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Ann Thorac Surg 2005;80:1424-1430
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Septal Myectomy for Obstructive Hypertrophic Cardiomyopathy in Pediatric Patients: Early and Late Results

^a Division of Cardiovascular Surgery, Mayo Clinic and Foundation, Rochester, Minnesota
^b Division of Pediatric Cardiology, Mayo Clinic and Foundation, Rochester, Minnesota

Accepted for publication March 28, 2005.

^_* Address reprint requests to Dr Dearani, Division of Cardiovascular Surgery, Mayo Clinic College of Medicine, 200 First Street, SW, Rochester, MN55905 (Email: jdearani{at}mayo.edu).

Presented at the Fifty-first Annual Meeting of the Southern Thoracic Surgical Association, Cancun, Mexico, Nov 2–4, 2004.

	Abstract

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

 
BACKGROUND: Symptomatic pediatric patients with obstructive hypertrophic cardiomyopathy (HCM) have a higher death rate (6% annually) compared with adults. Transaortic left ventricular septal myectomy provides excellent outcomes for adults with obstructive HCM. We sought to assess the effect of septal myectomy on late survival and outcome in pediatric patients with obstructive HCM.

METHODS: From 1975 to 2003, 56 pediatric patients underwent septal myectomy for obstructive HCM. Mean age at diagnosis was 6.3 ± 5.4 years. Ages at operation ranged from 2 months to 20 years (mean 11 ± 5.6 years). Concomitant procedures included mitral valve repair (n = 7), closure of atrial septal defect (n = 3), and other (n = 5).

RESULTS: After myectomy, mean left ventricular outflow tract (LVOT) gradient decreased from 103 ± 34 to 16 ± 12 mm Hg and mean degree of mitral regurgitation decreased from 2.0 ± 1.0 to 1.0 ± 0.3 (both p < 0.0001). There were no early deaths. Four patients underwent elective cardioverter defibrillator implantation and 1 patient received a permanent pacemaker. Follow-up ranged up to 29 years (mean, 8.6 ± 6.2). Cardiac reoperations were required in 8 patients: heart transplantation (n = 2), repeat myectomy (n = 2), mitral valve repair-replacement (n = 2), Konno-Rastan procedure (n = 1), and aortic valve replacement (n = 1). Age 14 years or less at operation was the only predictor of late reoperation (p = 0.017). Two patients died late; one suddenly without residual LVOT obstruction and one from chronic rejection after heart transplantation. Ninety-six percent of surviving patients were in New York Heart Association functional class I or II. Survival estimates at 5 and 10 years were 97% and 93%, respectively.

CONCLUSIONS: Septal myectomy is safe and effective in symptomatic pediatric patients with obstructive HCM. Late survivorship compares very favorably with the natural history of this disease.

	Introduction

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Hypertrophic cardiomyopathy (HCM) is a primary genetic myocardial disease characterized by heterogeneity of the disease process including its wide variation in clinical symptoms, hemodynamic characteristics, natural history, age at presentation, and risk for sudden death [1]. Hypertrophic cardiomyopathy usually is not recognized clinically until adulthood; presentation of this disease in childhood is associated with high mortality [2–4]. Although several other risk factors for mortality have been identified, including family history of sudden death, extreme septal hypertrophy, and history of syncope or nonsustained ventricular tachycardia [1, 5], left ventricular outflow tract (LVOT) obstruction has been found to be a strong independent predictor of disease progression to severe heart failure and death [1, 5, 6].

Left ventricular septal myectomy, also known as the Morrow procedure [7], has been the standard therapeutic option for those severely symptomatic patients with LVOT obstruction and associated mitral regurgitation who are unresponsive to maximal medical therapy [1, 8–11]. We previously reported the effectiveness of septal myectomy in a small pediatric subset in which there was relief of severe symptoms and LVOT obstruction and apparent improvement of late survivorship [12]. The aim of this study was to update this pediatric experience and add further information regarding early and late results up to 29 years of follow-up.

