Ann Thorac Surg 2010;89:459-464. doi:10.1016/j.athoracsur.2009.10.065
© 2010 The Society of Thoracic Surgeons
Original Articles: Adult Cardiac
Concomitant Septal Myectomy at the Time of Aortic Valve Replacement for Severe Aortic Stenosis
Nihan Kayalar, MD,
Hartzell V. Schaff, MD,
Richard C. Daly, MD,
Joseph A. Dearani, MD,
Soon J. Park, MD*
Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota
Accepted for publication October 23, 2009.
* Address correspondence to Dr Park, Division of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (Email: park.soon{at}mayo.edu).
Presented at the Poster Session of the Forty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 25–27, 2010.
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Abstract
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Background: Left ventricular outflow tract obstruction may be unmasked after a successful aortic valve replacement (AVR) for severe aortic stenosis in the setting of asymmetrical basal septal hypertrophy (ABSH). The quantitative assessment of the obstructive potential of ABSH adjacent to a severely stenotic valve can be challenging. We reviewed our experience with patients who underwent concomitant septal myectomy at the time of AVR for severe aortic stenosis.
Methods: During the 10-year period ending January 2009, 3,523 patients underwent AVR for the primary indication of severe aortic stenosis. Forty-seven of these patients underwent concomitant septal myectomy. Preoperative and postoperative echocardiograms, operative data, hospital course, morbidity, and mortality were assessed.
Results: The mean age of the group was 73 ± 11 years. The mean aortic valve area was 0.74 cm2 preoperatively. On preoperative transthoracic echocardiography, only 28% of the patients were considered to be at risk for possible left ventricular outflow tract obstruction. The mean left ventricular mass index decreased from 113.7 ± 24.3 g preoperatively to 90.0 ± 17.2 g at 1 year after the surgery (p < 0.001). The operative mortality was 2%. Complete heart block was observed in 2 patients (4.2%), and no iatrogenic ventricular septal defect was noted.
Conclusions: A quantitative assessment of the obstructive ABSH in the setting of severe aortic stenosis may be difficult preoperatively. Surgeons should inspect left ventricular outflow tract for possible obstructive ABSH at the time of AVR. Concomitant myectomy is a safe and effective procedure without additional complications and should be considered for patients with a preoperative or intraoperative diagnosis of ABSH even though dynamic obstruction was not demonstrated.
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Introduction
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Left ventricular outflow tract obstruction (LVOTO) may be caused by a primary disease such as hypertrophic cardiomyopathy or may be secondary to other processes such as systemic arterial hypertension or valvular aortic stenosis. These secondary causes of septal hypertrophy are usually associated with a uniform or symmetric distribution of left ventricular hypertrophy. However, in some patients there may be a nonuniform pattern of hypertrophy in which one portion of the ventricle shows a greater degree of thickening than other regions [1]. The presence of asymmetric basal septal hypertrophy (ABSH) contributing to LVOTO in the setting of valvular aortic stenosis (AS) is not uncommon and can be easily overlooked at the time of aortic valve replacement (AVR) resulting in residual LVOTO after AVR. Panza and Maron [2] have recommended concomitant myectomy at the time of AVR only when there is dynamic obstruction with systolic anterior motion of the mitral valve, whereas Turina [3] has advised more liberal use of septal myectomy during aortic valve replacement.
The aim of this study was to assess the role and safety of concomitant septal myectomy at the time of AVR for severe aortic stenosis.
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Patients and Methods
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Patient Population
We retrospectively identified patients who underwent concomitant septal myectomy among 3,523 patients who underwent AVR for the primary diagnosis of severe AS between January 2000 and January 2009. The Institutional Review Board of the Mayo Clinic approved this study (IRB no. 08-006099), and patients who gave individual consent have been included in the study. Patients with the diagnosis of hypertrophic cardiomyopathy or dynamic outflow tract obstruction with systolic anterior motion of mitral valve were excluded. We also excluded all patients who were diagnosed with known septal hypertrophy in the setting of less than severe aortic stenosis. Patients undergoing concomitant coronary bypass surgery or mitral valve repair/replacement for primary mitral valve pathology were included.
