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Ann Thorac Surg 2005;80:851-856
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Mechanisms for Recurrent Left Ventricular Outflow Tract Obstruction After Septal Myectomy for Obstructive Hypertrophic Cardiomyopathy

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

Accepted for publication March 28, 2005.

^_* Address reprint requests to Dr Dearani, 200 First St SW, Rochester, MN 55905 (Email: dearani.joseph{at}mayo.edu).

	Abstract

Top Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
BACKGROUND: Left ventricular septal myectomy provides excellent outcomes for symptomatic patients with severe obstructive hypertrophic cardiomyopathy. However, in a few patients, left ventricular outflow tract obstruction may recur and require repeat myectomy. We reviewed this subset of patients to assess the mechanisms of recurrence.

METHODS: From 1975 to July 2003, 610 septal myectomies were performed; 13 of these were repeat myectomies after classic myectomies performed at our institution (n = 6) or elsewhere (n = 7). Ages ranged from 4 to 70 years (mean, 32 ± 22). The interval between initial myectomy and repeat myectomy ranged from 13 months to 11 years (mean, 5.0 ± 3.7 years).

RESULTS: Mechanisms for obstruction included limited myectomy at the initial myectomy (n = 11), septal hypertrophy at the midventricular level (n = 8), and anomalous papillary muscles (n = 3). Mean intraoperative pressure gradients decreased from 82 ± 24 to 6.2 ± 4.4 mm Hg. No mitral valve replacement was performed, and there were no early deaths. Mean follow-up was 5.8 ± 5.8 years. There was one late death. All surviving patients were free from recurrence of outflow tract obstruction and were in the New York Heart Association functional class I or II.

CONCLUSIONS: Mechanisms for recurrent obstruction included limited myectomy at the initial operation, midventricular obstruction, anomalies of papillary muscles, and ventricular remodeling, especially in pediatric patients. Repeat myectomy can be performed with excellent outcomes. Need for reoperation may be reduced with current surgical approaches that include a more extended resection of the midventricular septum, relief of papillary muscle anomalies, and routine use of intraoperative transesophageal echocardiography.

	Introduction

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Patients with hypertrophic cardiomyopathy (HCM) may develop limiting symptoms due to dynamic left ventricular outflow tract obstruction (LVOTO) and associated mitral regurgitation caused by systolic anterior motion of the anterior mitral leaflet [1]. For those patients whose symptoms are unresponsive to maximal medical therapy, left ventricular septal myectomy has been the standard therapeutic option for both children and adults [2–10]. Initially good results are generally permanent and are associated with significant and persistent improvement in symptoms and exercise capacity [1]. However, after an apparently successful myectomy in a few patients, a substantial LVOT gradient may recur, which causes recurrent symptoms. This review sought to identify the mechanisms for recurrent LVOTO and to assess the results of repeat myectomy in this subgroup of patients.

	Patients and Methods

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Between April 1975 and July 2003, 610 left ventricular septal myectomy procedures were performed for obstructive HCM on the authors’ surgical services. Patients without HCM who underwent resection of fixed LVOTO for Shone’s complex or other diagnoses were excluded. Thirteen of the 610 operations were repeat myectomies for recurrent LVOTO after initial myectomy performed at our institution (n = 6) or elsewhere (n = 7). These 13 patients comprise the study population for this review. Two other patients who had undergone a previous myectomy and who required repeat operation for aortic valve replacement and mitral valve repair had concomitant repeat myectomies for minor residual gradients (peak systolic pressure gradients, 31 and 34 mm Hg, respectively); they were excluded from this review because the indications for reoperation were severe native cardiac valve regurgitation, not the minor degree of LVOTO. During the same time interval for this review, we had 1 patient who underwent alcohol septal ablation at our institution 5 years after a previous surgical myectomy that was also done at our institution. Conversely, we have had 3 patients who underwent surgical myectomy at our institution after failed alcohol ablations that were also done at our institution.

Demographic and other patient-related data were obtained from medical and surgical records. Follow-up information was obtained from subsequent clinical visits, written correspondence from local physicians, and telephone interviews with patients or families. Data were expressed as mean ± standard deviation. Continuous data were compared with a paired Student t test, and categorical data were analyzed with the ₂ or Fischer’s exact test. Statistical significance was considered to be p < 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 patients or families gave informed consent.

