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Residual and recurrent gradients after septal myectomy for hypertrophic cardiomyopathy—mechanisms of obstruction and outcomes of reoperation
Accepted Manuscript Residual and Recurrent Gradients after Septal Myectomy for Hypertrophic Cardiomyopathy – Mechanisms of Obstruction and Outcomes of Reoperation Yang Hyun Cho , M.D. Ph.D Eduard Quintana , M.D. FETCS Hartzell V. Schaff , M.D Rick A. Nishimura , M.D Joseph A. Dearani , M.D Martin D. Abel , M.D Steve Ommen , M.D PII:
S0022-5223(14)00568-6
DOI:
10.1016/j.jtcvs.2014.05.028
Reference:
YMTC 8617
To appear in:
The Journal of Thoracic and Cardiovascular Surgery
Received Date: 1 April 2014 Revised Date:
22 April 2014
Accepted Date: 5 May 2014
Please cite this article as: Cho YH, Quintana E, Schaff HV, Nishimura RA, Dearani JA, Abel MD, Ommen S, Residual and Recurrent Gradients after Septal Myectomy for Hypertrophic Cardiomyopathy – Mechanisms of Obstruction and Outcomes of Reoperation, The Journal of Thoracic and Cardiovascular Surgery (2014), doi: 10.1016/j.jtcvs.2014.05.028. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Title: Residual and Recurrent Gradients after Septal Myectomy for Hypertrophic Cardiomyopathy –
ACCEPTED MANUSCRIPT Mechanisms of Obstruction and Outcomes of Reoperation
Authors: Yang Hyun Cho*, M.D. Ph.D. 1,2, Eduard Quintana*, M.D. FETCS.1,3, Hartzell V. Schaff, M.D.1,
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Rick A. Nishimura, M.D.4, Joseph A. Dearani, M.D.1, Martin D. Abel, M.D. 5, Steve Ommen, M.D.4
Institution and Affiliations: Division of Cardiovascular Surgery, Mayo Clinic
2
Department of Thoracic and Cardiovascular Surgery. Samsung Medical Center, Sungkyunkwan University
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1
3
Universitat de Barcelona
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Division of Cardiovascular Disease, Mayo Clinic
5
Department of Anesthesiology, Mayo Clinic
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*Both authors contributed equally to this work
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School of Medicine, Seoul, Korea
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Word count: 2910
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Funding or Disclosure: none
Corresponding Author: Hartzell V. Schaff MD
Division of Cardiovascular Surgery Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 e-mail: [email protected] Phone: 507-255-7068 Fax: 507-255-8674 1
Abstract
ACCEPTED MANUSCRIPT Objective: The aims of this study were to identify the mechanism(s) of residual or recurrent left ventricular outflow tract (LVOT) obstruction in patients undergoing repeat septal myectomy for hypertrophic cardiomyopathy and to assess the early and late results of reoperation. Methods: From January, 1980 to June 2012, we performed 52 repeat myectomies in 51 patients. We
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reviewed medical records and preoperative transthoracic echocardiograms to evaluate adequacy of previous resection and mechanism of LVOT obstruction. Complications of previous and repeat myectomy, NYHA class, and survival were analyzed.
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Results: The mean interval from previous myectomy to reoperation was 43±51 months. In 6 patients (12%) residual/recurrent gradients were caused by isolated midventricular obstruction. In the remaining 46
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operations, the mechanisms of residual/recurrent gradients were identified as systolic anterior motion of mitral valve (SAM) related subaortic obstruction caused by inadequate length of previous subaortic septal excision in 31 patients (59% of the total) or a combination of inadequate length and inadequate depth of septectomy 13 patients (25%); two patients had both residual subaortic obstruction due to SAM and
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midventricular obstruction (4%). Preoperatively 96% of patients were in NYHA class III or IV, and postoperatively, 93.8% were class I or II (p<0.001). The 10-year survival following reoperation was 98 % and similar to an age and gender matched Minnesota population (p = 0.46).
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Conclusions: The most common cause of recurrent LVOT obstruction and symptoms in patients undergoing septal myectomy is inadequate length of septal excision. Reoperation is safe with excellent long-term
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survival and functional improvement.
Abstract word count: 250
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Ultra mini-Abstract: Repeat septal myectomy for recurrent left ventricular outflow tract obstruction
ACCEPTED MANUSCRIPT provides excellent surgical results as regards gradient relief and symptomatic improvement. The
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mechanisms of residual obstruction are usually related to the extent of previous myectomy.
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Introduction
ACCEPTED MANUSCRIPT Fixed or provocable left ventricular outflow tract (LVOT) obstruction is present in as many as 70% of patients with hypertrophic cardiomyopathy (HCM) [1]. In obstructive HCM, left ventricular outflow tract narrowing is caused by septal hypertrophy in combination with systolic anterior motion of the mitral valve (SAM); abnormal papillary muscle may also contribute to LVOT gradients [2]. Patients unresponsive to
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medical treatment and with favorable anatomy are good candidates for septal myectomy which predictably relieves gradients and secondary mitral valve regurgitation thus improving symptoms and exercise performance [3, 4]. A subset of patients undergoing myectomy may have residual or recurrent obstruction
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with persistence of symptoms, and even though risk of residual gradients is low, little is known of mechanism(s) of recurrent obstruction or outcome of reoperation [5]. Therefore, the aim of this study was to
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investigate the anatomic abnormalities leading to reoperation for myectomy and to document early and late results of reoperation.
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Methods
Patient Selection
From January 1980 to June 2012, 2,034 patients underwent septal myectomy for obstructive HCM at our
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Clinic. Among these, we then identified 51 patients who had 52 operations for the residual or recurrent obstruction after a previous surgical septal myectomy. We included only patients who had a primary
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diagnosis of HCM and did not include patients who had myectomy at the time of planned aortic valve replacement or patients who had SAM following mitral valve repair. This clinical study was reviewed and approved by the Mayo Clinic College of Medicine Institutional Review Board, and all patients agreed to clinical research authorization before operation. For capture of data related to this population we used information from our database and electronic medical record. Follow-up was obtained from health assessment questionnaires sent to patients and families 1, 3, 5, 10, and 15 years postoperatively and was supplemented by written correspondence from referral physicians or patients themselves and vital status from the Social Security Death Index. 4
All patients had resting or provoked gradients ≥50 mmHg determined preoperatively by means of
ACCEPTED MANUSCRIPT transthoracic Doppler echocardiography or invasive hemodynamic study if outflow tract gradients could not be determined by Doppler echocardiography. Echocardiographic studies were performed at baseline according to the recommendations of the American Society of Echocardiography [3]. LVOT gradients were measured with continuous-wave Doppler of the outflow tract from an apical window and calculated using
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the modified Bernoulli equation (gradient = 4v2, v = peak LVOT velocity). If a significant gradient was not obtained under basal conditions, a Valsalva maneuver and/or administration of amyl nitrate or exercise was used to provoke a gradient. If patients were stable in the operating room before cardiopulmonary bypass,
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pressure measurements were obtained again directly measuring intracavitary (LV) and aortic pressures [6]. Thirty-two of the 52 patients underwent first operation for septal myectomy elsewhere. The
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remaining 20 patients had initial operation at our institution, and this represents approximately 1% of patients having primary myectomy. Two patients had residual obstruction following two previous myectomies, and 3 patients had a previous percutaneous alcohol septal ablation.
