Gen Thorac Cardiovasc Surg DOI 10.1007/s11748-013-0353-y

CASE REPORT

Myectomy as an alternative solution for systolic anterior motion in a patient who underwent mitral valve repair Satoru Domoto • Kozo Morita • Hiroyuki Koike • Atsushi Iguchi • Kazuhiko Uwabe • Hiroshi Niinami

Received: 6 August 2013 / Accepted: 21 November 2013 Ó The Japanese Association for Thoracic Surgery 2013

Abstract Systolic anterior motion (SAM) of the mitral apparatus is a relatively frequent complication of mitral valve repair. When significant SAM persists despite intraoperative medical therapies, a second repair is generally required. We describe a rare case of SAM due to a hypertrophic septum in a patient who underwent mitral valve repair, with no preoperative obstruction of the left ventricular outflow tract. The present case of SAM was successfully treated only with transaortic septal myectomy. Therefore, myectomy might be considered as an alternative solution for SAM that is suspected to be caused by a hypertrophic septum after mitral valve repair.

undersized annuloplasty ring, second repair is needed [3, 4]. In our case, we used only transaortic septal myectomy to treat a patient with SAM due to a hypertrophic septum, which was not preoperatively diagnosed as left ventricular outflow tract (LVOT) obstruction on echocardiogram. Myectomy has been an established technique for LVOT obstruction associated with mitral regurgitation caused by SAM in patients with hypertrophic obstructive cardiomyopathy [5] and might be considered as an alternative solution for SAM due to hypertrophic septum after mitral valve repair.

Keywords Myectomy  Systolic anterior motion  Mitral valve repair

Case report

Introduction Systolic anterior motion (SAM) of the mitral valve sometimes develops after mitral valve repair surgery, at an estimated incidence rate of 6 %. Intraoperative medical therapies (increased mean arterial pressure, slow heart rate, increased preload, and avoidance of inotropes) would generally improve the situation [1, 2]. However, when significant SAM persists despite intraoperative medical therapies, usually caused by technical factors, including excessive posterior leaflet tissue and an inaccurately

S. Domoto (&)  K. Morita  H. Koike  A. Iguchi  K. Uwabe  H. Niinami Department of Cardiovascular Surgery, Saitama International Medical Center, Saitama Medical University, 1397-1 Yamane, Hidaka, Saitama 350-1298, Japan e-mail: [email protected]

A 71-year-old woman was referred to our institution for severe mitral regurgitation. A preoperative transthoracic echocardiogram showed a mitral posterior leaflet of the middle scallop prolapse and moderate tricuspid regurgitation. Left ventricular end-diastolic diameter was 54 mm and left ventricular end-systolic diameter was 26 mm. Ejection fraction (83 %), interventricular septal thickness (12 mm) and LVOT peak velocity (0.9 m/s) were within the reference range. Height of posterior mitral leaflet was 13 mm. The patient was operated for mitral valve repair and tricuspid annuloplasty. An intraoperative transesophageal echocardiogram obtained just before the operation revealed a mild hypertrophic septum (interventricular septal thickness was 14 mm); however, there were no findings of LVOT obstruction as well as previous transthoracic echocardiographic findings (Fig. 1). Posterior leaflet quadrangular resection of the middle scallop of the posterior leaflet with ruptured chordae was performed. A 28 mm Carpentier-Edwards Physio II Ring (Edwards LifeSciences, Irvine, CA, USA), sized in accordance with

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the true size of the anterior leaflet and reasonably sized for a 1.52 m2 body surface area was implanted. Tricuspid valve repair with an Edwards MC3 ring (Edwards LifeSciences) was also performed. During weaning from cardiopulmonary bypass, a transesophageal echocardiogram showed a significant SAM with LVOT obstruction and severe mitral regurgitation (Fig. 2a). The LVOT peak gradient was 143.5 mm Hg, and the SAM persisted despite intraoperative medical therapies. The residual height of posterior leaflet was 12 mm. Based on our suspicion that the SAM was mainly caused by the hypertrophic septum, we decided to perform transaortic septal myectomy. After a second cardioplegic arrest and transverse aortotomy, septal myectomy was performed through the aortic valve. Total resection was performed for the septal bulge measuring

20 mm wide, 18 mm long, and 9 mm deep. After aortic declamping, a transesophageal echocardiogram revealed complete regression of the SAM and LVOT obstruction (LVOT peak gradient, 2.6 mm Hg), and no mitral regurgitation (Fig. 2b). Histopathological findings of the hypertrophic septum were diffuse basophilic degeneration and focal fibrosis. The postoperative course was uneventful, and a predischarge transthoracic echocardiogram indicated no findings of SAM and mitral regurgitation.

