Aetna considers percutaneous transluminal septal myocardial ablation (PTSMA) by alcohol-induced septal branch occlusion medically necessary for hypertrophic obstructive cardiomyopathy (HOCM) in adults when all of the following criteria are met:
Member has severe symptoms (e.g., dyspnea, angina pectoris, [pre]syncope, palpitations or heart failure) for at least 6 months despite optimal drug therapy (e.g., beta-blockers, calcium-antagonists), dual chamber pacing therapy and/or ineffective previous surgical myotomy/myectomy; and
Member is classified as New York Heart Association class III or IV (see below); and
Member has a classical, asymmetric subaortic HOCM identified by echocardiography, and not a mid-ventricular, a concealed membranous subaortic stenosis, nor supravalvular form; and
Echocardiography shows left ventricular wall thickness of greater than 13 mm in adults in the absence of another cause for left ventricular hypertrophy; 15 mm in an athlete; and
Member has systolic anterior motion of the mitral valve on echocardiography; and
Member has a resting left ventricular outflow tract (LVOT) gradient of greater than 30 mm Hg or a stressed gradient of greater than 60 mm Hg, or member has less severe symptoms and LVOT of greater than 50 mm Hg at rest or greater than 100 mm Hg under stress; and
Member does not have coronary artery disease that would preclude performance of the procedure.
Aetna considers percutaneous transluminal septal myocardial ablation experimental and investigational for all other indications because of insufficient evidence of its safety and effectiveness.
Hypertrophic obstructive cardiomyopathy (HOCM), also known as idiopathic hypertrophic subaortic stenosis, is a primary, sometimes familial and genetically determined myocardial hypertrophy with an incidence of about 0.2 %. About 25 % of the patients have dynamic left ventricular outflow tract (LVOT) obstruction, which usually develops during puberty and increases in severity until the age of 18 to 20 years. Not infrequently, HOCM is diagnosed for the first time in the elderly.
Echocardiography is the primary method for diagnosing HOCM. This condition is characterized by a super-normally contracting left ventricle, asymmetric septal hypertrophy, which affects mainly the interventricular septum, increased ventricular wall thickness (left ventricular wall thickness of greater than 13 mm in adults in the absence of another cause for left ventricular hypertrophy; 15 mm in an athlete), and systolic anterior motion of the mitral valve. Although patients with hypertrophic cardiomyopathy usually have super-normal ejection fractions, they have thickened and poorly compliant left ventricles in which left ventricular filling pressure is markedly elevated and probably is responsible for most of the symptoms.
Cardiac hypertrophy is associated with LVOT obstruction in only a minority of HOCM patients. The LVOT gradient is generated by systolic anterior motion of a mitral valve leaflet and its coaptation with the interventricular septum. Left ventricular outflow tract obstruction does not generally increase during exercise because of adequate venous return, but it often worsens or becomes apparent in the immediate post-exercise period. Maneuvers that decrease preload or afterload or increase myocardial contractility, such as stress, dehydration, and sudden adoption of an erect posture often induce symptoms. The significance of the LVOT gradient has been debated, but it is now generally accepted that it is an important determinant of the clinical course.
Asymptomatic adult patients probably do not require therapy or risk stratification studies, unless there is a malignant family history of sudden death or occupational need (airline pilot). Management decisions are dominated by the need to address sometimes disabling symptoms of dyspnea, angina pectoris, stress-induced syncope, palpitations or heart failure, and risk of sudden death. Treatment of symptomatic patients with HOCM aims at reduction of the LVOT gradient and improvement of diastolic filling either by pharmacological therapy with negative inotropic drugs (beta-blockers, calcium-antagonists), permanent DDD pacemaker therapy (i.e., dual- chamber, dual-pacing, dual-sensing), or surgical myotomy/myectomy.
At least 10 % of patients with severe HCOM are unresponsive to medical therapy or report severe side effects of optimum doses of drugs. Successful DDD pacing at the apex of the right ventricle induces a paradoxic motion of the inter-ventricular septum away from the mitral valve, reducing LVOT obstruction. Long-term studies have uniformly confirmed that DDD pacing can reduce LVOT gradient and improve severe drug-refractory symptoms in most patients with HOCM, obviating the need for cardiac surgery. A large European study has demonstrated that when follow-up was sufficiently long to allow adaptive changes and to eliminate carryover effects, DDD pacing conferred substantial symptomatic and hemodynamic benefits. As some of the beneficial effects of DDD pacing become apparent after prolonged pacing, it is important to allow sufficient time for chronic DDD pacemaker therapy.
