Case Study
Systolic anterior motion of mitral valve with calcified annulus in octogenarians
Asian Cardiovascular & Thoracic Annals 21(4) 456–459 ß The Author(s) 2012 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492312455808 aan.sagepub.com
Haralabos Parissis, Umar Imran Hamid, Reubendra Jeganathan and Alastair Graham
Abstract Systolic anterior motion of the mitral leaflet causing left ventricular outflow tract obstruction is commonly seen in hypertrophic cardiomyopathy and also in patients with advanced mitral valve disease with excessive anterior leaflet tissue or a reduced aortic-mitral angle. We describe 2 octogenarians who presented with systolic mitral leaflet anterior motion in advanced mitral valve disease with severe mitral annular calcification and associated asymmetrical septal hypertrophy.
Keywords Aged, 80 and over, calcinosis, mitral valve annuloplasty, mitral valve insufficiency, ventricular outflow obstruction
Introduction Systolic anterior motion (SAM) of the mitral leaflet was first described in the 1960s, in association with hypertrophic cardiomyopathy.1 SAM of the mitral valve is defined as prolapse of the anterior leaflet into the left ventricular outflow tract (LVOT) during systole, causing LVOT obstruction with concomitant mitral valve regurgitation. The consequence is a drop in cardiac output. There are known factors such as small left ventricular cavity, hyperdynamic left ventricle, asymmetric septal hypertrophy, excessive anterior mitral leaflet tissue, use of a small prosthetic ring for mitral repair, and an elongated ascending aorta, which reduce the aortic-mitral angle and contribute to the development of SAM. Mitral annular calcification (MAC) has been suggested as a cause of SAM, but we believe this to be an association rather than a cause, because it is usually present in the setting of advanced mitral valve disease.
Case 1 An 86-year-old woman presented with worsening breathlessness on exertion. There was no significant medical history apart from hypertension. Her initial transthoracic echocardiogram at rest demonstrated mild mitral regurgitation with an elongated anterior leaflet, significant calcification of the mitral annulus, asymmetrical septal hypertrophy of 16 mm, with
preserved left ventricular function. The initial management plan was to treat her medically, but despite this, her symptoms continued to progress. Dobutamine stress echocardiography demonstrated an increase in the LVOT velocity from 2 to 6 ms 1 and a peak mean LVOT gradient of 62 mm Hg. This was associated with SAM (Figure 1(a)). Given her good comorbid status, surgery was offered. We opted to treat the underlying pathology by reducing the height of the anterior leaflet of the mitral valve and performing a septal myectomy, given her annular dimensions were within normal limits. The surgical approach was through a generous hockey-stick aortotomy, where a crescent of 8 2 mm of the anterior leaflet close to the annulus was excised, and a myectomy was performed. Intraoperative transesophageal echocardiography with dobutamine stress testing after termination of cardiopulmonary bypass did not demonstrate any SAM, with a residual peak LVOT velocity of 2 ms 1. Postoperative recovery was uneventful. Histology of
Department of Cardiothoracic Surgery, Royal Victoria Hospital, Belfast, UK Corresponding author: Haralabos Parissis, PhD, Cardiothoracic Department, Royal Victoria Hospital, West Wing, Grosvenor Road, Belfast BT12 6BA, UK. Email: [email protected]
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
Parissis et al.
457 was inserted, with careful attention to avoid any postoperative SAM, given the fact that no leaflet tissue was excised. Both a saline test and post-cardiopulmonary bypass intraoperative echocardiography demonstrated a trace of mitral regurgitation with no SAM. The postoperative course was complicated by acute renal failure and respiratory tract infection. The patient was discharged on postoperative day 19, and was doing well on follow-up.
Discussion
Figure 1. Transthoracic echocardiography in (a) case 1 and (b) case 2. The arrows indicate the prolapsed anterior mitral leaflet during systole, obstructing the left ventricular outflow tract.
the septal myectomy specimen showed no obliterative small vessel disease and no muscle fiber disarray or interstitial fibrosis. At follow-up, the patient remained clinically well with a significant improvement in exercise tolerance.
