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 Table of Contents  
IMAGING VIGNETTE
Year : 2022  |  Volume : 6  |  Issue : 3  |  Page : 293-297

Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy- Is Myocardial Contrast Echocardiography Mandatory?


Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka, India

Date of Submission15-Apr-2022
Date of Decision12-Jul-2022
Date of Acceptance21-Jul-2022
Date of Web Publication21-Sep-2022

Correspondence Address:
Dr. Arun B Shivashankarappa
Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bannergatta Road, Jayanagar, 9th Block, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_18_22

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  Abstract 

Alcohol septal ablation (ASA) is an effective treatment for symptomatic hypertrophic obstructive cardiomyopathy (HOCM). Although routine use of myocardial contrast echocardiography (MCE) in guiding ASA has been recommended by guidelines, it has not come into common clinical practice. Here, we present three cases of HOCM where MCE helped in decision-making.

Keywords: Alcohol septal ablation, hypertrophic obstructive cardiomyopathy, myocardial contrast echocardiography


How to cite this article:
Sastry SL, Shivashankarappa AB, Bhat P, Manjunath SC, Nanjappa MC. Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy- Is Myocardial Contrast Echocardiography Mandatory?. J Indian Acad Echocardiogr Cardiovasc Imaging 2022;6:293-7

How to cite this URL:
Sastry SL, Shivashankarappa AB, Bhat P, Manjunath SC, Nanjappa MC. Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy- Is Myocardial Contrast Echocardiography Mandatory?. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2022 [cited 2023 Feb 5];6:293-7. Available from: https://jiaecho.org/text.asp?2022/6/3/293/356636


  Introduction Top


Alcohol septal ablation (ASA) is increasingly used as an effective treatment option for symptomatic hypertrophic obstructive cardiomyopathy (HOCM) since 1995.[1],[2] Usually, obstruction is caused by systolic anterior motion (SAM) of the mitral valve toward the hypertrophied basal septum. The target of ASA is usually the first large septal branch, which most probably supplies the basal septum. However, there is considerable variability in its size, morphology, supplying territory, and collateralization with other septal branches.[3],[4] Multiple or atypically originating septal branches may further create a challenge. Considering these problems, guidance with myocardial contrast echocardiography (MCE) for the identification of a suitable target septal branch is a significant improvement in the technique of ASA.[5] Routine use of MCE in guiding ASA has been recommended by the European Society of Cardiology guidelines (class of recommendation: I) and the American Heart Association/American College of Cardiology guidelines (class of recommendation: I).[6],[7] However, it has not yet come into common clinical practice. Here, we discuss three cases of HOCM where MCE proved useful.


  Case Series Top


Case 1

A 33-year-old male presented with a history of dyspnea on exertion and chest pain for 3 months. Clinical examination revealed brisk pulse with a rate of 84 beats per min. His blood pressure was 130/80 mmHg. Apical impulse was heaving with palpable S4. Grade 3/6 mid-systolic murmur was present at the left lower sternal border. Electrocardiogram was normal. M-mode echocardiogram showed septal thickness of 26 mm and posterior wall thickness of 18 mm. There was SAM of mitral valve with peak left ventricular (LV) outflow tract (LVOT) gradient of 80 mmHg. There was moderate mitral regurgitation (MR) with posterolateral jet. LV systolic function was normal [Figure 1] and [Video 1].
Figure 1: Prealcohol septal ablation echocardiography of case 1. (a) Parasternal-long axis view showing septal thickness of 2.3 cm. (b) Color Doppler showing turbulence across LVOT. (c) Apical four-chamber view showing asymmetrical septal hypertrophy. (d) Color Doppler showing turbulence across LVOT. (e) Systolic anterior motion of the anterior mitral leaflet. (f) Peak LVOT gradient of 79 mmHg. LVOT: Left ventricular outflow tract

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[Additional file 1]

Video 1: Apical five-chamber view showing turbulence across left ventricular outflow tract in case 1.