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Etiology of recurrent obstruction
The site of recurrent obstruction was identified primarily by using a parasternal long-axis view. Images of the preoperative echocardiograms and operative records of all patients were reviewed by three
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authors (Y.H.C, E.Q, and H.V.S). In each patient, consensus was reached on the morphologic features causing obstruction. The previous myectomy site was visually evaluated. The presence of systolic anterior
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motion of the mitral valve was a marker of dynamic LVOT obstruction indicating residual or recurrent subaortic obstruction. A midventricular obstructive pattern was defined when there was no SAM and the midventricular septum was responsible for significant intracavitary gradient. The anatomy of papillary muscle was also reviewed as a possible cause of LVOT obstruction. Based on these findings, we categorized the mechanisms of recurrent obstructions as insufficient length of septal excision, inadequate depth of septal excision, midventricular obstruction, or obstruction due to an abnormal papillary muscle (Figure 1). An important goal of the study was to determine whether late LVOT obstruction might reflect regrowth of muscle in the area of prior myectomy. Thus, we analyzed further those patients from our Clinic 5
who had marked improvement in their clinical status initially after the previous myectomy. We then
ACCEPTED MANUSCRIPT compared Doppler echocardiograms obtained early after initial myectomy to studies obtained before reoperation to compare septal anatomy and the previous myectomy site.
Surgical procedure
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Operations were performed using standard methods for repeat median sternotomy; we employed normothermic cardiopulmonary bypass with single venous cannula, and antegrade cold blood cardioplegia for myocardial protection. . Exposure is facilitated by complete lysis of adhesions to allow the ventricles to
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collapse and to be displaced posteriorly. Next, an oblique aortotomy is made, and we prefer to situate this slightly closer to the sinotubular ridge than is usual for aortic valve replacement; the aortic incision is carried
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through the midpoint of the noncoronary aortic sinus of Valsalva to a level approximately 1 cm above the valve anulus. The edge of the proximal aorta is held out of the way with small stay sutures, and a cardiotomy sucker is placed through the aortic valve and used to depress the anterior leaflet of the mitral valve to protect it from injury. The right aortic valve cusp is collapsed against the sinus wall, where it will usually stay.
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The region of residual septal obstruction can be recognized by endocardial scar resulting from contact with the anterior mitral valve leaflet. The technique used for relief of residual subaortic obstruction is similar to that employed for primary operations. [7]. The septum is incised with a No. 10 scalpel blade just
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to the right of the nadir of the right aortic sinus. Incision in the septum is made upward and then leftward over to the anterior leaflet of the mitral valve. Scissors are used to complete excision of this initial portion of
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myocardium. A sponge stick is used to depress the right ventricle and to rotate the septum posteriorly, orienting the LV outflow anteriorly. The area of septal excision is then deepened and lengthened toward the apex of the heart, being certain to excise hypertrophied septum beyond endocardial scar, and the myectomy site is further enlarged with the use of pituitary rongeurs. Adequate septal myectomy usually yields 3 to 12 g of muscle, and the depth of resection depends on the thickness of the septum but is rarely less than 10 mm. If the level of obstruction was distant from the aortic valve precluding a transaortic access, an apical left ventriculotomy was performed to provide access to the midventricular septum[8]. To confirm complete relief of the LVOT obstruction, we used intraoperative echocardiography and routinely measured 6
simultaneous aortic and left ventricular pressure by direct needle puncture before and after myectomy.
ACCEPTED MANUSCRIPT Patients had the surgical ablative procedure performed either by a transaortic approach (45 patients), a transventricular myectomy (4 patients), or combined transaortic and transapical approach (3 patients). In addition to surgery to relieve obstruction caused by HCM, 19 concomitant procedures were performed in 16
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patients (Table 2).
Follow-up and Analysis
Statistical analyses were performed using SAS software (version 9.1; SAS Institute Inc, Cary, NC).
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Descriptive statistics for categorical variables are reported as frequency and percentage, and continuous variables are given as mean (± standard deviation). The Kaplan–Meier method was used to estimate late
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survival. Observed late survival was compared using a log-rank test to expected survival of an age- and sexmatched Minnesota population. In the analysis of functional status, we used the most current follow-up information.
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Results
The mean age at the time of repeat myectomy was 38.1±18.9 years, and 18 patients were men (35%). All patients had cardiac limitation at time of reoperation with symptoms of left heart failure, dyspnea and
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fatigability, despite medical treatment with one or two negative inotropic agents (Table 1). In addition, 11 patients (22%) had angina pectoris, and 7 (14%) had syncope. Formal exercise tests were recorded in 19
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patients whose functional aerobic capacity was 59±24 % of predicted. Among all patients, the symptom-free interval after the prior myectomy was 22±42 months, and repeat myectomy was performed at a mean of 43±51 months following the prior procedure (Table 2). At the time of reoperation, 5 patients had permanent transvenous pacemakers in place because of complete atrioventricular block related to the previous operation. Further, there were 9 patients with previous ICD (implantable cardio-defibrillator) implants, 5 as primary prevention and 4 as secondary prevention following resuscitation from sudden cardiac death. Dual chamber pacemaker implantations
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aimed at reducing LVOT gradients [9] were performed at different times before redo myectomy in 9
ACCEPTED MANUSCRIPT additional patients. Before reoperation, 4 subjects were in atrial fibrillation and the remaining patients were in sinus rhythm or paced as described above. Among patients without pacemakers, the electrocardiograms before repeat myectomy demonstrated normal conduction in 5 patients, left anterior fascicular block (LAFB) in 2
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patients, and left bundle branch block (LBBB) pattern in the remainder of the study patients. Mean peak-to-peak LVOT gradients measured intraoperatively before repeat myectomy were 54±30 mmHg at rest and 85±41 mmHg after provocation. After redo myectomy the maximum (provoked) mean
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peak-to-peak systolic gradients fell to 13±12 mmHg. After redo myectomy, 5 patients had an ICD implanted before hospital dismissal (2 patients developed new complete heart block), 2 patients with previous normal
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intraventricular conduction and 1 with LAFB conduction developed a new LBBB. After surgery, improvement of symptoms was common. Preoperatively 96% of patients were in NYHA class III or IV, and postoperatively, 93.8% were class I or II (p<0.001, Figure 2).
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Surgical findings and causes of recurrent obstruction
The pathological anatomic findings causing obstruction before reoperation were identified as inadequate length of excision in 31 patients (59%), a combination of inadequate length and inadequate depth of
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previous myectomy in 13 (25%), a combination of inadequate length and midventricular obstruction 2 (4%), and isolated midventricular obstruction in 6 patients (12%). One patient had abnormal papillary muscles
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combined with midventricular obstruction. Among 11 pediatric patients (<18 years old) in this series recurrence of obstruction was insufficient length of septectomy in 9 patients and mid ventricular obstruction in 2 patients.