Patient characteristics are summarized in Table 1. Ages at initial myectomy ranged from 2 months to 64 years (median, 26 years). All 13 patients had 1 or more recurrent symptoms and 9 were in the New York Heart Association functional class III or IV. Year of initial myectomy and intraoperative direct pressure measurements before and after initial myectomy are given in Table 2. In one patient (No. 3), a reliable pre-myectomy gradient could not be obtained because of unstable hemodynamics; the pre-myectomy gradient was taken from the preoperative cardiac catheterization.

Evaluation of the mechanism(s) for recurrent LVOTO was made at the time of reoperation by viewing the transesophageal echocardiogram and by direct inspection of the left ventricle and mitral valve. An assignment of a limited resection at the initial myectomy was made if the depth or width of the trough was inadequate or if the trough did not extend apically far enough to prevent systolic mitral–septal contact. An assignment of midventricular obstruction was made if the LVOT gradient occurred primarily at the midventricular level. The category of anomalous papillary muscle included any insertion of a papillary muscle directly into the anterior mitral leaflet, extensive fusion of a papillary muscle with the ventricular septum, or the presence of any abnormal chordae tendineae or accessory papillary muscles that contributed to the LVOTO [11–14]. It was recognized that left ventricular remodeling represents an important component of the pathophysiology of HCM and can be an important factor in altering LVOT dimensions [15]. However, at the time of repeat myectomy, it was not possible to determine the degree to which remodeling had contributed to the recurrent LVOTO.

Current Surgical Techniques "Extended Septal Myectomy"
Current surgical techniques emphasize ideal exposure of the subaortic region and mitral valve anatomy, an extended resection at the midventricular level, and relief of any papillary muscle anomalies (Fig 1).

View larger version (92K): [in this window] [in a new window]   Fig 1. Diagram showing two operative approaches for performing septal myectomy in obstructive hypertrophic cardiomyopathy. Typical outflow tract morphology with predominant basal septal hypertrophy and subaortic obstruction due primarily to systolic anterior motion of the mitral valve (center panel). Endocardial thickening at the line of apposition of the anterior mitral leaflet to the septum (friction lesion) is shown (center panel). (A) A standard rectangular myectomy trough (Morrow procedure) is created from 1 cm below the aortic valve apically to a point beyond the line of mitral–septal contact and intraventricular obstruction, allowing relief of the outflow tract gradient and preservation of sinus rhythm. (B) In the presence of muscular midcavity obstruction due to anomalous papillary muscles with direct insertion into the mitral valve or to extensive diffuse septal hypertrophy extending to the bases of the papillary muscles, a much more substantial myectomy is performed by combining the standard operation with an extended midventricular resection. The apical portion of the myectomy trough is much wider and includes the distal third of the right side of the septum (arrows). (Reprinted from [16] Dearani JA, Danielson GK. Obstructive hypertrophic cardiomyopathy: results of septal myectomy. In: Maron BJ, ed. Diagnosis and Management of Hypertrophic Cardiomyopathy. Malden, MA: Blackwell Futura; 2004:220–353, with permission.)

The classical portion of the resection is started by making two parallel longitudinal incisions in the septum; the first incision is made beneath the nadir of the right coronary cusp and the second is made beneath the commissure between the right and left coronary cusps. These incisions are connected superiorly with a third incision below the aortic annulus, and a deep wedge of septal tissue is resected. This classical resection is then extended in several ways, beginning with continued resection leftward (as viewed by the surgeon) toward the mitral valve annulus and apically to the papillary muscles. The apical third of the trough is then extended rightward by resection of posterior septal myocardium to obtain a much wider trough at the apex than the base. All redundant anomalous chordae are resected and any papillary muscle fusion to the septum or free wall is released (Fig 1) [11]. For midventricular obstruction due to diffuse septal hypertrophy, massively hypertrophied papillary muscles, or anomalous muscle bundles, an additional resection is made at the midventricular level and around the bases of the papillary muscles. After the patient is weaned from cardiopulmonary bypass, pressures are re-measured and transesophageal echocardiogram evaluation is repeated. In general, we would resume cardiopulmonary bypass for re-resection if the gradient was greater than 15 to 20 mm Hg. Additional technical details are given (see refs [16, 17]).