Left ventricular myotomy and myectomy (Morrow's procedure) has been the standard therapy for patients with severe symptoms (New York Heart Association (NYHA) functional class III to IV) that persist despite adequate pharmacotherapy and DDD pacing. Using an aortic root approach, this involves surgically removing enough muscle from the septum to sufficiently widen the outflow tract. The procedure improves or eliminates symptoms and LVOT gradient in 90 % of patients. The success of the procedure and the operative mortality are very much dependent on the skill and experience of the surgeon but may be as low as 1 to 2 %. Complications include heart block, ventricular septal defect, 1 to 2 % annual mortality during follow-up, late aortic valve incompetence, and LV dysfunction. Sometimes, a prosthetic mitral valve replacement must be done to eliminate systolic anterior motion and LVOT obstruction, but the patient requires life-long anti-coagulation and is subject to the risk of prosthetic malfunction.
In 1994, as an alternative to surgery, non-surgical percutaneous transluminal septal myocardial ablation (PTSMA) by alcohol-induced septal branch occlusion was introduced to decrease LVOT gradient and improve symptoms in patients with HOCM. This method was substantially improved by the introduction of echocardiographic guidance in 1996. With this guidance, the reduction in the LVOT gradient is optimized and ablation of inappropriate areas can be avoided. Consequently, the hemodynamic results and symptoms are improved, and the incidence of complications is reduced. The most common procedural complication is the development of high-grade trifascicular block necessitating implantation of a permanent pacemaker in 25 % of patients. Other complications include death, ventricular arrhythmias, and coronary artery dissection.
Percutaneous transluminal septal myocardial ablation involves transcatheter selection of 1 or 2 small septal branches of the left anterior descending artery, threading a small, short, low-pressure angioplasty balloon into position to occlude the artery, and the instillation of absolute alcohol into the myocardium. The resultant localized myocardial infarction reduces the amount of septal myocardium, opening up the LVOT. Compared with surgical myectomy, the literature shows that PTSMA has the advantage of being minimally invasive, easily repeated, and with relatively low major morbidity/mortality risk for patients with co-morbid conditions.
In one study, 70 % of patients during short-term follow-up showed impressive clinical improvement as well as diminution of intra-ventricular pressure gradient and a marked increase in maximal workload during exercise testing. During a 12-month follow-up period, there was a significant decrease of functional class, a reduced rate of syncope, and a reduced degree of mitral insufficiency. Exercise capacity, oxygen uptake and the cardiac index increased, intra-ventricular gradient, the end diastolic pressure of the left ventricle and the left atrial size decreased. Additionally, there was a decrease in the septal thickness with increase in the cross-sectional area of the outflow tract. PET examination showed an ablation-induced local myocardial defect. There was also evidence for improved diastolic function. Electrophysiological and Holter monitor studies indicated no increased arrhythmogenicity. The in-hospital mortality rate amounts to about 1.8 % and in 15 % of patients a second PTSMA is necessary.
There appears to be little doubt in the literature that favorable morphologic and functional results can be achieved by PTSMA, and that short-term follow-up studies show clinical and objective improvement, as well as further gradient reduction due to left ventricular remodeling. Currently, randomized, prospective studies of larger patient series are being conducted to compare the short- and long-term effects of PTSMA with the major treatment options (e.g., pharmacologic therapy, myotomy/myectomy, mitral valve replacement, pacemaker implantation). The outcomes of these studies will be needed to determine PTSMA’s ultimate role in the treatment of HOCM, as well as provide guidance concerning the optimal treatment of patients with HOCM.
The American Heart Association and the American College of Cardiology have no position statements on this procedure.
An assessment by the National Institute of Clinical Excellence (NICE, 2003) concluded that current evidence on the safety and efficacy of non-surgical reduction of the myocardial septum appears adequate to support the use of the procedure, provided that normal arrangements are in place for consent, audit and clinical governance.
Percutaneous transluminal septal myocardial ablation is best performed in centers with experience with this procedure. Patients treated with PTSMA should be entered into a registry of these procedures.