Mitral regurgitation and systolic anterior motion of mitral valve Preoperatively, mitral regurgitation (MR) was common, but the severity varied in relation to systolic anterior motion (SAM) of the mitral valve and dynamic outflow obstruction. If the mitral valve was structurally normal, regurgitation improved or disappeared after myectomy without additional direct procedures on the 8
valve itself. In 4 patients with intrinsic abnormalities of the mitral leaflets, direct valve repair was necessary
ACCEPTED MANUSCRIPT at the time of myectomy [10]. No patients required mitral valve replacement.
Early and late survival There was no in-hospital mortality, but 1 patient died after hospital dismissal within 30 days after surgery;
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postmortem examination revealed pulmonary embolism. There were 3 late mortalities. One patient with severe pulmonary hypertension died 13 years after surgery of unclear reasons. Another patient died of cancer 11 years after surgery, and there was another death of unknown cause 10 years after repeat
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myectomy. The Kaplan-Meier 10-year survival rate was 98% and at 15 years was 82%. Survival following repeat myectomy was similar to that of an age and gender matched Minnesota population (p = 0.46, Figure
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3).
Special attention was given to patients who had initial improvement in symptoms and had their first operation at our institution. Among these patients, post myectomy intraoperative LVOT gradients at initial operation averaged 9.2±8.2 mmHg, and symptoms recurred at an average of 38±24 months following initial
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septal myectomy. Detailed comparisons of intraoperative echocardiograms from the first procedure compared to studies performed just before redo myectomy showed no evidence of regrowth of subaortic septum. In 2 pediatric patients the recurrence could be attributed to septal muscle growth at the
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Discussion
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midventricular level, but interpretation of changes is difficult because of somatic growth.
Recurrent symptoms after myectomy for obstructive HCM may be caused by a variety of problems including left ventricular diastolic dysfunction, valvular abnormalities, development of coronary artery disease, medication related symptoms, arrhythmias, persistence of pulmonary arterial hypertension as well as dynamic or fixed left ventricular obstruction. Little is known about the real incidence of recurrent obstruction after a septal myectomy, but this subgroup of patients with symptoms and recurrent obstruction severe enough to require reoperation accounts for 1% of all HCM surgical practice.
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Recognition and management of residual or recurrent LVOT obstruction varies considerably
ACCEPTED MANUSCRIPT depending on the quality of clinical assessment and expertise available to this relatively small group of patients. Previously, we reported outcome of operation in 13 patients who had repeat myectomy at our Clinic from 1975 to 2003. In that report, the primary cause of LVOT obstruction was identified as limited resection. The present study provides more detailed information on the morphologic aspects of incomplete
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septal myectomy in a larger cohort of patients with extended follow-up. Assessment of preoperative echocardiograms and surgical findings revealed that the primary reason for incomplete myectomy was not carrying the septal excision far enough towards the apex during the first
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operation, and this was identified in 59% of patients. In an additional 25% of patients there was both inadequate length and depth of septal excision. Recurrent symptoms due to midventricular obstruction were
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less common (12%).
There are several technical factors that may limit exposure of the subaortic area and excision of septal muscle. Visualization of the subaortic septum is often more difficult in obese patients with thick chest walls and patients with greater anterior-posterior diameters of the thorax. Also, exposure may be poor
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because of small ascending aorta diameter and small aortic valve annulus size. Important also is the level of obstruction and its distance from the aortotomy. Despite the difficulties listed above, in almost all patients the site of subaortic obstruction can be identified by the presence of endocardial scar, the area of apposition
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with the anterior mitral valve leaflet during systolic anterior motion of the structure. It is important that septal excision be carried distally toward to the apex and past the visible endocardial scar.
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Understanding the anatomic basis for recurrent LVOT obstruction is important in order to avoid complications of myectomy. For example, widening the proximal area of septal excision in the clockwise direction would increase risk of injury to the atrioventricular conduction pathway and development of complete heart block. Also, deepening the region of previous myectomy, because of the mistaken assumption that this is the site of obstruction, invites iatrogenic ventricular septal defect. As a general rule, whenever SAM is present we first approach LVOT obstruction through an aortotomy and the aortic valve. On the other hand, when midventricular obstruction is present without SAM of the mitral valve, we favor exposure of the mid septum through an apical ventriculotomy. In the present 10
study 7 patients (14 %) underwent the transventricular approach for septal myectomy to relieve obstruction
ACCEPTED MANUSCRIPT completely, and it is likely that some of these patients would have been better served by this approach at initial operation. As is found with subaortic obstruction, there is endocardial scar that guides septal excision in patients with midventricular obstruction, and this is caused by contact of the papillary muscles with the septum. Midventricular obstruction can be readily exposed through an apical ventriculotomy and the
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procedure is safe with minimal complications related to incision of the ventricle. [11]. The evolution of gradients deserves a special comment. Review of the intraoperative courses of the first myectomy in patients from our institution (in patients with initial improvement) reveals that
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intraoperative LVOT gradients were minimal, mean 9.2 ± 8.2. This group had a recurrence of symptoms at 38 ± 24 months after the procedure, and comparison of septal morphology by echocardiography
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demonstrated that although gradients were acceptably low after initial myectomy, there was either some degree of septal bulging that persisted or midventricular obstruction was not appreciated initially. There was no evidence from these patients in whom direct comparison of echocardiograms was possible that there was regrowth of septal muscle responsible for obstruction. As previously described, the pediatric population is at
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increased risk of recurrent symptoms and need for reoperation due to limited transaortic access leading to incomplete resections [12]. It is unclear why patients had low gradients after initial myectomy, and it is possible that these were minimized by anesthetic effects [6] and/or that gradients developed later with global
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LV remodeling [13]. The time frame of reappearance of symptoms may have been influenced by impact of recovery from heart surgery itself, individual expectations and physician judgment. It is important, therefore,
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to measure intraoperative gradients accurately and compare this to intraoperative Doppler-echocardiographic findings. Provocative maneuvers should be performed (induction of a premature ventricular contraction or administration of isoproterenol) to confirm the absence of an inducible gradient. If additional resection is necessary, we remove more muscle from the distal septum rather than thinning further the initial myectomy site. This patient population is complex; nevertheless, operative mortality for repeat myectomy was very low. Patient survival and symptomatic improvement were similar to the larger group of patients having primary myectomy; indeed survival of these patients parallels a sex and age matched population. These 11
results emphasize the importance of identifying residual obstruction in patients with persistent symptoms
ACCEPTED MANUSCRIPT after a septal myectomy. The findings also highlight the importance of complete intraoperative assessment of septal myectomy at initial operation.
Conclusions
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Reoperation for recurrent obstruction in patients with HOCM is uncommon and but most often due to incomplete initial myectomy. The most frequent finding was failure to carry septal excision far enough
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toward the apex of the heart; mid ventricular obstruction may also lead to recurrent symptoms.