Case 2 An 80-year-old man presented with progressive exertional breathlessness. Transthoracic echocardiography at rest demonstrated bileaflet prolapse with mitral regurgitation, significant mitral annular calcification, and severe aortic stenosis. There was mild asymmetric septal hypertrophy with the suggestion of possible SAM, given the redundant anterior leaflet of the mitral valve (Figure 1(b)). Coronary angiography revealed 2-vessel coronary artery disease. He underwent mitral valve repair, bioprosthetic aortic valve replacement, and double-vessel coronary artery bypass with vein grafts to the left anterior descending and obtuse marginal arteries. At surgery, the findings were in keeping with advanced degenerative mitral valve disease, with elongated chordae to both leaflets and significant posterior annular calcification. Decalcification was carried out on the posterior annulus, with no patch required to restore left atrial-to-left ventricular continuity. The ‘‘respect and not resect’’ approach was applied with neochordae construction to both leaflets, with the aim of restoring competence. A size 30 Physio II ring
SAM usually occurs in the setting of intrinsic mitral valve disease, asymmetric septal hypertrophy, and conditions that predisposed to a reduction in the aorticmitral angle. SAM is classified as moderate when the LVOT maximum pressure gradient ranges between 20 and 50 mm Hg, and severe when the LVOT maximum pressure gradient is 50 mm Hg or greater.2 This report highlights 2 patients whose primary etiology was intrinsic mitral valve disease and who concurrently had mild to moderate asymmetric septal hypertrophy, likely to be secondary to hypertensive disease. Both patients had severe MAC that made the subsequent surgical management more difficult. MAC is a common finding in the elderly, usually with no clinical consequences. Although MAC has been implicated as a cause of SAM in at least one report, we believe it to be an association rather than a causative factor.3 In 88% of cases of MAC, the posterior annulus is involved, the calcification also involves the commissures in 10.5%, and the full circumference of the valve is involved in only 1.5% of cases.4 Following mitral valve repair, SAM can occur when there is a discrepancy between the amount of valvular tissue and the mitral valve orifice area. Major anatomic factors incriminated in the genesis of LVOT obstruction include degenerative mitral valve disease with excess leaflet tissue, a small left ventricular cavity, hyperdynamic left ventricle, asymmetric septal hypertrophy, and conditions that narrow the aortic-mitral angle. Furthermore, following mitral repair, LVOT obstruction occurs when the mitral coaptation line is displaced anteriorly. Therefore, repairs that leave a relatively tall posterior leaflet or use a small annuloplasty ring can result in an anteriorly displaced coaptation line, and therefore SAM. Appropriate measures to prevent this include reduction of the posterior leaflet height to 1.5 cm or less with a sliding- or foldingplasty technique or insertion of neochordae. It is important not to neglect the fact that myxomatous mitral valve disease is a spectrum of varying amounts of excess leaflet tissue with or without annular dilatation. Therefore, appropriate selection of ring size is of great importance in preventing SAM.