The patient was started on tablet metoprolol succinate 25 mg bid and gradually increased to 100 mg bid. He continued to have dyspnea, and peak LVOT gradient remained high at 75 mmHg. Hence, we planned for ASA as the patient was not willing for surgical myectomy.

LV angiogram and coronary angiogram (CAG) were done [Figure 2]. LV angiogram showed banana-shaped LV cavity, with subaortic obstruction and moderate MR. The peak gradient across LVOT was 110 mmHg. CAG showed normal epicardial coronaries. The first septal branch (S1) was 2.0 mm in size and suitable for ASA.
Figure 2: LV angiogram and alcohol septal ablation of case 1. (a and b) LV angiogram showing banana-shaped LV cavity during systole. (c) Target septal branch (S1). (d and e) Wire passed into S1. (f) OTW balloon inflated in S1. LV: Left ventricular, OTW: Over-the-wire

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Exchange length 0.014” floppy wire was placed in the possible target septal branch; S1 of left anterior descending artery and 2.0 mm × 10 mm over-the-wire (OTW) balloon was passed over the wire and inflated. 0.2 ml of a myocardial contrast agent (Definity, Lantheus Medical Imaging, North Billerica, Massachusetts, USA), diluted with 1 ml of water, was injected into the target septal branch distal to inflated OTW balloon. There was contrast opacification of the left-side portion of the basal septum, which was adjacent to flow acceleration in LVOT. There was no contrast opacification of any other structures such as right ventricular (RV) free wall and papillary muscles [Figure 3] and [Video 2]. Hence, we concluded S1 to be the target septal branch and injected 0.5 ml of alcohol into S1 taking care to avoid reflux of alcohol out of the septal branch. After this, peak LVOT gradient was measured which was still high. Hence, we repeated two more intracoronary injections of 0.5 ml of alcohol. After the third injection, the peak LVOT gradient reduced to 30 mmHg [Figure 3] and [Video 3]. The patient had an uneventful intraprocedural and postprocedural course. After 2 days, the peak LVOT gradient increased to 60 mmHg with mild SAM. However, the patient had improvement in symptoms. At 2 months of follow-up, the peak LVOT gradient reduced to 26 mmHg, which was maintained during further follow-up.
Figure 3: Echocardiography during ASA of case 1. (a and b) Myocardial contrast echocardiogram showing contrast opacification of left-side portion of basal septum, adjacent to LVOT flow acceleration. (c) Post-ASA echocardiogram color Doppler showing reduced turbulence across LVOT. (d) Post-ASA, gradient reduced to 30 mmHg. ASA: Alcohol septal ablation, LVOT: Left ventricular outflow tract

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[Additional file 2]

Video 2: Myocardial contrast echocardiography showing contrast opacification of left-side portion of basal septum in case 1.

[Additional file 3]

Video 3: Decreased turbulence across left ventricular outflow tract after alcohol septal ablation in case 1.

Case 2

A 48-year-old male presented with typical angina. Clinical examination showed pulse rate of 70 beats per min and blood pressure 138/80 mmHg. Cardiac examination revealed features suggestive of HOCM. Electrocardiogram showed LV hypertrophy with systolic strain. M-mode echocardiogram showed septal thickness of 19 mm and posterior wall thickness of 13 mm. There was SAM of the mitral valve with the peak LVOT gradient of 71 mmHg. There was mild MR. LV systolic function was normal [Figure 4], [Video 4] and [Video 5].
Figure 4: Echocardiogram of case 2. (a) Apical four-chamber view showing asymmetrical septal hypertrophy. (b) Apical five-chamber view showing turbulence across LVOT. (c) Basal septal thickness of 2.02 cm. (d) Peak LVOT gradient of 139 mmHg. (e) Myocardial contrast echocardiography showing opacification of right-side portion of the basal septum. LVOT: Left ventricular outflow tract

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[Additional file 4]

Video 4: Apical four-chamber view showing asymmetrical basal septal hypertrophy in case 2.