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Acknowledgments
ACCEPTED MANUSCRIPT The authors would like to acknowledge Zhuo Li for statistical analysis, Judy Lenoch for data retrieval,
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Michael King for creation of surgical illustrations and Mark Zang for echocardiographic imaging support.
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References
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Maron, M.S., et al., Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction. Circulation, 2006. 114(21): p. 2232-9.
2.
Minakata, K., et al., Extended septal myectomy for hypertrophic obstructive cardiomyopathy with
3.
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anomalous mitral papillary muscles or chordae. J Thorac Cardiovasc Surg, 2004. 127(2): p. 481-9. Gersh, B.J., et al., 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart
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Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg, 2011. 142(6): p. e153203.
Ommen, S.R., et al., Long-term effects of surgical septal myectomy on survival in patients with
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4.
obstructive hypertrophic cardiomyopathy. Journal of the American College of Cardiology, 2005. 46(3): p. 470-6. 5.
Minakata, K., et al., Mechanisms for recurrent left ventricular outflow tract obstruction after septal
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myectomy for obstructive hypertrophic cardiomyopathy. The Annals of Thoracic Surgery, 2005. 80(3): p. 851-6. 6.
Ashikhmina, E.A., et al., Intraoperative direct measurement of left ventricular outflow tract
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gradients to guide surgical myectomy for hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg, 2011. 142(1): p. 53-9.
Schaff, H.V. and S.M. Said, Transaortic Extended Septal Myectomy for Hypertrophic
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7.
Cardiomyopathy. Operative Techniques in Thoracic and Cardiovascular Surgery, 2012. 17(4): p. 238-250. 8.
Said, S.M., et al., Transapical approach for apical myectomy and relief of midventricular obstruction in hypertrophic cardiomyopathy. Journal of cardiac surgery, 2012. 27(4): p. 443-8.
9.
Erwin, J.P., 3rd, et al., Dual chamber pacing for patients with hypertrophic obstructive cardiomyopathy: a clinical perspective in 2000. Mayo Clin Proc, 2000. 75(2): p. 173-80.
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10.
Wan, C.K., et al., What is the best surgical treatment for obstructive hypertrophic cardiomyopathy
ACCEPTED MANUSCRIPT and degenerative mitral regurgitation? Ann Thorac Surg, 2009. 88(3): p. 727-31; discussion 731-2. 11.
Kunkala, M.R., et al., Transapical approach to myectomy for midventricular obstruction in hypertrophic cardiomyopathy. The Annals of Thoracic Surgery, 2013. 96(2): p. 564-70.
12.
Minakata, K., et al., Septal myectomy for obstructive hypertrophic cardiomyopathy in pediatric
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patients: early and late results. The Annals of Thoracic Surgery, 2005. 80(4): p. 1424-9; discussion 1429-30.
Deb, S.J., et al., Septal myectomy results in regression of left ventricular hypertrophy in patients with
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hypertrophic obstructive cardiomyopathy. The Annals of Thoracic Surgery, 2004. 78(6): p. 2118-22.
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13.
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Tables
ACCEPTED MANUSCRIPT Table 1. Clinical and echocardiographic data of 51 patients having repeat myectomy for obstructive hypertrophic cardiomyopathy Variable
Value
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Clinical data Age (yr)
38.1 ± 18.9
Male
18 (35%) 1.8 ± 0.4
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BSA (m2) Hypertension
History of stroke NYHA III-IV Previous percutaneous alcohol septal ablation
Preop pacemaker Patient history of sudden death
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Family history of sudden death
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Preoperative ICD
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Chronic atrial fibrillation
5 (10%) 4 (8%) 4 (8%) 49 (96%) 3 (6%) 9 (18%) 9 (18%) 4 (8%) 7 (14%) 51 (100%)
Preoperative Diuretics
17 (33%)
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Preoperative beta-blocker/calcium channel blockers/both
Complications from previous myectomy Iatrogenic VSD
4 (8%)
Complete AV block
5 (10%)
Aortic valve injury
6 (12%)
Procedures combined with previous myectomy Aortic valve replacement
2 (4%)
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CABG
3 (6%)
ACCEPTED MANUSCRIPT Iatrogenic VSD repair
3 (7%)
Mitral valve repair
6 (12%)
Measurements 54 ± 30
Provoked LVOT gradient (mmHg)
85 ± 41
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Resting LVOT gradient (mmHg)
LV Ejection fraction (%)
71.2 ± 7.8
Basal septal thickness (mm)
20.5 ± 7
13.3 ± 3.8
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Posterior wall (mm) LVDED (mm)
LA volumen index (ml/m2) LV mass index (gr/m2) Severity of diastolic disfunction (0-4 grades)
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LVDES (mm)
43 ± 6 24 ± 5 47 ± 16 171 ± 74 2.4 ± 0.9
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Right ventricular systolic pressure (mmHg) / Systemic systolic pressure (mmHg)
35.4%
60 ± 24
Preoperative systolic anterior motion of mitral valve
46 (88%)
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Preoperative exercise test (% functional aerobic capacity predicted per age). *
Mitral regurgitation (≥ moderate)
37 (73%)
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Data shown as n (%) or mean ± SD *available data in 19 patients
Abbreviations: LV, left ventricle; LVDED, left ventricular end diastolic diameter; LVDES, left ventricular end systolic diameter; LA, left atrium.
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Table 2. Intraoperative and postoperative data of 51 patients having repeat myectomy for obstructive
ACCEPTED MANUSCRIPT hypertrophic cardiomyopathy Variable
Value
Intraoperative data following repeat myectomy 63 ± 37
Aortic occlusion time (min)
45 ± 27
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Extracorporeal circulation time
Grams of septal tissue removed (gr)
5.4 ± 4.1
Systolic anterior motion of mitral valve (≥ mild)
0
0
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Mitral valve regurgitation > mild Residual transventricular gradient (mmHg)
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Concomitant procedures Aortic valve repair CABG ASD closure
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Tricuspid valve repair Tumor removal Aortic valve replacement
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Mitral valve repair VSD repair
13 ± 12
1 (2%) 1 (2%) 1 (2%) 2 (4%) 2 (4%) 4 (8%) 4 (8%) 4 (8%)
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Related surgical complications Aortic valve injury
0
New complete auriculoventricular block
2 (4%)
New iatrogenic VSD
2 (4%)
ICU/hospital data Intubation > 24 h
4 (8%)
ICU stay (median days)
1
18
Hospital days (median days)
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ACCEPTED MANUSCRIPT Data shown as n (%) or mean ± SD Abbreviations: CABG, coronary artery bypass grafting; ASD, atrial septal defect; VSD, ventricular septal
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defect; ICU, intensive care unit
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Figure legends
ACCEPTED MANUSCRIPT Figure 1. Three types of recurrence after septal myectomy for hypertrophic obstructive cardiomyopathy with their respective parasternal long axis echocardiographic views. A: inadequate length and depth of excision, B:
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inadequate length of excision, C: midventricular obstruction at the level of papillary muscles.
Figure 2.