Patient Characteristics
In all, 47 patients were included in the study. The mean age of the patients was 73.1 ± 11.2 years (range, 28 to 91), and 32 were female (68%). The mean body surface area was 1.85 ± 0.19 m2 (range, 1.49 m2 to 2.25 m2). The majority of patients had calcific stenosis of either a normal tricuspid (72%) or congenitally bicuspid aortic valve (18%). Major symptoms were dyspnea (70%), angina (28%) and syncope or presyncope (11%). Five patients were asymptomatic, and the indication for operation was worsening aortic stenosis on echocardiography. Hypertension (72%), coronary artery disease (40%), diabetes mellitus (17%), and history of cerebrovascular accident (17%) were commonly found comorbidities. The patients' preoperative data are summarized in Table 1.
Echocardiography
The diagnosis of severe aortic stenosis was confirmed preoperatively by echocardiography within 2 weeks of surgery. All patients underwent echocardiographic study intraoperatively (transesophageal echocardiography) and before hospital discharge after AVR. Standard parasternal, apical, subcostal, and suprasternal views were obtained. Left ventricular diameter and thickness were measured using M-mode echocardiography. Left ventricular mass was calculated using the Penn formula described by Devereux [4]. Left ventricular mass was indexed by dividing left ventricular mass (in grams) by body surface area. Continuous-wave, pulsed-wave, and color Doppler studies were done to assess the peak transvalvular gradient, the mean transvalvular gradient, and the effective orifice area of the aortic valve. The peak and mean gradients were calculated by the modified Bernoulli equation. The effective orifice area was calculated by the simplified continuity equation. Asymmetric basal hypertrophy was considered to be present when there is disproportionate thickening of the anterior ventricular septum relative to the posterior left ventricular free wall (septal-free wall ratio > 1.3).
Operative Technique
After median sternotomy, standard methods of extracorporeal circulation and cold blood cardioplegic arrest were employed. After excision of the calcified valve and debridement of the annulus, the subaortic area was inspected carefully. A potential need for concomitant myectomy was suspected in 13 patients (28%) because preoperative echocardiography demonstrated prominent bulging of septal muscle into the LVOT (Fig 1). In an additional 13 patients (28%), intraoperative transesophageal echocardiography revealed prominent septal hypertrophy protruding into the outflow tract. In the remaining 21 patients (45%), the decision to perform myectomy was made by the operating surgeon based on direct inspection of LVOT after excision of the native aortic valve. In these patients, neither preoperative nor intraoperative echocardiography suggested a prominent septal hypertrophy, which may cause LVOTO (Fig 2). The myectomy included resection of septal muscle from the nadir of the right aortic sinus to the commissure between the left and right cusps as in septal myectomy for hypertrophic obstructive cardiomyopathy (HOCM). The mean muscle mass excised was 0.8 ± 0.61 g. It should be noted that the septal myectomy performed in these patients is limited compared with that for HOCM, which usually yields 3 to 12 g of muscle [5].
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Fig 1. Patient with aortic stenosis, septal wall thickening, and significant outflow tract gradient. (A) Transthoracic echocardiography, apical long-axis view: acceleration of flow begins at mid ventricle (small arrows), adjacent to thickened septal wall (star). The aortic valve is denoted by thick arrow. (B) Continuous-wave Doppler (CW) through the outflow tract and aortic valve: the signal shows two different flow accelerations, one late-peaking, dynamic, in the mid ventricle (small arrows), and the other late peaking through the aortic valve (long arrow). (Ao = aorta; LA = left atrium; LV = left ventricle.)
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Fig 2. Another patient with aortic stenosis without outflow tract obstruction. (A) Transthoracic echocardiography, apical long-axis view: acceleration of flow begins just before the aortic valve (small arrows). The septum is not thickened (star). The aortic valve is denoted by thick arrow. (B) Continuous wave Doppler (CW) through the outflow tract and aortic valve: the signal shows the characteristic late-peaking flow acceleration of severe aortic stenosis (long arrow). The weak minimal flow acceleration in the outflow tract is denoted by the small arrows. (Ao = aorta; LA = left atrium; LV = left ventricle.)
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Bioprosthetic valves were the most common choice, for 85% of the patients. The aortic root enlargement was necessary in 3 patients in whom the aortotomy was extended through the aortomitral curtain. Either an autologous or bovine pericardial patch was incorporated in closing the aortotomy incision starting at the base of the aortic annulus [6].