Zhang and colleagues (2011) retrospectively summarized the effect of non-medical therapies for pediatric patients with HOCM. From November 2008 to June 2010, 4 children with drug-refractory HOCM were admitted to the authors' hospital. Their ages were 14, 7, 9 and 6 years old, respectively. Their body weights were 38, 17, 21.5 and 17 kg, respectively. Before operation, the LVOT gradients were 60, 147, 58 and 114 mm Hg (1 mm Hg = 0.133 kPa), respectively; mitral regurgitation (MR) areas were 2.2, 7.3 cm(2) and 2.9 cm(2), respectively, except that it was trivial in 1 case. Percutaneous transluminal septal myocardial ablation was performed in case 1 and 2. Septal myectomy (SM) was performed in case 3 and 4. Follow-up was first performed right after operation or before discharge, then 1 month, 3 months, 6 months, and 12 months after operation, and then once-yearly. The follow-up period was 1 to 18 (9.3 +/- 8.1) months. All patients experienced relieved symptoms; 3 of them had their NYHA functional class improved except case 2. Echocardiography revealed that LVOT gradients right after operations were 38, 79, 20 and 0 mm Hg, respectively, suggesting significant improvement of LVOT obstruction in all patients. During follow-up, case 2 suffered from recurrence of LVOT obstruction, while the other 3 cases showed sustained relief. In the last follow-up, the LVOT gradients of the 4 patients were 19, 168, 16 and 0 mm Hg, respectively. Echocardiography also revealed that MRs of all patients were significantly reduced, even in case 2 whose LVOT gradient rebounded, with no recurrence during follow-up. Severe complications were absent, such as ventricular septum perforation, cardiac tamponade, ventricular tachycardia or ventricular fibrillation. No one suffered from complete heart block. Transient complete right bundle branch block (CRBBB) was observed in case 1 after PTSMA and converted to intra-ventricular block after 1 month. Complete left bundle branch block (CLBBB) was present in both case 3 and 4, who received SM. In case 4, it converted to intra-ventricular block after 1 month while in case 3 CLBBB persisted. The authors concluded that the initial experience showed that PTSMA and SM were safe and effective for drug-refractory symptomatic HOCM children, with satisfactory short-term results. They stated that further studies are needed to evaluate the long-term results and complications.
The New York Heart Association (NYHA) classification is as follows:
Patients with cardiac disease but without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.
Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.
CPT Codes / HCPCS Codes / ICD-9 Codes
There is no specific CPT code for percutaneous transluminal septal myocardial ablation:
Other HCPCS codes related to the CPB:
Catheter, extravascular tissue ablation, any modality (insertable)
ICD-9 codes covered if selection criteria are met:
Coronary atherosclerosis [CAD could preclude performance of procedure]
428.0 - 428.9
Syncope and collapse [presyncope]
Other dyspnea and respiratory abnormalities
Cardiac pacemaker in situ
The above policy is based on the following references:
Nagueh SF, Lakkis NM, Middleton KJ, et al. Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation. 1999;99(3):344-347.
Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: Results with respect to intraprocedural myocardial contrast echocardiography. Circulation. 1998;98(22):2415-2421.
Nagueh SF, Lakkis NM, He ZX, et al. Role of myocardial contrast echocardiography during nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol. 1998;32(1):225-229.
Seggewiss H, Gleichmann U, Faber L, et al. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: Acute results and 3-month follow-up in 25 patients. J Am Coll Cardiol. 1998;31(2):252-258.
Lerakis S, Sheahan RG, Stouffer GA. Hypertrophic cardiomyopathy: Presentation and pathophysiology. Am J Med Sci. 1997;314(5):324-329.
Knight C, Kurbaan AS, Seggewiss H, et al. Nonsurgical septal reduction for hypertrophic obstructive cardiomyopathy: Outcome in the first series of patients. Circulation. 1997;95(8):2075-2081.
Sigwart U. Nonsurgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet. 1995;346:211–214
Lakkis NM, Nagueh SF, Kleiman NS, et al. Echocardiography-guided ethanol septal reduction for hypertrophic obstructive cardiomyopathy. Circulation. 1998;98:1750–1755
Spirito P. Alcohol septal ablation in the management of obstructive hypertrophic cardiomyopathy. Ital Heart J. 2000;1(11):721-725.
Maron BJ. Role of alcohol septal ablation in treatment of obstructive hypertrophic cardiomyopathy. Lancet. 2000;355(9202):425-426.
Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic cardiomyopathy. Curr Cardiol Rep. 2001;3(2):160-166.
Cheng TO. Transcatheter alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Circulation. 1999;100(11):1252.
Kim JJ. Improvement in exercise capacity and exercise blood pressure response after transcoronary alcohol ablation therapy of septal hypertrophy in hypertrophic cardiomyopathy. Am J Cardiol. 1999;83(8):1220-1223.
No authors listed. Alcohol injections replace surgery for patients with hypertrophic cardiomyopathy. Harv Heart Lett. 1999;9(5):4.
Kuhn H. Transcoronary ablation of septal hypertrophy (TASH): A new treatment option for hypertrophic obstructive cardiomyopathy. Z Kardiol. 2000;89(Suppl 4):IV41-IV54.