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Change in NYHA functional class after repeat myectomy. Most patients had improvement in symptoms and
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were in class I or II (93.8 %) at last follow-up.
Figure 3.
A: Kaplan-Meyer survival curve of patients who had repeat septal myectomy (solid curve). B: The survival
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was not inferior (p = 0.46) to that of an age and gender matched population (dashed curve).
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ACCEPTED MANUSCRIPT
S0022-5223(14)00568-6
DOI:
10.1016/j.jtcvs.2014.05.028
Reference:
YMTC 8617
To appear in:
The Journal of Thoracic and Cardiovascular Surgery
Received Date: 1 April 2014 Revised Date:
22 April 2014
Accepted Date: 5 May 2014
Please cite this article as: Cho YH, Quintana E, Schaff HV, Nishimura RA, Dearani JA, Abel MD, Ommen S, Residual and Recurrent Gradients after Septal Myectomy for Hypertrophic Cardiomyopathy – Mechanisms of Obstruction and Outcomes of Reoperation, The Journal of Thoracic and Cardiovascular Surgery (2014), doi: 10.1016/j.jtcvs.2014.05.028. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
Title: Residual and Recurrent Gradients after Septal Myectomy for Hypertrophic Cardiomyopathy –
ACCEPTED MANUSCRIPT Mechanisms of Obstruction and Outcomes of Reoperation
Authors: Yang Hyun Cho*, M.D. Ph.D. 1,2, Eduard Quintana*, M.D. FETCS.1,3, Hartzell V. Schaff, M.D.1,
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Rick A. Nishimura, M.D.4, Joseph A. Dearani, M.D.1, Martin D. Abel, M.D. 5, Steve Ommen, M.D.4
Institution and Affiliations: Division of Cardiovascular Surgery, Mayo Clinic
2
Department of Thoracic and Cardiovascular Surgery. Samsung Medical Center, Sungkyunkwan University
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1
3
Universitat de Barcelona
4
Division of Cardiovascular Disease, Mayo Clinic
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Department of Anesthesiology, Mayo Clinic
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*Both authors contributed equally to this work
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School of Medicine, Seoul, Korea
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Funding or Disclosure: none
Corresponding Author: Hartzell V. Schaff MD
Division of Cardiovascular Surgery Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 e-mail: [email protected] Phone: 507-255-7068 Fax: 507-255-8674 1
Abstract
ACCEPTED MANUSCRIPT Objective: The aims of this study were to identify the mechanism(s) of residual or recurrent left ventricular outflow tract (LVOT) obstruction in patients undergoing repeat septal myectomy for hypertrophic cardiomyopathy and to assess the early and late results of reoperation. Methods: From January, 1980 to June 2012, we performed 52 repeat myectomies in 51 patients. We
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reviewed medical records and preoperative transthoracic echocardiograms to evaluate adequacy of previous resection and mechanism of LVOT obstruction. Complications of previous and repeat myectomy, NYHA class, and survival were analyzed.
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Results: The mean interval from previous myectomy to reoperation was 43±51 months. In 6 patients (12%) residual/recurrent gradients were caused by isolated midventricular obstruction. In the remaining 46
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operations, the mechanisms of residual/recurrent gradients were identified as systolic anterior motion of mitral valve (SAM) related subaortic obstruction caused by inadequate length of previous subaortic septal excision in 31 patients (59% of the total) or a combination of inadequate length and inadequate depth of septectomy 13 patients (25%); two patients had both residual subaortic obstruction due to SAM and
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midventricular obstruction (4%). Preoperatively 96% of patients were in NYHA class III or IV, and postoperatively, 93.8% were class I or II (p<0.001). The 10-year survival following reoperation was 98 % and similar to an age and gender matched Minnesota population (p = 0.46).
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Conclusions: The most common cause of recurrent LVOT obstruction and symptoms in patients undergoing septal myectomy is inadequate length of septal excision. Reoperation is safe with excellent long-term
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survival and functional improvement.
Abstract word count: 250
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Ultra mini-Abstract: Repeat septal myectomy for recurrent left ventricular outflow tract obstruction
ACCEPTED MANUSCRIPT provides excellent surgical results as regards gradient relief and symptomatic improvement. The
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mechanisms of residual obstruction are usually related to the extent of previous myectomy.
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Introduction
ACCEPTED MANUSCRIPT Fixed or provocable left ventricular outflow tract (LVOT) obstruction is present in as many as 70% of patients with hypertrophic cardiomyopathy (HCM) [1]. In obstructive HCM, left ventricular outflow tract narrowing is caused by septal hypertrophy in combination with systolic anterior motion of the mitral valve (SAM); abnormal papillary muscle may also contribute to LVOT gradients [2]. Patients unresponsive to
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medical treatment and with favorable anatomy are good candidates for septal myectomy which predictably relieves gradients and secondary mitral valve regurgitation thus improving symptoms and exercise performance [3, 4]. A subset of patients undergoing myectomy may have residual or recurrent obstruction
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with persistence of symptoms, and even though risk of residual gradients is low, little is known of mechanism(s) of recurrent obstruction or outcome of reoperation [5]. Therefore, the aim of this study was to
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investigate the anatomic abnormalities leading to reoperation for myectomy and to document early and late results of reoperation.
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Methods
Patient Selection
From January 1980 to June 2012, 2,034 patients underwent septal myectomy for obstructive HCM at our
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Clinic. Among these, we then identified 51 patients who had 52 operations for the residual or recurrent obstruction after a previous surgical septal myectomy. We included only patients who had a primary
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diagnosis of HCM and did not include patients who had myectomy at the time of planned aortic valve replacement or patients who had SAM following mitral valve repair. This clinical study was reviewed and approved by the Mayo Clinic College of Medicine Institutional Review Board, and all patients agreed to clinical research authorization before operation. For capture of data related to this population we used information from our database and electronic medical record. Follow-up was obtained from health assessment questionnaires sent to patients and families 1, 3, 5, 10, and 15 years postoperatively and was supplemented by written correspondence from referral physicians or patients themselves and vital status from the Social Security Death Index. 4
All patients had resting or provoked gradients ≥50 mmHg determined preoperatively by means of
ACCEPTED MANUSCRIPT transthoracic Doppler echocardiography or invasive hemodynamic study if outflow tract gradients could not be determined by Doppler echocardiography. Echocardiographic studies were performed at baseline according to the recommendations of the American Society of Echocardiography [3]. LVOT gradients were measured with continuous-wave Doppler of the outflow tract from an apical window and calculated using
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the modified Bernoulli equation (gradient = 4v2, v = peak LVOT velocity). If a significant gradient was not obtained under basal conditions, a Valsalva maneuver and/or administration of amyl nitrate or exercise was used to provoke a gradient. If patients were stable in the operating room before cardiopulmonary bypass,
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pressure measurements were obtained again directly measuring intracavitary (LV) and aortic pressures [6]. Thirty-two of the 52 patients underwent first operation for septal myectomy elsewhere. The
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remaining 20 patients had initial operation at our institution, and this represents approximately 1% of patients having primary myectomy. Two patients had residual obstruction following two previous myectomies, and 3 patients had a previous percutaneous alcohol septal ablation.