Overall, 17 patients (36%) underwent concomitant coronary bypass surgery, 6 (13%) had concomitant mitral valve replacement, and 4 (9%) had aortoplasty or replacement of ascending aorta. Operative data of patients are summarized in Table 2.
Patient Follow-Up
Late follow-up was obtained by review of medical records, Social Security Death Index, and by postal questionnaire.
Statistical Methods
Statistical analyses were performed using SAS 9.13 (SAS Institute, Cary, NC). Data are expressed as mean values ± SD for continuous variables and as numbers with percentage for categorical variables. Preoperative and postoperative measurements were compared using a Student's paired t test. A p value of 0.05 or less was considered statistically significant for all comparisons. The follow-up period for each patient was calculated from the date of operation to the date of death or last contact. The survival rate was calculated using Kaplan-Meier analysis.
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Results
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Early Postoperative Data and Follow-Up
The operative mortality was 2%. The single death was due to multisystem organ failure of an 86-year-old woman who had undergone concomitant mitral valve replacement as well as AVR and myectomy 35 days earlier. Three patients (6%) required permanent pacemaker implantation after the surgery, 2 for complete heart block and 1 for sinus node dysfunction. Transient postoperative atrial fibrillation was observed in 23 patients (49%). Two patients had a stroke without major residual defects. The mean hospital stay was 9.6 ± 6.1 days (range, 5 to 35). Five patients required a prolonged intensive care unit or hospital stay owing to respiratory problems associated with the preexisting chronic lung disease.
The mean follow-up interval for patients was 43.1 ± 27.6 months, ranging from 4 to 96 months. The survival rates at 1, 3, and 5 years were 98%, 92%, and 87%, respectively (Fig 3). Five patients died after 20, 24, 58, 70, and 83 months, 1 of cerebral hemorrhage, 1 of peritoneal carcinoma, and 3 of unknown causes. None of the patients required reoperation.
Hemodynamic Measurements
The peak and mean aortic gradients were 106.8 ± 31.9 mm Hg and 63.5 ± 19.2 mm Hg, respectively, preoperatively. Postoperatively, the aortic transvalvular gradients were measured before the hospital discharge and at 1 year after the surgery. The peak and mean gradients decreased significantly to 29.5 ± 11.7 mm Hg and 18.2 ± 6.5 mm Hg, respectively. The aortic valve area increased from 0.74 ± 0.11 cm2 to 1.68 ± 0.49 cm2 as summarized in Table 3.
Left Ventricular Mass and Geometry
Left ventricular remodeling due to aortic valve stenosis was documented by increased left ventricular mass, left ventricular mass index, and interventricular septum thickness preoperatively. These values decreased over time after AVR and septal myectomy. The details are presented in Table 4.
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Comment
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Based on available data, approximately 10% of patients with severe aortic valve stenosis have asymmetric basal septal thickening relative to the posterior left ventricular free wall [2, 7]. The incidence is 1.3% in this series. One of the reasons for this discrepancy is the exclusion of patients with known HOCM or with demonstrated dynamic outflow tract obstruction. We also excluded patients with less than severe aortic stenosis and inappropriately thick interventricular septum to make sure that only patients with septal hypertrophy secondary to aortic stenosis are included in the study. The presence of ABSH and the need for concomitant myectomy may present a dilemma for surgeons performing AVR. Some clinicians have recommended a concomitant septal myectomy at the time of AVR when there is associated dynamic outflow tract obstruction [2, 8], and we agree with this approach. However, there are few data on management of patients having AVR who demonstrate marked asymmetric septal hypertrophy without systolic anterior motion.
The rationale for performing concomitant myectomy is to remove a potential cause of subaortic obstruction from hypertrophic septum after AVR [2, 3, 7]. Residual obstruction may lead to problems early and late postoperatively. Early after operation, obstruction can be aggravated by inotropic stimulation used to treat low cardiac output or hypotension; this may be further complicated by volume changes and bleeding. Once hemodynamic decompensation develops, beta-blockers may fail to help or hypotension may preclude their use [3]. Ayerbe and coworkers [9] have advised prophylactic myectomy during aortic valve replacement in patients with either demonstrable dynamic subaortic gradient or marked septal hypertrophy. In their experience, 6% of patients had a dynamic aortic gradient at 1 year after AVR [9]. We can only speculate as to whether LVOT obstruction would or would not have developed obstruction in our patients had we only performed AVR.
