectomy resulted in a "more complete" relief of LVOT obstruction than did ASA (6). Another issue that needs attention, and perhaps should be studied in the future, is that of myocardial scarring that is induced by ASA and the potential for ventricular tachyarrhythmias. Also, there are many other potential reasons for suboptimal results following ASA. A recent study (7) highlighted other important mitral subvalvular aspects leading to a failed ASA. It demonstrated the multifactorial etiology of dynamic LVOT obstruction, which includes mitral apparatus abnormalities, such as anterior displacement of the papillary muscles leaflet elongation and anteriorly displaced coaptation of the mitral valve leaflets. We have also observed abnormal chordae attachment to the base of the anterior mitral leaflet resulting in systolic "buckling" of and dynamic LVOT obstruction, even in the setting of a normal-sized upper septum. In fact, 1 large surgical series identified abnormalities of the mitral valve in 19% of patients undergoing surgical myectomy, which required further modification of surgical technique to relieve obstruction (8). A priori identification of such abnormalities might be crucial for an optimal result following ASA.
As aptly described in a recent editorial by Sigwart (9), "ASA was never devised to replace surgery for symptomatic patients with HOCM. It was intended to provide those patients, young and old, who have favorable (and accessible) anatomy, with an alternative to open heart surgery through the induction of a meaningful septal necrosis." In conclusion, we stand by our assertion that at present, based on all the available data, surgical myectomy is the preferred option for young patients with drug refractory HOCM and for those with additional structural changes in the mitral valve, papillary muscles, and coronary arteries. Furthermore, the most important step in the management of patients with HOCM, even before they get to either the surgical suite or the catheterization laboratory, is to identify the exact etiology of dynamic outflow tract obstruction.
* Department of Cardiovascular Medicine, Heart and Vascular Institute, Desk J1-5, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio 44195 (Email: desaim2{at}ccf.org).
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REFERENCES
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- Kwon DH, Kapadia SR, Tuzcu EM, et al. Long-term outcomes in high-risk symptomatic patients with hypertrophic cardiomyopathy undergoing alcohol septal ablation J Am Coll Cardiol Intv 2008;1:432-438.[Abstract/Free Full Text]
- Sorajja P, Valeti U, Nishimura RA, et al. Outcome of alcohol septal ablation for obstructive hypertrophic cardiomyopathy Circulation 2008;118:131-139.[Abstract/Free Full Text]
- Fernandes VL, Nagueh SF, Wang W, Roberts R, Spencer 3rd WH. A prospective follow-up of alcohol septal ablation for symptomatic hypertrophic obstructive cardiomyopathy—the Baylor experience (1996–2002) Clin Cardiol 2005;28:124-130.[Web of Science][Medline]
- Kuhn H, Gietzen FH, Leuner C, et al. Transcoronary ablation of septal hypertrophy (TASH): a new treatment option for hypertrophic obstructive cardiomyopathy Z Kardiol 2000;89(Suppl 4):IV41-IV54.[CrossRef][Medline]
- 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]
- Valeti US, Nishimura RA, Holmes DR, et al. Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with hypertrophic obstructive cardiomyopathy J Am Coll Cardiol 2007;49:350-357.[Abstract/Free Full Text]
- Delling FN, Sanborn DY, Levine RA, et al. Frequency and mechanism of persistent systolic anterior motion and mitral regurgitation after septal ablation in obstructive hypertrophic cardiomyopathy Am J Cardiol 2007;100:1691-1695.[CrossRef][Web of Science][Medline]
- Minakata K, Dearani JA, Nishimura RA, Maron BJ, Danielson GK. Extended septal myectomy for hypertrophic obstructive cardiomyopathy with anomalous mitral papillary muscles or chordae J Thorac Cardiovasc Surg 2004;127:481-489.[Abstract/Free Full Text]
- Sigwart U. Catheter treatment for hypertrophic obstructive cardiomyopathy: for seniors only? Circulation 2008;118:107-108.[Free Full Text]
Related Article
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Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy: The Joys Are Brief: The Results Are Lasting
- Neeraj Parakh and Balram Bhargava
J. Am. Coll. Cardiol. Intv. 2009 2: 74.
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