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Etiology of recurrent obstruction
The site of recurrent obstruction was identified primarily by using a parasternal long-axis view. Images of the preoperative echocardiograms and operative records of all patients were reviewed by three
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authors (Y.H.C, E.Q, and H.V.S). In each patient, consensus was reached on the morphologic features causing obstruction. The previous myectomy site was visually evaluated. The presence of systolic anterior
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motion of the mitral valve was a marker of dynamic LVOT obstruction indicating residual or recurrent subaortic obstruction. A midventricular obstructive pattern was defined when there was no SAM and the midventricular septum was responsible for significant intracavitary gradient. The anatomy of papillary muscle was also reviewed as a possible cause of LVOT obstruction. Based on these findings, we categorized the mechanisms of recurrent obstructions as insufficient length of septal excision, inadequate depth of septal excision, midventricular obstruction, or obstruction due to an abnormal papillary muscle (Figure 1). An important goal of the study was to determine whether late LVOT obstruction might reflect regrowth of muscle in the area of prior myectomy. Thus, we analyzed further those patients from our Clinic 5
who had marked improvement in their clinical status initially after the previous myectomy. We then
ACCEPTED MANUSCRIPT compared Doppler echocardiograms obtained early after initial myectomy to studies obtained before reoperation to compare septal anatomy and the previous myectomy site.
Surgical procedure
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Operations were performed using standard methods for repeat median sternotomy; we employed normothermic cardiopulmonary bypass with single venous cannula, and antegrade cold blood cardioplegia for myocardial protection. . Exposure is facilitated by complete lysis of adhesions to allow the ventricles to
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collapse and to be displaced posteriorly. Next, an oblique aortotomy is made, and we prefer to situate this slightly closer to the sinotubular ridge than is usual for aortic valve replacement; the aortic incision is carried
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through the midpoint of the noncoronary aortic sinus of Valsalva to a level approximately 1 cm above the valve anulus. The edge of the proximal aorta is held out of the way with small stay sutures, and a cardiotomy sucker is placed through the aortic valve and used to depress the anterior leaflet of the mitral valve to protect it from injury. The right aortic valve cusp is collapsed against the sinus wall, where it will usually stay.
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The region of residual septal obstruction can be recognized by endocardial scar resulting from contact with the anterior mitral valve leaflet. The technique used for relief of residual subaortic obstruction is similar to that employed for primary operations. [7]. The septum is incised with a No. 10 scalpel blade just
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to the right of the nadir of the right aortic sinus. Incision in the septum is made upward and then leftward over to the anterior leaflet of the mitral valve. Scissors are used to complete excision of this initial portion of
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myocardium. A sponge stick is used to depress the right ventricle and to rotate the septum posteriorly, orienting the LV outflow anteriorly. The area of septal excision is then deepened and lengthened toward the apex of the heart, being certain to excise hypertrophied septum beyond endocardial scar, and the myectomy site is further enlarged with the use of pituitary rongeurs. Adequate septal myectomy usually yields 3 to 12 g of muscle, and the depth of resection depends on the thickness of the septum but is rarely less than 10 mm. If the level of obstruction was distant from the aortic valve precluding a transaortic access, an apical left ventriculotomy was performed to provide access to the midventricular septum[8]. To confirm complete relief of the LVOT obstruction, we used intraoperative echocardiography and routinely measured 6
simultaneous aortic and left ventricular pressure by direct needle puncture before and after myectomy.
ACCEPTED MANUSCRIPT Patients had the surgical ablative procedure performed either by a transaortic approach (45 patients), a transventricular myectomy (4 patients), or combined transaortic and transapical approach (3 patients). In addition to surgery to relieve obstruction caused by HCM, 19 concomitant procedures were performed in 16
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patients (Table 2).
Follow-up and Analysis
Statistical analyses were performed using SAS software (version 9.1; SAS Institute Inc, Cary, NC).
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Descriptive statistics for categorical variables are reported as frequency and percentage, and continuous variables are given as mean (± standard deviation). The Kaplan–Meier method was used to estimate late
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survival. Observed late survival was compared using a log-rank test to expected survival of an age- and sexmatched Minnesota population. In the analysis of functional status, we used the most current follow-up information.
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Results
The mean age at the time of repeat myectomy was 38.1±18.9 years, and 18 patients were men (35%). All patients had cardiac limitation at time of reoperation with symptoms of left heart failure, dyspnea and
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fatigability, despite medical treatment with one or two negative inotropic agents (Table 1). In addition, 11 patients (22%) had angina pectoris, and 7 (14%) had syncope. Formal exercise tests were recorded in 19
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patients whose functional aerobic capacity was 59±24 % of predicted. Among all patients, the symptom-free interval after the prior myectomy was 22±42 months, and repeat myectomy was performed at a mean of 43±51 months following the prior procedure (Table 2). At the time of reoperation, 5 patients had permanent transvenous pacemakers in place because of complete atrioventricular block related to the previous operation. Further, there were 9 patients with previous ICD (implantable cardio-defibrillator) implants, 5 as primary prevention and 4 as secondary prevention following resuscitation from sudden cardiac death. Dual chamber pacemaker implantations
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aimed at reducing LVOT gradients [9] were performed at different times before redo myectomy in 9
ACCEPTED MANUSCRIPT additional patients. Before reoperation, 4 subjects were in atrial fibrillation and the remaining patients were in sinus rhythm or paced as described above. Among patients without pacemakers, the electrocardiograms before repeat myectomy demonstrated normal conduction in 5 patients, left anterior fascicular block (LAFB) in 2
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patients, and left bundle branch block (LBBB) pattern in the remainder of the study patients. Mean peak-to-peak LVOT gradients measured intraoperatively before repeat myectomy were 54±30 mmHg at rest and 85±41 mmHg after provocation. After redo myectomy the maximum (provoked) mean
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peak-to-peak systolic gradients fell to 13±12 mmHg. After redo myectomy, 5 patients had an ICD implanted before hospital dismissal (2 patients developed new complete heart block), 2 patients with previous normal
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intraventricular conduction and 1 with LAFB conduction developed a new LBBB. After surgery, improvement of symptoms was common. Preoperatively 96% of patients were in NYHA class III or IV, and postoperatively, 93.8% were class I or II (p<0.001, Figure 2).
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Surgical findings and causes of recurrent obstruction
The pathological anatomic findings causing obstruction before reoperation were identified as inadequate length of excision in 31 patients (59%), a combination of inadequate length and inadequate depth of
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previous myectomy in 13 (25%), a combination of inadequate length and midventricular obstruction 2 (4%), and isolated midventricular obstruction in 6 patients (12%). One patient had abnormal papillary muscles
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combined with midventricular obstruction. Among 11 pediatric patients (<18 years old) in this series recurrence of obstruction was insufficient length of septectomy in 9 patients and mid ventricular obstruction in 2 patients.