[Additional file 5]

Video 5: Apical five-chamber view showing turbulence across left ventricular outflow tract in case 2.

The patient was initiated on tablet metoprolol succinate 50 mg bid, despite which he was symptomatic. Hence, he was considered for ASA. LV angiogram showed subaortic stenosis with peak LVOT gradient of 100 mmHg with mild MR. CAG showed normal epicardial coronaries. Second septal branch (S2) was a 2-mm vessel and identified as a possible target for ASA [Figure 5]. Definity contrast was injected into the target septal branch distal to inflated OTW balloon. There was contrast opacification of predominantly right-side portion of the basal septum, which was not adjacent to LVOT flow acceleration [Figure 4], [Video 6] and [Video 7]. Hence, ASA was abandoned, and the patient was referred for septal myectomy. Following septal myectomy, the patient improved with a reduction in LVOT gradient to 22 mmHg.
Figure 5: CAG and target septal branch assessment of case 2. (a) CAG showing second septal branch to be a possible target septal branch. (b) Wire passed into LAD. (c) OTW balloon passed over the wire into second septal branch. (d) OTW balloon inflated in second septal branch. CAG: Coronary angiogram, LAD: Left anterior descending artery, OTW: Over-the-wire

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[Additional file 6]

Video 6: Myocardial contrast echocardiography showing contrast opacification of right-side portion of basal septum in case 2.

[Additional file 7]

Video 7: Myocardial contrast echocardiography (sepia) showing contrast opacification of right-side portion of basal septum in case 2.

Case 3

A 32-year-old male presented with a history of dyspnea for 3 months. On evaluation, he was found to have HOCM with severe MR. There was no mitral valve abnormality. The patient was initiated on metoprolol succinate 50 mg OD, later which was increased to 100 mg bid. Despite this, he continued to be symptomatic. Hence, he was taken up for ASA. CAG showed S1 to be a suitable target for ASA [Figure 6]. Then, MCE was performed by injecting Definity contrast into S1. It showed enhancement of mid-septum facing the RV. Basal septum was not enhanced. Hence, the procedure was abandoned. He was referred for surgical myectomy.
Figure 6: Coronary angiogram and target septal branch assessment of case 3. (a) CAG showing first septal branch to be a possible target septal branch. (b) Wire passed into first septal branch. (c) OTW balloon passed over the wire into first septal branch. (d) OTW balloon inflated in S1. CAG: Coronary angiogram, OTW: Over-the-wire

Click here to view



  Discussion Top


For MCE during ASA, an echocardiographic contrast agent (e.g., Definity, Optison, SonoVue) is administered through the central lumen of the balloon catheter under the guidance of transthoracic two-dimensional echocardiography and color Doppler. Injection into the optimal septal branch causes an obvious opacification of the septal area, adjacent to maximal flow acceleration that involves the point of contact between the mitral valve and the septum during systole. MCE can alter the interventional strategy by guiding the need to change the target septal branch or sometimes even abandon the procedure if the proper septal branch cannot be identified. Alcohol is injected only when the correct target septal branch is identified. MCE evaluates whether the selected septal branch also perfuses other distant areas of LV or RV myocardium or papillary muscles.[8] Amount of alcohol administered can also be estimated based on the opacified areas of the basal septum by MCE.[9] The precise identification of the target septal region helps in reducing the amount of alcohol injected without compromising the hemodynamic results.[10],[11],[12] The use of MCE during ASA has been shown to improve the hemodynamic result and decrease the complication risk, thus ensuring the safety of the procedure.[5],[13]

In one series by Faber et al., among 337 patients, the use of MCE abandoned the procedure in 8% of cases and changed the target septal branch in 11% of cases.[13] Determination of the target vessel by MCE was associated with a higher rate of acute (92% vs. 70%; P = 0.01) and mid-term (94% vs. 64%; P = 0.01) success.[5] Further, it reduced the incidence of permanent pacemaker requirement after ASA from 17% to 7%.[5] A study by Monakier et al. has shown that the use of MCE is associated with decrease in infarct size.[14]

In our experience of three cases of HOCM, ASA had to be abandoned in two patients because MCE showed opacification of the area of the septum not adjacent to LVOT flow acceleration.