	Results

Top Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Intraoperative Findings and Mechanisms of LVOTO
More than one mechanism for obstruction was identified in many patients (Table 2). The most common mechanisms appeared to be limited resection at the initial myectomy (n=11) and obstruction at the midventricular level (n=8). Mitral valve or papillary muscle anomalies were mechanisms of obstruction in 3 patients; these included marked anterior displacement of the anterolateral papillary muscle (n = 2), false chordae to the free wall and septum (n = 1), accessory papillary muscle (n = 1), and redundant mitral leaflet tissue attached to the lateral wall of the left ventricle (n = 1). A leftward shift of the septal trough contributed to LVOTO 6 years after initial myectomy in a 70-year-old patient.

Hemodynamic Measurements
Peak systolic pressure gradients were assessed intraoperatively by direct pressure measurements before and after myectomy (Table 2). In 2 patients (Nos. 1, 4), reliable pre-myectomy gradients could not be obtained due to unstable hemodynamics; their pre-myectomy gradients were taken from preoperative cardiac catheterization and echocardiographic data, respectively. Mean peak systolic pressure gradients decreased significantly from 82 ± 24 to 6.2 ± 4.4 mm Hg after repeat myectomy (p < 0.001). Mitral valve regurgitation was graded from I (mild) to IV (severe); mean grade of mitral regurgitation by intraoperative transesophageal echocardiogram also decreased significantly from 1.9 ± 1.0 to 1.1 ± 0.5 (p < 0.05). No mitral valve repairs were required, and no mitral valve was replaced. Three patients (Nos. 8, 11, and 12) underwent concomitant procedures for preexisting pathology as described in Table 2.

Early Results
There were no early deaths. An iatrogenic ventricular septal defect was repaired with a patch through the aortotomy in 1 patient (no. 1); this patient also required a pacemaker. One patient underwent temporary reintubation for respiratory failure, and 1 had nonsustained ventricular tachycardia develop postoperatively who received an implantable cardioverter defibrillator.

Late Results
Follow-up information was obtained on all patients; mean follow-up was 5.8 ± 5.8 years. There was 1 late death; patient 1 died of cancer at age 81 (11 years after repeat myectomy). One patient required mitral valve replacement for severe mitral regurgitation 10 years after repeat myectomy; the cause of regurgitation was degenerative disease without any evidence of LVOTO. All surviving patients were in the New York Heart Association functional class I or II and were free from recurrence of significant LVOTO by follow-up echocardiography.

	Comment

Top Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
Transaortic left ventricular septal myectomy has been the standard surgical procedure for symptomatic patients with severe obstructive HCM unresponsive to medical therapy since the late 1960s [3, 5]. It has been shown that septal myectomy significantly decreases LVOT gradient and associated mitral regurgitation and provides excellent long-term outcomes [1–8]. However, in some patients symptoms may recur after myectomy; the causes may include ventricular diastolic or systolic dysfunction, progressive mitral regurgitation, arrhythmias, or recurrent LVOTO. Little has been reported to date regarding the pathophysiology of recurrent LVOTO after septal myectomy.

As observed at repeat myectomy, the cardiac anatomy in 11 of 13 patients in this review showed limited septal resections, mostly in depth or width, or both, as mechanisms of recurrent LVOTO. Limited resections also occurred when the initial resection was not carried far enough apically to permanently relieve the obstruction, especially at the midventricular level in patients who had diffuse septal hypertrophy (n = 8). It has been demonstrated that the mitral valve is elongated and the area is enlarged in many patients with obstructive HCM [12], and experience has shown that for complete relief of LVOTO, septal resections must be carried apically far enough to prevent contact of the anterior mitral leaflet with the septum during systole.

Although the basic transaortic approach for performing a septal myectomy has been known for over 40 years, the operation remains technically challenging and results are operator dependent to a high degree [2]. Incisions or excisions made too deep create ventricular septal defects or ventricular perforations. Poor visualization of the anatomy below the aortic valve can result in injury to mitral leaflets or chordae. Incorrect placement of incisions or excessive traction can produce complete heart block. Inadequate myocardial protection of the hypertrophied heart can cause difficulty in defibrillation and low cardiac output. The aortic valve is always at risk for injury from instruments passed through the valve and manipulated within the ventricle. Therefore it is understandable that overly conservative surgical attitudes may sometimes prevail, resulting in limited myocardial resection and consequent incomplete relief or early return of LVOTO and symptoms.