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
458
Asian Cardiovascular & Thoracic Annals 21(4)
The mechanism of SAM in septal hypertrophy implicates raised flow velocities in the outflow tract that create a Venturi effect that pulls the mitral valve leaflet towards the septum, thus obstructing ventricular outflow.5,6 However, anterior motion of the mitral valve could begin prior to ventricular ejection and aortic valve opening, a finding that the Venturi effect could not explain.7 In this case, possible anterior and inward displacement of the papillary muscles and elongation of the valve leaflets are factors that create slack in the leaflets, predisposing to SAM. Pridie and Oakley8 suggested that an abnormally directed and dyssynchronous papillary muscle contraction could pull the anterior mitral leaflet into the LVOT during systole. The forward positioning of the mitral valve at the onset of systole, together with forces that may be generated as blood is ejected through this narrowed LVOT, may result in a Venturi effect.9 The mitral valve may then be sucked up into the outflow tract to produce the obstruction and the gradient. Finally, there are no objective guides on the extent of reduction of the anterior mitral leaflet height or resection of septal hypertrophy to correct SAM. Efforts should be made to reduce the posterior mitral leaflet height to less than 1.5 cm, something clearly achievable with various manoeuvres (sliding or folding plasty). The only way to reduce anterior mitral leaflet height would be elliptical resection of the central portion of the leaflet, basically on visual inspection, which is not widely applicable in repair techniques. Lastly, optimal sizing and avoidance of small rings somehow preserves anteroposterior diameter and indirectly relates to anterior mitral leaflet height. Septal myectomy as described by Morrow10 is carried out via an aortotomy, the hypertrophied muscle is excised using a scalpel. Modifications, as per Mayo Clinic maneuvers for more reproducible resection, could also considered.11 Care should be taken when using a scalpel, to achieve a smooth uniform excision of the hypertrophied septum, without leaving ridges and furrows. Finally, the amount of muscle to be removed is directly related to the judgment and experience of the operator. Digital palpation, although a rather crude measure, confirms the depth of resection. Lastly, not only the thickness but also the length of septal resection deep into the left ventricular cavity should be assessed under direct vision. Both of these cases illustrate the complex surgical decision-making in patients with advanced age and concomitant intrinsic mitral valve disease with asymmetric hypertrophy. To make matters worse, there was severe MAC. The first patient had a relatively easy operation, only by the fact that her annular dimensions were preserved, and by altering the height of the anterior leaflet and performing a septal myectomy, we
corrected the flow dynamics and removed SAM. The 2nd patient unfortunately had more complex mitral valve disease, and therefore both leaflet and annular pathology needed correcting, without altering the thickness of the septum. Both patients made a good recovery and are symptomatically better. These cases highlight that appropriate understanding of the mechanism of SAM is of great significance because it tailors the operation accordingly, and can be straightforward as in the first patient, or complex reconstructive mitral valve surgery as seen in the 2nd patient. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflicts of interest statement None declared.
References 1. Shah PM, Gramiak R and Kramer DH. Ultrasound localization of left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy. Circulation 1969; 40: 3–11. 2. Brown ML, Abel MD, Click RL, Morford RG, Dearani JA, Sundt TM, et al. Systolic anterior motion after mitral valve repair: is surgical intervention necessary? J Thorac Cardiovasc Surg 2007; 133: 136–143. 3. Lindvall K and Herrlin B. Mitral annulus calcification, systolic anterior motion of the anterior mitral leaflet and outflow obstruction in two patients without hypertrophic cardiomyopathy. Acta Med Scand 1981; 209: 513–518. 4. Carpentier AF, Pellerin M, Fuzellier JF and Relland JY. Extensive calcification of the mitral valve anulus: pathology and surgical management. J Thorac Cardiovasc Surg 1996; 111: 718. 5. Maron BJ, Bonow RO, Cannon 3rd RO, Leon MB and Epstein SE. Hypertrophic cardiomyopathy. Interrelations of clinical manifestations, pathophysiology, and therapy (1). N Engl J Med 1987; 316: 780–789. 6. Maron BJ, Bonow RO, Cannon 3rd RO, Leon MB and Epstein SE. Hypertrophic cardiomyopathy. Interrelations of clinical manifestations, pathophysiology, and therapy (2). N Engl J Med 1987; 316: 844–852. 7. Jiang L, Levine RA, King ME and Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. Am Heart J 1987; 113: 633–644. 8. Pridie RB and Oakley CM. Mechanism of mitral regurgitation of hypertrophic obstructive cardiomyopathy. Br Heart J 1970; 32: 203–208.
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
Parissis et al.
459
9. Henry WL, Clark CE, Griffith JM and Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy. Am J Cardiol 1975; 35: 337–345. 10. Morrow AG. Hypertrophic subaortic stenosis. Operative methods used to relieve left ventricular outflow obstruction. J Thorac Cardiovasc Surg 1978; 76: 423–430.
11. Schaff HV. Septal myectomy: how I do it. AATS Conference, San Francisco, USA, April 28–May 2 2012, 92nd Annual meeting. Available at: http://store.eventarchives.com/archive/aats/2012/sessions/player.html?sid=12040107.13. Accessed July 03, 2012.