	Patients and Methods

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Between April 1975 and April 2003, 56 patients who were age 20 years or younger underwent operation for obstructive HCM on the authors' surgical services. We excluded patients having severe obstruction of both right and left ventricular outflow tracts who underwent biventricular resection (n = 9). Patient characteristics are summarized in Table 1. Ages at diagnosis ranged from 2 days to 19 years (mean, 6.3 ± 5.4; median, 5 years) and ages at operation ranged from 2 months to 20 years (mean, 11 ± 5.6; median, 14 years). Patient distributions were similar for age groups 0 to 5 years (n = 12, 21%), 6 to 10 years (n = 15, 27%), 11 to 15 years (n = 15, 27%), and 16 to 20 years (n = 14, 25%). The diagnosis of obstructive HCM was based on clinical evaluation and on cardiac catheterization or echocardiography, or both. Cardiac catheterization was essential in the early part of the series but is now performed only when additional information, such as evaluation of dynamic obstruction under monitored conditions in patients for whom satisfactory echocardiographic pressure gradients cannot be obtained during exercise, is required. The indications for operation in the majority of patients were limiting symptoms unresponsive to optimal medical therapy associated with LVOT gradients 50 mm Hg or greater at rest or with provocation (preferably utilizing physiologic exercise). Seven asymptomatic patients were referred for operation because they had resting LVOT gradients in excess of 85 to 100 mm Hg. New York Heart Association (NYHA) functional classes are shown in Figure 1. Preoperative cardiac medications are shown in Table 1. Twelve patients had undergone prior dual chamber pacemaker implantation with no or only temporary improvement of symptoms and LVOT gradients, and 4 patients had undergone implantation of a cardioverter defibrillator (ICD) for prevention of sudden death. Prior operations are shown in Table 1. No patient had a previous attempted catheter-based alcohol septal ablation.

View larger version (24K): [in this window] [in a new window]   Fig 1. New York Heart Association functional class before operation and at late follow-up. (Black columns = before operation; grey columns = late follow-up.)

Current Surgical Techniques
As detailed in previous publications [13–16], our technique of septal myectomy has evolved from the classic Morrow myectomy to a more extended myectomy. This includes resection apically to the bases of the papillary muscles and resection leftward (as viewed by the surgeon) toward the mitral valve. The apical third of the trough is then extended rightward by resecting posterior septal myocardium, effectively making a much wider trough at the apex than at the base. If desired, the base of the resected area can then be deepened with a pituitary rongeur. When abnormal mitral subvalvular apparatus is present, we divide all attachments that exist between the lateral edge of the anterior leaflet and ventricular septum and between the papillary muscle(s) and septum. It is important to maintain intact all chordal attachments to the leading edge of the anterior leaflet. The presence of a direct papillary muscle insertion into the anterior mitral leaflet may be accompanied by fusion of the papillary muscle to the septum. Surgical myectomy is performed in the extended fashion and, in addition, the papillary muscle is incised off of the septum down to its base. Details of operation, including the importance of providing excellent myocardial protection, a quiet, dry field, and optical magnification with fiberoptic lighting have been described previously [13–16].

Since the late 1980s, transesophageal echocardiography (TEE) has become an essential adjunct in the operating room for performing septal myectomy. Transesophageal echocardiography is performed in all patients after induction of general anesthesia with particular attention to the cardiac anatomy, mitral valve function, and thickness of the ventricular septum. The TEE evaluation is repeated after the patient is weaned from cardiopulmonary bypass to confirm adequacy and extent of the resection. Transesophageal echocardiography can quantify and localize any residual gradients, exclude an iatrogenic ventricular septal defect, and confirm satisfactory competence of the mitral and aortic valves.

With regard to postoperative medications for pediatric patients after septal myectomy, our practice has been to place patients on a moderate dose of beta-blocker. Although hard evidence is lacking, historically both beta-blockers and surgery appear to have given incremental reductions in mortality, especially sudden death.

Statistical Analysis
Demographic and other patient-related data were obtained from Mayo Clinic medical records. Follow-up information was obtained from subsequent clinic visits, written correspondence from local physicians, and mailed questionnaires to patients or families. The rank sum test was used to compare continuous variables. The probability of survival and survivorship free of reoperation were estimated by the Kaplan-Meier method. The associations of potential risk factors for reoperation were assessed with log-rank tests and the Cox proportional hazards model. Data were expressed as mean ± standard deviation and statistical significance was considered at p less than 0.05. Early operative mortality was defined as death occurring within 30 days of operation or at any time during the index hospitalization. This study was approved by the Mayo Foundation Institutional Review Board, and all patients or families gave written informed consent.