It might be argued that the hypertrophic septum would have normalized as the left ventricular hypertrophy regresses over time after AVR. However, the gradient across the left ventricular outflow tract can persist in patients with unresected ABSH. Tasca and associates [10] reported that left ventricular mass regression was significantly greater in patients who underwent AVR and concomitant myectomy compared with patients undergoing only AVR. Perhaps the better regression of left ventricular hypertrophy noted with concomitant myectomy was due to more effective reduction in LVOT gradient. Then, it seems only logical to resect obstructive muscle mass with a simple additional procedure that does not increase the operative risk.
In patients with valvular aortic stenosis, the contribution of ABSH to the transaortic gradient cannot be established by pressure measurements alone, and although left ventriculography can show septal hypertrophy and subaortic narrowing, it is not a reliable index for severity of asymmetrical ABSH [3]. Asymmetric basal septal hypertrophy may also be hard to document on echocardiography in the presence of severe aortic stenosis. Transesophageal echocardiography may be better than transthoracic approach for identifying basal septal hypertrophy [11]. Conversely, basal septal hypertrophy is readily visible during intraoperative inspection of LVOT after resection of aortic valve, and digital exploration may help to estimate extent of obstruction and adequacy of resection. These findings were confirmed in our study population as well. Only about one fourth of patients were suspected to have septal hypertrophy on transthoracic echocardiogram, but transesophageal echocardiography demonstrated ABSH in an additional one fourth of patients. Certain features such as marked septal thickness, heterogenous distribution of hypertrophy, the presence of systolic anterior motion of the mitral valve, and familial distribution may help to differentiate concomitant HOCM [2]. However, these factors are not present in patients with fixed obstruction due to ABSH, and proximity of the subaortic stenosis to aortic valve makes it even more difficult to diagnose the presence of a subaortic gradient. In this study, nearly one half of the patients had no echocardiographic findings suggestive of ABSH even though all of them underwent myectomy for obstructive ABSH based on intraoperative inspection of LVOT. The indication for myectomy was the surgeon's subjective decision, but the presence of a prominent septal ridge protruding into the LVOT, confirmed by digital exploration, was the main determinant of decision for resection.
Although septal myectomy is a commonly performed procedure with a minimal morbidity and mortality in HOCM patients [5, 12, 13], it involves young patients with significant septal hypertrophy. Performing a concomitant septal myectomy at the time of AVR may not have a similar safety profile for it mostly involves elderly patients with less well defined hypertrophic septum and more friable tissue. Our experience seems to indicate that the concomitant myectomy does not increase the operative risk. We did not encounter any surgical complications such as iatrogenic ventricular septal defect. Although our incidence of permanent pacemaker implantation appears to be high (6%), only 2 of these patients (4%) had a complete AV block. One patient required a pacemaker for the sinus node dysfunction. The reported incidence of permanent pacemaker requirement after AVR for aortic stenosis is approximately 4% [14], and it could be higher (6.5%) among elderly patients [15].
We observed a female preponderance in the current series (68%), whereas the female population constituted 37% of 3,523 patients who underwent AVR for AS (p < 0.001). It is difficult to differentiate whether female sex is associated with the actual increase in hypertrophy or whether a smaller LVOT diameter accentuated the concern for a potential obstruction. The majority of patients had a history of hypertension (72%), although this was not significantly higher than that in the overall AVR group (69%; p = 0.1). It is conceivable that long-standing hypertension superimposed on severe aortic stenosis may cause more prominent ventricular hypertrophy. Our patients' peak and mean preoperative aortic gradients were higher than those reported in the literature for the AVR population [16-18]. The presence of these risk factors may suggest an increased likelihood of having ABSH that may require myectomy at the time of AVR for severe aortic stenosis.
One of the weaknesses of this study is being a retrospective review. Also, because the decision for septal myectomy was mostly based on the intraoperative assessment by the operating surgeon, there is no control group to compare whether myectomy improve outcome.
In conclusion, in patients undergoing AVR for severe AS, the presence of obstructive ABSH may be underappreciated on echocardiography. Female sex, history of hypertension, and high aortic gradients in patients with severe aortic stenosis should raise a suspicion for the presence of ABSH. Surgeons are obliged to inspect the LVOT for possible concomitant myectomy at the time of AVR. It seems logical to resect obstructive muscle mass with a simple additional procedure that does not increase the operative risk. Therefore, concomitant myectomy should be considered for patients with a preoperative or intraoperative diagnosis of ABSH, even though dynamic obstruction is not demonstrated.