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
Systolic anterior motion of mitral valve with calcified annulus in octogenarians
Asian Cardiovascular & Thoracic Annals 21(4) 456–459 ß The Author(s) 2012 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492312455808 aan.sagepub.com
Haralabos Parissis, Umar Imran Hamid, Reubendra Jeganathan and Alastair Graham
Abstract Systolic anterior motion of the mitral leaflet causing left ventricular outflow tract obstruction is commonly seen in hypertrophic cardiomyopathy and also in patients with advanced mitral valve disease with excessive anterior leaflet tissue or a reduced aortic-mitral angle. We describe 2 octogenarians who presented with systolic mitral leaflet anterior motion in advanced mitral valve disease with severe mitral annular calcification and associated asymmetrical septal hypertrophy.
Keywords Aged, 80 and over, calcinosis, mitral valve annuloplasty, mitral valve insufficiency, ventricular outflow obstruction
Introduction Systolic anterior motion (SAM) of the mitral leaflet was first described in the 1960s, in association with hypertrophic cardiomyopathy.1 SAM of the mitral valve is defined as prolapse of the anterior leaflet into the left ventricular outflow tract (LVOT) during systole, causing LVOT obstruction with concomitant mitral valve regurgitation. The consequence is a drop in cardiac output. There are known factors such as small left ventricular cavity, hyperdynamic left ventricle, asymmetric septal hypertrophy, excessive anterior mitral leaflet tissue, use of a small prosthetic ring for mitral repair, and an elongated ascending aorta, which reduce the aortic-mitral angle and contribute to the development of SAM. Mitral annular calcification (MAC) has been suggested as a cause of SAM, but we believe this to be an association rather than a cause, because it is usually present in the setting of advanced mitral valve disease.
Case 1 An 86-year-old woman presented with worsening breathlessness on exertion. There was no significant medical history apart from hypertension. Her initial transthoracic echocardiogram at rest demonstrated mild mitral regurgitation with an elongated anterior leaflet, significant calcification of the mitral annulus, asymmetrical septal hypertrophy of 16 mm, with
preserved left ventricular function. The initial management plan was to treat her medically, but despite this, her symptoms continued to progress. Dobutamine stress echocardiography demonstrated an increase in the LVOT velocity from 2 to 6 ms 1 and a peak mean LVOT gradient of 62 mm Hg. This was associated with SAM (Figure 1(a)). Given her good comorbid status, surgery was offered. We opted to treat the underlying pathology by reducing the height of the anterior leaflet of the mitral valve and performing a septal myectomy, given her annular dimensions were within normal limits. The surgical approach was through a generous hockey-stick aortotomy, where a crescent of 8 2 mm of the anterior leaflet close to the annulus was excised, and a myectomy was performed. Intraoperative transesophageal echocardiography with dobutamine stress testing after termination of cardiopulmonary bypass did not demonstrate any SAM, with a residual peak LVOT velocity of 2 ms 1. Postoperative recovery was uneventful. Histology of
Department of Cardiothoracic Surgery, Royal Victoria Hospital, Belfast, UK Corresponding author: Haralabos Parissis, PhD, Cardiothoracic Department, Royal Victoria Hospital, West Wing, Grosvenor Road, Belfast BT12 6BA, UK. Email: [email protected]
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
Parissis et al.
457 was inserted, with careful attention to avoid any postoperative SAM, given the fact that no leaflet tissue was excised. Both a saline test and post-cardiopulmonary bypass intraoperative echocardiography demonstrated a trace of mitral regurgitation with no SAM. The postoperative course was complicated by acute renal failure and respiratory tract infection. The patient was discharged on postoperative day 19, and was doing well on follow-up.
Discussion
Figure 1. Transthoracic echocardiography in (a) case 1 and (b) case 2. The arrows indicate the prolapsed anterior mitral leaflet during systole, obstructing the left ventricular outflow tract.
the septal myectomy specimen showed no obliterative small vessel disease and no muscle fiber disarray or interstitial fibrosis. At follow-up, the patient remained clinically well with a significant improvement in exercise tolerance.