	Results

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Early Results
Concomitant procedures were performed in 15 patients, all for preexisting conditions. The most common procedure was transaortic mitral valve repair with or without anterior leaflet plication (n = 6) and transatrial commissuroplasty (n = 1). Other concomitant procedures included closure of atrial septal defect or patent foramen ovale (n = 3), resection of associated discrete membranous subaortic stenosis (n = 2), division of left anterior descending muscle bridge (n = 1), aortic valve repair (n = 1), and ICD placement with epicardial electrode patches (n = 1). Mitral valve replacement was not necessary in any patient. The mean cardiopulmonary bypass time and aortic cross-clamp time were 78 ± 27 minutes and 51 ± 18 minutes, respectively.

Hemodynamic measurements and echocardiographic data are shown in Table 2. The LVOT gradients were assessed by preoperative transthoracic echocardiography, intraoperative direct pressure measurements pre- and postmyectomy, and predischarge transthoracic echocardiography. The degree of reduction of mean LVOT gradients was highly significant (p < 0.0001). Intraoperative assessment of mitral regurgitation by TEE pre- and postmyectomy showed a concomitant highly significant reduction of mean echocardiographic grade (p < 0.0001). There was no significant change in aortic regurgitation grade.

Late Results
Clinical follow-up was obtained in 54 of 56 patients (2 patients outside of North America were lost to follow-up). The mean follow-up was 8.6 ± 6.2 years (range, 0.5 to 29 years). There were 2 late deaths. One patient died at age 9 from chronic rejection 3 years after orthotropic heart transplantation. The other died suddenly at age 22, 5 years after septal myectomy; the peak echocardiographic LVOT gradient was only 16 mm Hg one year prior to death and the patient had been doing well clinically.

Cardiac reoperations were required in 8 patients; there were no deaths related to reoperation. The mean duration between septal myectomy and reoperation was 6.2 ± 3.9 years (range, 1.2 to 12 years). Freedom from reoperation for any reason was 100%, 93%, and 82% at 1, 5, and 10 years, respectively (Fig 2). The procedures included repeat septal myectomy in 2, heart transplantation in 2, Konno-Rastan procedure with myectomy in 1, mitral valve repair with incidental repeat myectomy in 1, mitral valve replacement in 1, and aortic valve replacement in 1. The indications for heart transplantation were restrictive cardiomyopathy 6 years after successful myectomy in one patient and severe biventricular outflow tract obstruction 6 years after myectomy in the other patient. Only 4 of the 8 reoperations were required primarily for recurrent LVOT obstruction; freedom from reoperation for recurrent LVOT obstruction was 100%, 98%, and 94% at 1, 5, and 10 years, respectively (Fig 2). On univariate analysis, young age at operation ( 14 years) was the only variable associated with late reoperation (log-rank, p = 0.017). In the youngest age group (0–5 years old), we found no difference in symptoms or indications for operation compared with the older patients. There were no early deaths in either group. Neither late death occurred in the youngest group. However, all 4 reoperations for recurrent LVOT obstruction were in the youngest age group. The small number of events precluded multivariable analysis.

View larger version (16K): [in this window] [in a new window]   Fig 2. Freedom from reoperation for all causes and for recurrent left ventricular outflow tract obstruction (LVOTO). (— = reoperation for all causes; – – – = reoperation for LVOTO.)

Follow-up echocardiographic data were obtained from 38 patients (Table 2). The mean interval between the dates of operation and the most recent echocardiograms was 7.3 ± 6.3 years (median, 4.8). The mean peak LVOT gradient remained low at 11 ± 20 mm Hg and the median gradient was 0 mm Hg. The degrees of mitral and aortic regurgitation remained in the insignificant range for the majority of patients.

Of the 52 known survivors, 96% were in NYHA functional class I or II (Fig 1). However, 4 patients developed important reductions of left ventricular systolic function (ejection fraction < 40%) and are being followed closely. Survival estimates at 5 and 10 years were 97% and 93%, respectively (Fig 3). The survival curve for symptomatic pediatric patients with HCM who were treated nonsurgically was derived from the report by McKenna and colleagues [3].