Faber L. Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy: Long term follow up of the first series of 25 patients. Heart. 2000;83(3):326-331.
Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic cardiomyopathy. Curr Cardiol Rep. 2001;3(2):160-166.
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(7):1994-2000.
Mutlak D, Gruberg L, Reisner S, et al. Non-surgical myocardial reduction in hypertrophic obstructive cardiomyopathy. Isr Med Assoc J. 2002;4(2):86-90.
Jiang T, Wu X, Jia C, et al. Percutaneous transluminal septal myocardial ablation in patients with hypertrophic obstructive cardiomyopathy. Chin Med J (Engl). 2002;115(1):26-30.
Kovacic JC, Muller D. Hypertrophic cardiomyopathy: State-of-the-art review, with focus on the management of outflow obstruction. Intern Med J. 2003;33(11):521-529.
National Institute for Clinical Excellence (NICE). Interventional procedure overview of non-surgical reduction of myocardial septum. London, UK: NICE; November 2003. Available at: http://www.nice.org.uk/page.aspx?o= 90963. Accessed September 13, 2005.
Li ZQ, Cheng TO, Zhang WW, et al. Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy: The Chinese experience in 119 patients from a single center. Int J Cardiol. 2004;93(2-3):197-202.
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(2):231-235.
National Institute for Clinical Excellence (NICE). Non-surgical reduction of myocardial septum. Interventional Procedure Guidance 40. London, UK: NICE; February 2004. Available at: http://www.nice.org.uk/page.aspx?o=104270. Accessed September 13, 2005.
van der Lee C, ten Cate FJ, Geleijnse ML, et al. Percutaneous versus surgical treatment for patients with hypertrophic obstructive cardiomyopathy and enlarged anterior mitral valve leaflets. Circulation. 2005;112(4):482-488.
Zeng Z, Wang F, Dou X, et al. Comparison of percutaneous transluminal septal myocardial ablation versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy--a meta analysis. Int J Cardiol. 2006;112(1):80-84.
Murphy RT, Ratliff NB, Lever HM, Kapadia SR. Use of percutaneous transluminal septal myocardial ablation for relief of outflow tract obstruction in cardiac amyloidosis: A novel therapeutic target. Catheter Cardiovasc Interv. 2006;68(4):637-641.
Seggewiss H, Rigopoulos A, Welge D, et al. Long-term follow-up after percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Clin Res Cardiol. 2007;96(12):856-863.
Hosokawa Y, Takano H, Ohno T, et al. Impact of percutaneous transluminal septal myocardial ablation on refractory paroxysmal atrial fibrillation in patients with hypertrophic obstructive cardiomyopathy. Angiology. 2008;59(3):329-334.
Welge D, Seggewiss H, Fassbender D, et al. Long-term follow-up after percutaneous septal ablation in hypertrophic obstructive cardiomyopathy. Dtsch Med Wochenschr. 2008;133(39):1949-1954.
van der Lee C, Scholzel B, ten Berg JM, et al. Usefulness of clinical, echocardiographic, and procedural characteristics to predict outcome after percutaneous transluminal septal myocardial ablation. Am J Cardiol. 2008;101(9):1315-1320.
Faber L, Welge D, Hering D, et al. Percutaneous septal ablation after unsuccessful surgical myectomy for patients with hypertrophic obstructive cardiomyopathy. Clin Res Cardiol. 2008;97(12):899-904.
Llamas-Esperón GA, Loera Pinales A, Sandoval Navarrete S, et al. Percutaneous transluminal septal myocardial ablation in patients with obstructive septal hypertrophic myocardiopathy. Acute results and 3-year follow-up. Arch Cardiol Mex. 2009;79(1):33-40.
Gersh BJ, Maron BJ, Bonow RO, et al.; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines; American Association for Thoracic Surgery; American Society of Echocardiography; American Society of Nuclear Cardiology; Heart Failure Society of America; Heart Rhythm Society; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;124(24):2761-2796.
Zhang X, Li YF, Xie B, et al. Non-drug treatment for hypertrophic obstructive cardiomyopathy in children. Zhonghua Er Ke Za Zhi. 2011;49(5):381-385.
Jensen MK, Almaas VM, Jacobsson L, et al. Long-term outcome of percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: A Scandinavian multicenter study. Circ Cardiovasc Interv. 2011;4(3):256-265.
Jensen MK, Havndrup O, Hassager C, et al. Survival and sudden cardiac death after septal ablation for hypertrophic obstructive cardiomyopathy. Scand Cardiovasc J. 2011;45(3):153-160.
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