Case 2 An 80-year-old man presented with progressive exertional breathlessness. Transthoracic echocardiography at rest demonstrated bileaflet prolapse with mitral regurgitation, significant mitral annular calcification, and severe aortic stenosis. There was mild asymmetric septal hypertrophy with the suggestion of possible SAM, given the redundant anterior leaflet of the mitral valve (Figure 1(b)). Coronary angiography revealed 2-vessel coronary artery disease. He underwent mitral valve repair, bioprosthetic aortic valve replacement, and double-vessel coronary artery bypass with vein grafts to the left anterior descending and obtuse marginal arteries. At surgery, the findings were in keeping with advanced degenerative mitral valve disease, with elongated chordae to both leaflets and significant posterior annular calcification. Decalcification was carried out on the posterior annulus, with no patch required to restore left atrial-to-left ventricular continuity. The ‘‘respect and not resect’’ approach was applied with neochordae construction to both leaflets, with the aim of restoring competence. A size 30 Physio II ring
SAM usually occurs in the setting of intrinsic mitral valve disease, asymmetric septal hypertrophy, and conditions that predisposed to a reduction in the aorticmitral angle. SAM is classified as moderate when the LVOT maximum pressure gradient ranges between 20 and 50 mm Hg, and severe when the LVOT maximum pressure gradient is 50 mm Hg or greater.2 This report highlights 2 patients whose primary etiology was intrinsic mitral valve disease and who concurrently had mild to moderate asymmetric septal hypertrophy, likely to be secondary to hypertensive disease. Both patients had severe MAC that made the subsequent surgical management more difficult. MAC is a common finding in the elderly, usually with no clinical consequences. Although MAC has been implicated as a cause of SAM in at least one report, we believe it to be an association rather than a causative factor.3 In 88% of cases of MAC, the posterior annulus is involved, the calcification also involves the commissures in 10.5%, and the full circumference of the valve is involved in only 1.5% of cases.4 Following mitral valve repair, SAM can occur when there is a discrepancy between the amount of valvular tissue and the mitral valve orifice area. Major anatomic factors incriminated in the genesis of LVOT obstruction include degenerative mitral valve disease with excess leaflet tissue, a small left ventricular cavity, hyperdynamic left ventricle, asymmetric septal hypertrophy, and conditions that narrow the aortic-mitral angle. Furthermore, following mitral repair, LVOT obstruction occurs when the mitral coaptation line is displaced anteriorly. Therefore, repairs that leave a relatively tall posterior leaflet or use a small annuloplasty ring can result in an anteriorly displaced coaptation line, and therefore SAM. Appropriate measures to prevent this include reduction of the posterior leaflet height to 1.5 cm or less with a sliding- or foldingplasty technique or insertion of neochordae. It is important not to neglect the fact that myxomatous mitral valve disease is a spectrum of varying amounts of excess leaflet tissue with or without annular dilatation. Therefore, appropriate selection of ring size is of great importance in preventing SAM.
