Percutaneous Transluminal Septal Myocardial Ablation (PTSMA)

Number: 0558

Table Of Contents

Policy
Applicable CPT / HCPCS / ICD-10 Codes
Background
References


Policy

Scope of Policy

This Clinical Policy Bulletin addresses percutaneous transluminal septal myocardial ablation (PTSMA).

  1. Medical Necessity

    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:

    1. 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
    2. Member is classified as New York Heart Association class III or IV (see below); and
    3. Member has a classical, asymmetric subaortic HOCM identified by echocardiography, and not a mid-ventricular, a concealed membranous subaortic stenosis, nor supravalvular form; and
    4. 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
    5. Member has systolic anterior motion of the mitral valve on echocardiography; and
    6. 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
    7. Member does not have coronary artery disease that would preclude performance of the procedure.
  2. Experimental and Investigational

    Aetna considers percutaneous transluminal septal myocardial ablation experimental and investigational for all other indications because of insufficient evidence of its safety and effectiveness.


Table:

CPT Codes / HCPCS Codes / ICD-10 Codes

Code Code Description

Information in the [brackets] below has been added for clarification purposes.   Codes requiring a 7th character are represented by "+":

There is no specific CPT code for percutaneous transluminal septal myocardial ablation:

CPT codes covered if selection criteria are met:

93583 Percutaneous transcatheter septal reduction therapy (eg, alcohol septal ablation) including temporary pacemaker insertion when performed

Other HCPCS codes related to the CPB: :

C1886 Catheter, extravascular tissue ablation, any modality (insertable)

ICD-10 codes covered if selection criteria are met:

I42.1 Obstructive hypertrophic cardiomyopathy

Background

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.

Akita and colleagues (2018) stated that plasma brain natriuretic peptide (BNP) levels are associated with clinical outcomes in patients with HOCM.  However, the prognostic value of plasma BNP level changes before and after PTSMA remains unclear.  These researchers examined if repeated BNP measurements following PTSMA provide prognostic information regarding the response to PTSMA in patients with drug-refractory HOCM.  They measured the plasma BNP levels serially before and after PTSMA, and evaluated the relationship between the changes in plasma BNP levels and clinical improvement in 47 patients.  The patients were assigned to 2 groups based on the reduction in the NYHA class greater than or equal to 1 (good responder) or less than 1 (poor responder) before and after PTSMA.  The Kansas City Cardiomyopathy Questionnaire (KCCQ) was used to measure health status.  The plasma BNP levels gradually decreased after PTSMA, although the levels plateaued 3 months until 12 months after PTSMA.  Although the plasma BNP levels and resting LVOT peak pressure gradient before PTSMA were comparable between the groups, the ratio of the BNP levels before and after PTSMA in the good responder group was significantly lower than that in the poor responder group (0.43; range of 0.24 to 0.68) versus 0.78 (range of 0.62 to 0.93), p = 0.002).  The KCCQ score changes in the good responder group were significantly higher than those in the poor responder group.  The authors concluded that the plasma BNP level ratio was associated with long-term clinical improvement of heart failure (HF) following PTSMA for drug-refractory HOCM.

Percutaneous Transluminal Septal Myocardial Ablation for the Treatment of Severe but Asymptomatic Hypertrophic Obstructive Cardiomyopathy

Arslan and colleagues (2021) noted that symptoms justify invasive treatment in HOCM patients with LVOT obstruction.  Adverse structural and functional changes (re-modeling) in the heart occur preceding heart failure and sudden cardiac death.  Early invasive treatment in asymptomatic patients may reverse adverse re-modeling to the same extent as in symptomatic patients.  These researchers examined the impact of PTSMA on re-modeling in asymptomatic patients with HOCM and severe LVOT obstruction.  Reverse re-modeling after PTSMA in severe but asymptomatic LVOT obstruction (RASTA) study is a prospective, randomized, single-blind trial (ClinicalTrials.gov number: NCT04230551).  A total of 10 asymptomatic HOCM patients with an exertional LVOT gradient greater than or equal to 50 mmHg (or greater than 30 mmHg in rest) are randomized 1:1 to PTSMA versus conservative therapy, in the absence of mitral valve disease or other indications for cardiac surgery; 5 symptomatic (reference group) will undergo PTSMA according to the current guidelines.  Re-modeling is evaluated using extensive cardiac imaging with trans-thoracic echocardiography (TTE) and late gadolinium enhancement cardiac magnetic resonance (CMR) at baseline and during follow-up at 1, 12, and 24 months.  Extracellular volume fraction, global, and regional strain analysis, geometry, pressure gradients and changes in four-dimensional (4D) velocity mapping are primary parameters to study (reversal of) adverse re-modeling.  The authors concluded that the RASTA study gives insight in cardiac re-modeling that may occur in asymptomatic patients after PTSMA.  It will provide arguments whether to pursue (or not) a larger trial with clinical endpoints in asymptomatic HOCM patients with severe LVOT obstruction.


Glossary of Terms 

Table: Glossary of Terms
Term Definition
Hypertrophic Cardiomyopathy A disease in which the heart muscle becomes thickened (hypertrophied), making it hard for the heart to pump blood
New York Heart Association (NYHA) Classification Provides a way to classify the extent of heart failure; a tool used for risk stratification which classifies patients in one of four categories based on their limitations during physical activity, limitations/symptoms in regards to normal breathing, varying degrees in shortness of breath and or angina pain
Percutaneous Passing through the skin 
Transluminal Passing across or performed by way of a lumen of a blood vessel

Appendix 

Table: New York Heart Association (NYHA) Classification
Class Classification
Class I Patients with cardiac disease but without resulting limitation of physical activity.  Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
Class II 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.
Class III

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.

Class IV 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.

References

The above policy is based on the following references:

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