  Conclusion Top


MCE helps in appropriate case selection for ASA in patients with HOCM. It enhances the success and safety of the procedure.

Acknowledgment

We would like to acknowledge all the cardiac catheterization and echocardiography laboratory staff at our center.

Declaration of patient consent

The authors declare that they have obtained consent from patients. Patients have given their consent for their images and other clinical information to be reported in the journal. Patients understand that their names will not be published and due efforts will be made to conceal their identity but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995;346:211-4.  Back to cited text no. 1
    
2.
Seggewiss H. Percutaneous transluminal septal myocardial ablation: A new treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J 2000;21:704-7.  Back to cited text no. 2
    
3.
Singh M, Edwards WD, Holmes DR Jr., Tajil AJ, Nishimura RA. Anatomy of the first septal perforating artery: A study with implications for ablation therapy for hypertrophic cardiomyopathy. Mayo Clin Proc 2001;76:799-802.  Back to cited text no. 3
    
4.
Rigopoulos A, Sepp R, Palinkas A, Ungi I, Kremastinos DT, Seggewiss H. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy: Collateral vessel communication between septal branches. Int J Cardiol 2006;113:e67-9.  Back to cited text no. 4
    
5.
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;98:2415-21.  Back to cited text no. 5
    
6.
Elliott PM, Anastasakis A, Borger MA, Borggrefe M, Cecchi F, Charron P, et al. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy. The Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology. Eur Heart J 2014;35:2733-79.  Back to cited text no. 6
    
7.
Ommen SR, Mital S, Burke MA, Day SM, Deswal A, Elliott P, et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2020;142:e558-631.  Back to cited text no. 7
    
8.
Losi MA, Nistri S, Galderisi M, Betocchi S, Cecchi F, Olivotto I, et al. Echocardiography in patients with hypertrophic cardiomyopathy: Usefulness of old and new techniques in the diagnosis and pathophysiological assessment. Cardiovasc Ultrasound 2010;8:7.  Back to cited text no. 8
    
9.
Rigopoulos AG, Seggewiss H. A decade of percutaneous septal ablation in hypertrophic cardiomyopathy. Circ J 2011;75:28-37.  Back to cited text no. 9
    
10.
Veselka J, Procházková S, Duchonová R, Bolomová-Homolová I, Pálenícková J, Tesar D, 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;63:231-5.  Back to cited text no. 10
    
11.
Faber L, Welge D, Fassbender D, Schmidt HK, Horstkotte D, Seggewiss H. One-year follow-up of percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy in 312 patients: Predictors of hemodynamic and clinical response. Clin Res Cardiol 2007;96:864-73.  Back to cited text no. 11
    
12.
Veselka J, Zemánek D, Tomasov P, Homolová S, Adlová R, Tesar D. Complications of low-dose, echo-guided alcohol septal ablation. Catheter Cardiovasc Interv 2010;75:546-50.  Back to cited text no. 12
    
13.
Faber L, Seggewiss H, Welge D, Fassbender D, Schmidt HK, Gleichmann U, et al. Echo-guided percutaneous septal ablation for symptomatic hypertrophic obstructive cardiomyopathy: 7 years of experience. Eur J Echocardiogr 2004;5:347-55.  Back to cited text no. 13
    
14.
Monakier D, Woo A, Puri T, Schwartz L, Ross J, Jamorski M, 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;94:1515-22.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

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