View larger version (15K): [in this window] [in a new window]   Fig 3. Probability of patient survival after septal myectomy compared with survival curve for symptomatic pediatric patients with hypertrophic cardiomyopathy treated nonsurgically as reported by McKenna and colleagues [3]. (— = survival after myectomy; – – – = survival without myectomy.)

	Comment

Top Abstract Introduction Patients and Methods Results Comment Discussion Acknowledgments References

It has been observed that progression of left ventricular hypertrophy may be more rapid in children and adolescents than in the adult population [17]. Patients who have a diagnosis of HCM made in childhood are often asymptomatic, and sudden death as an initial presentation is more common [1, 18]. Symptomatic patients with HCM who present in childhood have a higher death rate than symptomatic adults, with annual mortality as high as 6% [1–4]. In addition to young age at presentation, several other risk factors for mortality have been identified, including a family history of sudden death, extreme septal hypertrophy, history of syncope, history of sustained or nonsustained ventricular tachycardia, and abnormal blood pressure response with exercise [1, 5]. With regard to electrophysiologic strategy, we advocate ICD placement for all patients who have had one or more clinical episodes of ventricular tachyarrhythmia; ie, for secondary prevention. For patients with known significant risk factors, a strong case can be made for ICD placement for primary prevention of sudden death [19]. Electrophysiologic testing may be helpful in selected cases, but overall has not been able to separate clearly those patients who are at risk for sudden death from those who are not.

Importantly, LVOT obstruction has been found to be a strong independent predictor of disease progression to severe heart failure, stroke, and death (relative risk 4.4) [6]. As shown in the current study in this pediatric subgroup, the degree of reduction of LVOT gradients as well as mitral regurgitation were highly significant after septal myectomy, and late follow-up echocardiography demonstrated that pressure gradients and degree of mitral regurgitation continued to be low in the vast majority of patients. This sustained reduction of gradients to insignificant levels after myectomy may be the primary reason for the highly significant improvement in late patient survival compared to the natural history of the disease (Fig 3).

Although late mortality is reduced significantly by myectomy, sudden deaths are not entirely prevented, as illustrated by the one patient early in this series who died suddenly 5 years after successful myectomy (she was asymptomatic with a peak LVOT gradient of only 16 mm Hg one year prior to death). However, she had other risk factors in addition to young age at presentation, which included a history of nonsustained ventricular tachycardia and syncope preoperatively, and also ventricular tachycardia early postoperatively. These episodes were treated with atenolol and amiodarone. Additionally, the ventricular septum was 40 mm in diameter, which is now recognized to be a risk factor for death [1, 5]. For such a patient today, an ICD would probably be considered preferable treatment for primary prevention of sudden death [1, 19].

Although the basic transaortic approach for performing a septal myectomy has been known for over 40 years, the operation remains technically challenging and the results are operator dependent [1]. While myectomy can be performed successfully in pediatric patients and even infants, adequate resection may be compromised by the small size of the aorta and limited visibility of the midventricular region. Poor visualization of the anatomy below the aortic valve can result in injury to mitral leaflets or chordae, and incorrect placement of incisions or excessive traction can produce heart block. Incisions or excisions made too deep create ventricular septal defects or ventricular perforations, and the aortic valve is always at risk for injury from instruments passed through the valve and manipulated within the ventricle. These limitations, especially inadequate exposure of the mitral subvalvular apparatus, account in part for the need for reoperation at a later age for some pediatric patients [14].

We and others [14, 20] have observed that children appear to have an increased risk of reoperation for recurrent LVOT obstruction compared to adults. In addition to the aforementioned technical limitations related to pediatric patients, it is likely that ventricular remodeling also contributes to the need for reoperation in some patients [21]. It is known that left ventricular remodeling in children with HCM is characterized by progression of hypertrophy, particularly during adolescence [17]. We anticipate that with our current preference for an extended myectomy, which entails a much wider resection of obstructing myocardium, especially at midventricular level, together with inspection and treatment of papillary muscle and chordal anomalies, the need for subsequent operations for recurrent LVOT obstruction will decrease.