Mitral regurgitation and systolic anterior motion of mitral valve Preoperatively, mitral regurgitation (MR) was common, but the severity varied in relation to systolic anterior motion (SAM) of the mitral valve and dynamic outflow obstruction. If the mitral valve was structurally normal, regurgitation improved or disappeared after myectomy without additional direct procedures on the 8
valve itself. In 4 patients with intrinsic abnormalities of the mitral leaflets, direct valve repair was necessary
ACCEPTED MANUSCRIPT at the time of myectomy [10]. No patients required mitral valve replacement.
Early and late survival There was no in-hospital mortality, but 1 patient died after hospital dismissal within 30 days after surgery;
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postmortem examination revealed pulmonary embolism. There were 3 late mortalities. One patient with severe pulmonary hypertension died 13 years after surgery of unclear reasons. Another patient died of cancer 11 years after surgery, and there was another death of unknown cause 10 years after repeat
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myectomy. The Kaplan-Meier 10-year survival rate was 98% and at 15 years was 82%. Survival following repeat myectomy was similar to that of an age and gender matched Minnesota population (p = 0.46, Figure
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Special attention was given to patients who had initial improvement in symptoms and had their first operation at our institution. Among these patients, post myectomy intraoperative LVOT gradients at initial operation averaged 9.2±8.2 mmHg, and symptoms recurred at an average of 38±24 months following initial
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septal myectomy. Detailed comparisons of intraoperative echocardiograms from the first procedure compared to studies performed just before redo myectomy showed no evidence of regrowth of subaortic septum. In 2 pediatric patients the recurrence could be attributed to septal muscle growth at the
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Discussion
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midventricular level, but interpretation of changes is difficult because of somatic growth.
Recurrent symptoms after myectomy for obstructive HCM may be caused by a variety of problems including left ventricular diastolic dysfunction, valvular abnormalities, development of coronary artery disease, medication related symptoms, arrhythmias, persistence of pulmonary arterial hypertension as well as dynamic or fixed left ventricular obstruction. Little is known about the real incidence of recurrent obstruction after a septal myectomy, but this subgroup of patients with symptoms and recurrent obstruction severe enough to require reoperation accounts for 1% of all HCM surgical practice.
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Recognition and management of residual or recurrent LVOT obstruction varies considerably
ACCEPTED MANUSCRIPT depending on the quality of clinical assessment and expertise available to this relatively small group of patients. Previously, we reported outcome of operation in 13 patients who had repeat myectomy at our Clinic from 1975 to 2003. In that report, the primary cause of LVOT obstruction was identified as limited resection. The present study provides more detailed information on the morphologic aspects of incomplete
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septal myectomy in a larger cohort of patients with extended follow-up. Assessment of preoperative echocardiograms and surgical findings revealed that the primary reason for incomplete myectomy was not carrying the septal excision far enough towards the apex during the first
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operation, and this was identified in 59% of patients. In an additional 25% of patients there was both inadequate length and depth of septal excision. Recurrent symptoms due to midventricular obstruction were
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less common (12%).
There are several technical factors that may limit exposure of the subaortic area and excision of septal muscle. Visualization of the subaortic septum is often more difficult in obese patients with thick chest walls and patients with greater anterior-posterior diameters of the thorax. Also, exposure may be poor
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because of small ascending aorta diameter and small aortic valve annulus size. Important also is the level of obstruction and its distance from the aortotomy. Despite the difficulties listed above, in almost all patients the site of subaortic obstruction can be identified by the presence of endocardial scar, the area of apposition
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with the anterior mitral valve leaflet during systolic anterior motion of the structure. It is important that septal excision be carried distally toward to the apex and past the visible endocardial scar.
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Understanding the anatomic basis for recurrent LVOT obstruction is important in order to avoid complications of myectomy. For example, widening the proximal area of septal excision in the clockwise direction would increase risk of injury to the atrioventricular conduction pathway and development of complete heart block. Also, deepening the region of previous myectomy, because of the mistaken assumption that this is the site of obstruction, invites iatrogenic ventricular septal defect. As a general rule, whenever SAM is present we first approach LVOT obstruction through an aortotomy and the aortic valve. On the other hand, when midventricular obstruction is present without SAM of the mitral valve, we favor exposure of the mid septum through an apical ventriculotomy. In the present 10
study 7 patients (14 %) underwent the transventricular approach for septal myectomy to relieve obstruction
ACCEPTED MANUSCRIPT completely, and it is likely that some of these patients would have been better served by this approach at initial operation. As is found with subaortic obstruction, there is endocardial scar that guides septal excision in patients with midventricular obstruction, and this is caused by contact of the papillary muscles with the septum. Midventricular obstruction can be readily exposed through an apical ventriculotomy and the
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procedure is safe with minimal complications related to incision of the ventricle. [11]. The evolution of gradients deserves a special comment. Review of the intraoperative courses of the first myectomy in patients from our institution (in patients with initial improvement) reveals that
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intraoperative LVOT gradients were minimal, mean 9.2 ± 8.2. This group had a recurrence of symptoms at 38 ± 24 months after the procedure, and comparison of septal morphology by echocardiography
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demonstrated that although gradients were acceptably low after initial myectomy, there was either some degree of septal bulging that persisted or midventricular obstruction was not appreciated initially. There was no evidence from these patients in whom direct comparison of echocardiograms was possible that there was regrowth of septal muscle responsible for obstruction. As previously described, the pediatric population is at
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increased risk of recurrent symptoms and need for reoperation due to limited transaortic access leading to incomplete resections [12]. It is unclear why patients had low gradients after initial myectomy, and it is possible that these were minimized by anesthetic effects [6] and/or that gradients developed later with global
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LV remodeling [13]. The time frame of reappearance of symptoms may have been influenced by impact of recovery from heart surgery itself, individual expectations and physician judgment. It is important, therefore,
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to measure intraoperative gradients accurately and compare this to intraoperative Doppler-echocardiographic findings. Provocative maneuvers should be performed (induction of a premature ventricular contraction or administration of isoproterenol) to confirm the absence of an inducible gradient. If additional resection is necessary, we remove more muscle from the distal septum rather than thinning further the initial myectomy site. This patient population is complex; nevertheless, operative mortality for repeat myectomy was very low. Patient survival and symptomatic improvement were similar to the larger group of patients having primary myectomy; indeed survival of these patients parallels a sex and age matched population. These 11
results emphasize the importance of identifying residual obstruction in patients with persistent symptoms
ACCEPTED MANUSCRIPT after a septal myectomy. The findings also highlight the importance of complete intraoperative assessment of septal myectomy at initial operation.
Conclusions
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Reoperation for recurrent obstruction in patients with HOCM is uncommon and but most often due to incomplete initial myectomy. The most frequent finding was failure to carry septal excision far enough
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toward the apex of the heart; mid ventricular obstruction may also lead to recurrent symptoms.
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Acknowledgments
ACCEPTED MANUSCRIPT The authors would like to acknowledge Zhuo Li for statistical analysis, Judy Lenoch for data retrieval,
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Michael King for creation of surgical illustrations and Mark Zang for echocardiographic imaging support.