Discussion Previous studies have identified several important lesions of SAM after mitral valve repair, including a mismatch

Fig. 1 Preoperative transesophageal echocardiogram showing the mitral posterior leaflet prolapse and slight hypertrophic septum (a). Color Doppler echocardiogram shows anteriorly directed mitral regurgitation jet and no findings of LVOT obstruction (b)

Fig. 2 Intraoperative transesophageal echocardiogram obtained during weaning from the first cardiopulmonary bypass, showing significant SAM with LVOT obstruction and severe mitral regurgitation (a). The SAM improved after the septal myectomy (b)

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between the mitral valve annular dimension and the amount of leaflet tissue present, and the anterior displacement of the coaptation point. However, other mechanisms are also likely involved in the pathogenesis of SAM. The dynamic cause of SAM has been described as the anterior leaflet being drawn into the outflow tract by either a pulling (Venturi) or pushing (drag) phenomenon. Early systolic ejection flow through the outflow tract creates a drag effect on a redundant anterior leaflet tissue and the potential for LVOT obstruction by drawing the tip of the anterior leaflet into the outflow. In addition, it also creates turbulence to the flow, causing a Venturi effect on the anterior leaflet and the potential for mitral regurgitation [3, 6]. Preoperatively, despite the presence of a hypertrophic septum in our case, SAM was not detected by the detailed echocardiographic study. The severe mitral posterior leaflet with ruptured chordae, which was independent of SAM, might have reduced the early systolic ejection flow through the outflow tract, consequently abolishing the SAM. When we repaired the independent mitral valve disease, the SAM became apparent. The fundamental components leading to SAM can be divided into patient and technical risk factors related to the mitral valve repair. Patient risk factors include a narrow aortomitral angle, a bulging left ventricular septum, and a hyperdynamic small left ventricle [7]. Technical risk factors include excessive posterior leaflet tissue and an undersized annuloplasty ring [4]. When a significant SAM persists despite intraoperative medical therapies, usually caused by technical factors, removal of the prosthetic ring, repeat complex leaflet repair, and even valve replacement are required [3, 4]. In particular, although quadrangular resection is widely used as a standard procedure for posterior leaflet prolapse, this technique predisposes patients to SAM because it leaves a relatively tall posterior leaflet [8]. We confirmed that the main cause of the SAM in the present case was the hypertrophic septum rather than the technical factors; therefore, we decided to perform transaortic septal myectomy because we found no findings of excessive posterior leaflet tissue, or excess anterior leaflet extending beyond the coaptation point on the intraoperative transesophageal echocardiogram. Moreover, we found no significant difference between the preoperative and postoperative left ventricular diameters and ejection fractions. Myectomy has been an established treatment method for LVOT obstruction and concomitant mitral regurgitation, both caused by SAM, in patients with hypertrophic obstructive cardiomyopathy [5]. According to a recent report by Said et al. [7], a bulging angulated subaortic septum, which is characterized by an angle the of long axis of the left ventricle and aorta ([60°) with a discrete septal

bulge ([1.5 cm from the proximal septum, with normal midseptal thickness), may be a risk factor for SAM after mitral valve repair. The authors suggested that treatment should include septal myectomy with valvuloplasty. However, SAM seemed difficult to predict based on the preoperative transthoracic echocardiographic findings in the present case because the findings that indicated bulging subaortic septum (aortomitral angle \60°, \1.5 cm from the proximal septum) could not even be retrospectively detected. Therefore, when a hypertrophic septum is diagnosed by intraoperative transesophageal echocardiogram in a patient who has undergone mitral valve repair, the surgeon should consider concomitant septal myectomy, which from a surgical standpoint is easy to perform, requires only a short additional cross clamping time, and does not require manipulation of the previously repaired valve. In conclusion, myectomy might be considered as an alternative solution for SAM due to hypertrophic septum after mitral valve repair. Conflict of interest conflict of interest.

Satoru Domoto and other co-authors have no

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Myectomy as an alternative solution for systolic anterior motion in a patient who underwent mitral valve repair.

Systolic anterior motion (SAM) of the mitral apparatus is a relatively frequent complication of mitral valve repair. When significant SAM persists des...
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