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
458
Asian Cardiovascular & Thoracic Annals 21(4)
The mechanism of SAM in septal hypertrophy implicates raised flow velocities in the outflow tract that create a Venturi effect that pulls the mitral valve leaflet towards the septum, thus obstructing ventricular outflow.5,6 However, anterior motion of the mitral valve could begin prior to ventricular ejection and aortic valve opening, a finding that the Venturi effect could not explain.7 In this case, possible anterior and inward displacement of the papillary muscles and elongation of the valve leaflets are factors that create slack in the leaflets, predisposing to SAM. Pridie and Oakley8 suggested that an abnormally directed and dyssynchronous papillary muscle contraction could pull the anterior mitral leaflet into the LVOT during systole. The forward positioning of the mitral valve at the onset of systole, together with forces that may be generated as blood is ejected through this narrowed LVOT, may result in a Venturi effect.9 The mitral valve may then be sucked up into the outflow tract to produce the obstruction and the gradient. Finally, there are no objective guides on the extent of reduction of the anterior mitral leaflet height or resection of septal hypertrophy to correct SAM. Efforts should be made to reduce the posterior mitral leaflet height to less than 1.5 cm, something clearly achievable with various manoeuvres (sliding or folding plasty). The only way to reduce anterior mitral leaflet height would be elliptical resection of the central portion of the leaflet, basically on visual inspection, which is not widely applicable in repair techniques. Lastly, optimal sizing and avoidance of small rings somehow preserves anteroposterior diameter and indirectly relates to anterior mitral leaflet height. Septal myectomy as described by Morrow10 is carried out via an aortotomy, the hypertrophied muscle is excised using a scalpel. Modifications, as per Mayo Clinic maneuvers for more reproducible resection, could also considered.11 Care should be taken when using a scalpel, to achieve a smooth uniform excision of the hypertrophied septum, without leaving ridges and furrows. Finally, the amount of muscle to be removed is directly related to the judgment and experience of the operator. Digital palpation, although a rather crude measure, confirms the depth of resection. Lastly, not only the thickness but also the length of septal resection deep into the left ventricular cavity should be assessed under direct vision. Both of these cases illustrate the complex surgical decision-making in patients with advanced age and concomitant intrinsic mitral valve disease with asymmetric hypertrophy. To make matters worse, there was severe MAC. The first patient had a relatively easy operation, only by the fact that her annular dimensions were preserved, and by altering the height of the anterior leaflet and performing a septal myectomy, we
corrected the flow dynamics and removed SAM. The 2nd patient unfortunately had more complex mitral valve disease, and therefore both leaflet and annular pathology needed correcting, without altering the thickness of the septum. Both patients made a good recovery and are symptomatically better. These cases highlight that appropriate understanding of the mechanism of SAM is of great significance because it tailors the operation accordingly, and can be straightforward as in the first patient, or complex reconstructive mitral valve surgery as seen in the 2nd patient. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflicts of interest statement None declared.
References 1. Shah PM, Gramiak R and Kramer DH. Ultrasound localization of left ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy. Circulation 1969; 40: 3–11. 2. Brown ML, Abel MD, Click RL, Morford RG, Dearani JA, Sundt TM, et al. Systolic anterior motion after mitral valve repair: is surgical intervention necessary? J Thorac Cardiovasc Surg 2007; 133: 136–143. 3. Lindvall K and Herrlin B. Mitral annulus calcification, systolic anterior motion of the anterior mitral leaflet and outflow obstruction in two patients without hypertrophic cardiomyopathy. Acta Med Scand 1981; 209: 513–518. 4. Carpentier AF, Pellerin M, Fuzellier JF and Relland JY. Extensive calcification of the mitral valve anulus: pathology and surgical management. J Thorac Cardiovasc Surg 1996; 111: 718. 5. Maron BJ, Bonow RO, Cannon 3rd RO, Leon MB and Epstein SE. Hypertrophic cardiomyopathy. Interrelations of clinical manifestations, pathophysiology, and therapy (1). N Engl J Med 1987; 316: 780–789. 6. Maron BJ, Bonow RO, Cannon 3rd RO, Leon MB and Epstein SE. Hypertrophic cardiomyopathy. Interrelations of clinical manifestations, pathophysiology, and therapy (2). N Engl J Med 1987; 316: 844–852. 7. Jiang L, Levine RA, King ME and Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. Am Heart J 1987; 113: 633–644. 8. Pridie RB and Oakley CM. Mechanism of mitral regurgitation of hypertrophic obstructive cardiomyopathy. Br Heart J 1970; 32: 203–208.
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
Parissis et al.
459
9. Henry WL, Clark CE, Griffith JM and Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy. Am J Cardiol 1975; 35: 337–345. 10. Morrow AG. Hypertrophic subaortic stenosis. Operative methods used to relieve left ventricular outflow obstruction. J Thorac Cardiovasc Surg 1978; 76: 423–430.
11. Schaff HV. Septal myectomy: how I do it. AATS Conference, San Francisco, USA, April 28–May 2 2012, 92nd Annual meeting. Available at: http://store.eventarchives.com/archive/aats/2012/sessions/player.html?sid=12040107.13. Accessed July 03, 2012.
Downloaded from aan.sagepub.com at GEORGIAN COURT UNIV on April 30, 2015