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References
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- Hess OM, Schneider J, Turina M, Carroll JD, Rothlin M, Krayenbuehl HP. Asymmetric hypertrophy in patients with aortic stenosis: an adaptive mechanism or a coexistence of hypertrophic cardiomyopathy? J Am Coll Cardiol 1983;1:783-789.[Medline]
- Panza JA, Maron BJ. Valvular aortic stenosis and asymmetric septal hypertrophy: diagnostic considerations and clinical and therapeutic implications Eur Heart J 1988;9:71-76.[Free Full Text]
- Turina M. Asymmetric septal hypertrophy should be resected during aortic valve replacement Z Kardiol 1986;75(Suppl 2):198-200.[Medline]
- Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method Circulation 1977;55:613-618.[Abstract/Free Full Text]
- Brown ML, Schaff HV. Surgical management of hypertrophic cardiomyopathy in 2007: what is new? World J Surg 2008;32:350-354.[Medline]
- Dhareshwar J, Sundt TM, Dearani JA, Schaff HV, Cook DJ, Orszulak TA. Aortic root enlargement: what are the operative risks? J Thorac Cardiovasc Surg 2007;134:916-924.[Abstract/Free Full Text]
- Hess OM, Schneider J, Turina M, Carroll JD, Rothlin M, Krayenbuehl HP. Asymmetric septal hypertrophy in patients with aortic stenosis: an adaptive mechanism or a coexistence of hypertrophic cardiomyopathy? J Am Coll Cardiol 1983;1:783-789.[Medline]
- Schulte HD, Bircks W, Horstkotte D, Kerstholt J, Preusse CJ, Winter J. Asymmetric septal hypertrophy (ASH) in valvular aortic stenosis should not be resected at the time of surgery Z Kardiol 1986;75:201-206.[Medline]
- López Ayerbe J, Evangelista Masip A, Armada Romero E, et al. Predictive factors of abnormal dynamic intraventricular gradient after valve replacement in severe aortic stenosis Rev Esp Cardiol 2002;55:127-134.[Medline]
- Tasca G, Amaducci A, Parrella PV, et al. Myectomy-myotomy associated with aortic valve replacement for aortic stenosis: effects on left ventricular mass regression Ital Heart J 2003;4:865-871.[Medline]
- Niranjan G, Karagounis A, Asimakopoulos G, Wahed S, Chandrasekaran V. A case series of myectomy: a review of its current application as an adjunct procedure J Card Surg 2008;23:391-393.[Medline]
- Dearani JA, Ommen SR, Gersh BJ, Schaff HV, Danielson GK. Surgery insight: septal myectomy for obstructive hypertrophic cardiomyopathy—the Mayo Clinic experience Nat Clin Pract Cardiovasc Med 2007;4:503-512.[Medline]
- Smedira NG, Lytle BW, Lever HM, et al. Current effectiveness and risks of isolated septal myectomy for hypertrophic obstructive cardiomyopathy Ann Thorac Surg 2008;85:127-133.[Abstract/Free Full Text]
- Erdogan HB, Kayalar N, Ardal H, et al. Risk factors for requirement of permanent pacemaker implantation after aortic valve replacement J Card Surg 2006;21:211-215.[Medline]
- Morell VO, Daggett WM, Pezzella AT, Moran JM, Bitran D. Aortic stenosis in the elderly: result of aortic valve replacement J Cardiovasc Surg (Torino) 1996;37(Suppl 1):33-35.[Medline]
- Khan SS, Siegel RJ, DeRobertis MA, et al. Regression of hypertrophy after Carpentier-Edwards pericardial aortic valve replacement Ann Thorac Surg 2000;69:531-535.[Abstract/Free Full Text]
- Ding WH, Lam YY, Kaya MG, et al. Echocardiographic predictors of left ventricular functional recovery following valve replacement surgery for severe aortic stenosis Int J Cardiol 2008;128:178-184.[Medline]
- Schoen SP, Zimmermann TF, Rosenberger C, et al. Nomograms for severity of aortic valve stenosis using peak aortic valve pressure gradient and left ventricular ejection fraction Eur J Echocardiogr 2009 Jan 20[e-pub ahead of print].
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Abstract
Introduction