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References
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Maron, M.S., et al., Hypertrophic cardiomyopathy is predominantly a disease of left ventricular outflow tract obstruction. Circulation, 2006. 114(21): p. 2232-9.
2.
Minakata, K., et al., Extended septal myectomy for hypertrophic obstructive cardiomyopathy with
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anomalous mitral papillary muscles or chordae. J Thorac Cardiovasc Surg, 2004. 127(2): p. 481-9. Gersh, B.J., et al., 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart
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Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg, 2011. 142(6): p. e153203.
Ommen, S.R., et al., Long-term effects of surgical septal myectomy on survival in patients with
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obstructive hypertrophic cardiomyopathy. Journal of the American College of Cardiology, 2005. 46(3): p. 470-6. 5.
Minakata, K., et al., Mechanisms for recurrent left ventricular outflow tract obstruction after septal
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myectomy for obstructive hypertrophic cardiomyopathy. The Annals of Thoracic Surgery, 2005. 80(3): p. 851-6. 6.
Ashikhmina, E.A., et al., Intraoperative direct measurement of left ventricular outflow tract
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gradients to guide surgical myectomy for hypertrophic cardiomyopathy. J Thorac Cardiovasc Surg, 2011. 142(1): p. 53-9.
Schaff, H.V. and S.M. Said, Transaortic Extended Septal Myectomy for Hypertrophic
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Cardiomyopathy. Operative Techniques in Thoracic and Cardiovascular Surgery, 2012. 17(4): p. 238-250. 8.
Said, S.M., et al., Transapical approach for apical myectomy and relief of midventricular obstruction in hypertrophic cardiomyopathy. Journal of cardiac surgery, 2012. 27(4): p. 443-8.
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Erwin, J.P., 3rd, et al., Dual chamber pacing for patients with hypertrophic obstructive cardiomyopathy: a clinical perspective in 2000. Mayo Clin Proc, 2000. 75(2): p. 173-80.
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10.
Wan, C.K., et al., What is the best surgical treatment for obstructive hypertrophic cardiomyopathy
ACCEPTED MANUSCRIPT and degenerative mitral regurgitation? Ann Thorac Surg, 2009. 88(3): p. 727-31; discussion 731-2. 11.
Kunkala, M.R., et al., Transapical approach to myectomy for midventricular obstruction in hypertrophic cardiomyopathy. The Annals of Thoracic Surgery, 2013. 96(2): p. 564-70.
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Minakata, K., et al., Septal myectomy for obstructive hypertrophic cardiomyopathy in pediatric
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patients: early and late results. The Annals of Thoracic Surgery, 2005. 80(4): p. 1424-9; discussion 1429-30.
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hypertrophic obstructive cardiomyopathy. The Annals of Thoracic Surgery, 2004. 78(6): p. 2118-22.
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Tables
ACCEPTED MANUSCRIPT Table 1. Clinical and echocardiographic data of 51 patients having repeat myectomy for obstructive hypertrophic cardiomyopathy Variable
Value
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Clinical data Age (yr)
38.1 ± 18.9
Male
18 (35%) 1.8 ± 0.4
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BSA (m2) Hypertension
History of stroke NYHA III-IV Previous percutaneous alcohol septal ablation
Preop pacemaker Patient history of sudden death
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Family history of sudden death
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Preoperative ICD
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Chronic atrial fibrillation
5 (10%) 4 (8%) 4 (8%) 49 (96%) 3 (6%) 9 (18%) 9 (18%) 4 (8%) 7 (14%) 51 (100%)
Preoperative Diuretics
17 (33%)
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Preoperative beta-blocker/calcium channel blockers/both
Complications from previous myectomy Iatrogenic VSD
4 (8%)
Complete AV block
5 (10%)
Aortic valve injury
6 (12%)
Procedures combined with previous myectomy Aortic valve replacement
2 (4%)
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CABG
3 (6%)
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3 (7%)
Mitral valve repair
6 (12%)
Measurements 54 ± 30
Provoked LVOT gradient (mmHg)
85 ± 41
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Resting LVOT gradient (mmHg)
LV Ejection fraction (%)
71.2 ± 7.8
Basal septal thickness (mm)
20.5 ± 7
13.3 ± 3.8
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Posterior wall (mm) LVDED (mm)
LA volumen index (ml/m2) LV mass index (gr/m2) Severity of diastolic disfunction (0-4 grades)
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LVDES (mm)
43 ± 6 24 ± 5 47 ± 16 171 ± 74 2.4 ± 0.9
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Right ventricular systolic pressure (mmHg) / Systemic systolic pressure (mmHg)
35.4%
60 ± 24
Preoperative systolic anterior motion of mitral valve
46 (88%)
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Preoperative exercise test (% functional aerobic capacity predicted per age). *
Mitral regurgitation (≥ moderate)
37 (73%)
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Data shown as n (%) or mean ± SD *available data in 19 patients
Abbreviations: LV, left ventricle; LVDED, left ventricular end diastolic diameter; LVDES, left ventricular end systolic diameter; LA, left atrium.
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Table 2. Intraoperative and postoperative data of 51 patients having repeat myectomy for obstructive
ACCEPTED MANUSCRIPT hypertrophic cardiomyopathy Variable
Value
Intraoperative data following repeat myectomy 63 ± 37
Aortic occlusion time (min)
45 ± 27
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Extracorporeal circulation time
Grams of septal tissue removed (gr)
5.4 ± 4.1
Systolic anterior motion of mitral valve (≥ mild)
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0
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Mitral valve regurgitation > mild Residual transventricular gradient (mmHg)
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Concomitant procedures Aortic valve repair CABG ASD closure
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Tricuspid valve repair Tumor removal Aortic valve replacement
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Mitral valve repair VSD repair
13 ± 12
1 (2%) 1 (2%) 1 (2%) 2 (4%) 2 (4%) 4 (8%) 4 (8%) 4 (8%)
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Related surgical complications Aortic valve injury
0
New complete auriculoventricular block
2 (4%)
New iatrogenic VSD
2 (4%)
ICU/hospital data Intubation > 24 h
4 (8%)
ICU stay (median days)
1
18
Hospital days (median days)
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ACCEPTED MANUSCRIPT Data shown as n (%) or mean ± SD Abbreviations: CABG, coronary artery bypass grafting; ASD, atrial septal defect; VSD, ventricular septal
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defect; ICU, intensive care unit
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Figure legends
ACCEPTED MANUSCRIPT Figure 1. Three types of recurrence after septal myectomy for hypertrophic obstructive cardiomyopathy with their respective parasternal long axis echocardiographic views. A: inadequate length and depth of excision, B:
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inadequate length of excision, C: midventricular obstruction at the level of papillary muscles.
Figure 2.
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Change in NYHA functional class after repeat myectomy. Most patients had improvement in symptoms and
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were in class I or II (93.8 %) at last follow-up.
Figure 3.
A: Kaplan-Meyer survival curve of patients who had repeat septal myectomy (solid curve). B: The survival
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was not inferior (p = 0.46) to that of an age and gender matched population (dashed curve).
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