Three patients in this review had anomalies of mitral papillary muscles or chordae that appeared to contribute to the LVOTO. Such anomalies, if unrecognized and untreated, can lead to intraoperative death or incomplete or only temporary relief of obstruction [13]. Perhaps the most important of these anomalies is anomalous papillary muscle insertion directly into the anterior mitral leaflet [11–14]. Mitral valve replacement has been advocated by some as the best surgical solution for this serious anomaly, but we prefer to perform an extended septal myectomy in order to eliminate the potential long-term consequences of prosthetic valves and anticoagulant therapy [11]. Other anomalies of mitral subvalvular apparatus include extensive fusion of papillary muscles with the ventricular septum or left ventricular free wall, abnormal chordae tendineae (false cords) that attach to the ventricular septum or free wall, and accessory papillary muscles, all of which may tether the mitral leaflets toward the septum and produce LVOTO [11]. Additional mechanisms of dynamic LVOTO include midventricular obstruction secondary to severely hypertrophied papillary muscles or other muscle bundles and anterior displacement of the anterolateral papillary muscle [12].

We and others have observed that children appear to have an increased risk of reoperation after myectomy for obstructive HCM compared with adult populations [4, 9]. It has been shown that in nonoperated patients with HCM, left ventricular hypertrophy often rapidly progresses during the adolescent years [15]. Left ventricular wall thickness may increase dramatically (> 100%) during a few months or years, and the distribution of hypertrophy may become more diffuse [18]. This raises the possibility that recurrence of LVOTO after successful myectomy in pediatric patients might be due in part to regrowth of septal myocardium or to other types of left ventricular remodeling such as changes in wall thickness and reduction of cavity size [15]. Another possible explanation for the increased need for reoperation in pediatric patients is that extended septal resections may be compromised by the small size of the aorta and limited visibility of the midventricular region.

The role that ventricular remodeling plays in recurrent LVOTO in adult patients is even less well understood, but remodeling likely contributed to the progressive increase in LVOT gradients and symptoms seen in most patients in this review. For the 9 patients whose hemodynamic data at the initial myectomy were available, the mean gradients had been reduced from 86 mm Hg before myectomy to 20 mm Hg after myectomy, and most had significant improvement in symptoms. The gradients for the same 9 patients then increased progressively to a mean gradient of 87 mm Hg at the time of repeat myectomy (mean interval, 6 years later). At the time of repeat myectomy, it was not possible to determine the relative importance of limited resection versus subsequent remodeling as causes of the recurrent LVOTO. However, it is probable that short intervals between primary myectomy and re-myectomy suggest limited resection and longer intervals suggest remodeling as the major contributor. Nevertheless, a more extensive initial resection as currently performed would arguably have delayed or prevented recurrent LVOTO in some of these patients.

The 70-year-old patient who underwent repeat myectomy 6.1 years after initial myectomy had the same surgeon for both operations. The anatomy of reoperation was unusual; the septal trough, especially the right wall of the trough, had migrated leftward relative to the orientation of the aortic cusps, allowing anterior mitral leaflet contact with the septum in systole. It is known that in elderly patients the aortic root migrates rightward relative to the left ventricle (sigmoid septum); this narrows the LVOT, and in some patients it produces systolic mitral–septal contact and dynamic LVOTO [19, 20]. The relative roles of remodeling of the septal trough versus the development of a sigmoid septum in this patient’s recurrent LVOTO are unknown.

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 they are not appropriate for children, nor for those who have fixed obstruction present instead of obstructive HCM, nor for patients who have LVOTO due to papillary muscle anomalies, nor for patients with unfavorable septal artery anatomy [21]. As experience increases and lengthens with newer alternatives to surgery, the results can be compared with more than 40 years of experience with septal myectomy.

We conclude that dynamic LVOTO does recur after classic septal myectomy for obstructive HCM in a small number of patients. Mechanisms for recurrent obstruction include limited resection at the initial operation, midventricular obstruction, anomalies of the papillary muscles, and ventricular remodeling, especially in pediatric patients. Repeat myectomy can be performed with excellent outcomes. Need for reoperation may be reduced with current surgical approaches that include a more extended resection of the midventricular septum, relief of papillary muscle anomalies, and routine use of intraoperative transesophageal echocardiography.

	Acknowledgments

Top Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
We appreciate the statistical support received from the Center for Patient-Oriented Research at the Mayo Clinic in Rochester, Minnesota.

	References

Top Abstract Introduction Patients and Methods Results Comment Acknowledgments 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 Hartzell V. Schaff 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. Related Collections Congenital - acyanotic