Dual-chamber pacing and percutaneous transluminal alcohol septal ablation have recently been advocated for treatment of obstructive HCM. Their comparative merits versus septal myectomy continue to be evaluated. These techniques have been effective in selected patients, but are not appropriate for children, for those in whom fixed obstruction is present instead of obstructive HCM, for patients in whom LVOT obstruction is due to papillary muscle anomalies, or for patients with unfavorable septal artery anatomy. As experience increases and lengthens with newer alternatives to surgery, the results can be compared with the more than 40 years of experience with septal myectomy.

We conclude that extended septal myectomy can be performed in symptomatic pediatric patients having obstructive HCM with very low mortality and excellent relief of symptoms. Early significant reductions in LVOT obstruction and degree of mitral regurgitation are maintained at late follow-up in most patients. Late survivorship compares very favorably with the natural history of this disease.

	Discussion

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DR WALTER H. MERRILL (Cincinnati, OH): I would like to congratulate the authors on achieving outstanding results in a technically demanding procedure and a challenging group of patients. In my opinion this is a landmark paper, which firmly establishes myectomy of the outflow tract as a safe and efficacious procedure, which provides long lasting symptomatic improvement and survival benefit in patients with hypertrophic obstructive cardiomyopathy. I have four questions for the authors.

Are there any patients who are too young or too small to undergo this procedure? Secondly, what is the minimal septal thickness required in order for the operation to be efficacious and safe? What are the current recommendations of your group regarding either concomitant or subsequent placement of a defibrillator? And finally, in those patients who have recurrent outflow tract obstruction is there an anatomic subset for which you might recommend alcohol septal ablation as opposed to repeat myectomy? Thank you.

DR MINAKATA: Thank you very much for your kind comments and questions, Dr Merrill. First, with regard to the age at operation, 20% of the patients in the current study were age less than or equal to 5 years. This procedure is often compromised, especially in the small children, by the small size of the aorta and left ventricular outflow tract. It can be difficult to expose the basal and midventricular septum in those patients. Although it is possible to perform myectomy in small children, reoperation is more likely due to recurrent LVOT (left ventricular outflow tract) obstruction or other cardiac causes after successful initial operation. In fact, as shown in the presentation, younger age at operation is a strong predictor for late reoperation.

In response to the second question, there are no definite requirements of the thickness of the septum. Since the obstruction of LVOT in this disease is dynamic, careful evaluation of the hemodynamics and anatomical issue is mandatory by echocardiogram to decide the candidacy of the operation.

Regarding the ICD (implantable cardioverter defibrillator) placement, it has been shown that there are several risk factors for sudden death, such as marked septal hypertrophy over 30 mm, nonsustained V tach or sustained V tach by Holter ECG (electrocardiogram), history of syncope, and finally, history of sudden death in family member. If the patient has any of these, even if the patient is asymptomatic, we should consider implantation of an ICD. At late follow-up in this study, we found that an ICD was implanted in nine patients. The current trend is that we should have a low threshold to implant this device to prevent sudden death.

Finally, with regard to the alcohol ablation therapy, which was introduced to the clinical practice recently, it has been shown that the early and midterm results are favorable; as good as those of the surgical septal myectomy, although there is no data which shows the long-term survival and benefit. A recent study of alcohol ablation showed that the effectiveness of the procedure may not be long lasting. Also, there are contraindications for septal alcohol ablation: for example, patients with intrinsic mitral valve disease or abnormal mitral subvalvular apparatus. For the subgroup of the obstructive HCM (hypertrophic cardiomyopathy) patients who have abnormal mitral subvalvular apparatus, we believe that our extended septal myectomy is the best therapeutic option as we presented at AATS (American Association for Thoracic Surgery) last year and published in JTCVS (Journal of Thoracic Cardiovascular Surgery) this year.

In general, septal myectomy is the gold standard method of treatment. At the present time, septal artery ablation is not recommended in children.

	Acknowledgments

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We acknowledge with appreciation Dr Kevin Greason and Dr John Seccombe for early data collection. We thank the Mayo Clinic Division of Biostatistics for statistical support, Judy K. Lenoch for assistance with data collection and analysis, and Evon Heimer for excellent secretarial support.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Kenji Minakata Joseph A. Dearani Gordon K. Danielson Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Minakata, K. Articles by Danielson, G. K. Search for Related Content PubMed PubMed Citation Articles by Minakata, K. Articles by Danielson, G. K.