BACKGROUND: The purpose of this study is to determine etiologic factors of systolic anterior motion (SAM) of the mitral valve after repair. METHODS: We describe 6 patients with mitral valve repair (MVRep) for degenerative mitral valve disease and a bulging angulated subaortic septum that seemed a risk factor for SAM. RESULTS: No patient had a hypertrophic cardiomyopathy diagnosis. All patients had an angulated septum (angle of long axis of left ventricle and aorta, >60°) with a discrete septal bulge (proximal septum, ≥1.5 cm with normal midseptal thickness). One patient had severe mitral regurgitation and became hypotensive intraoperatively, with a SAM. He had successful valve repair and septal myectomy. In 2 patients, the bulging septum was not appreciated preoperatively, and SAM developed postoperatively, causing symptomatic left ventricular (LV) outflow tract (LVOT) obstruction and recurrent mitral regurgitation. At reoperation, SAM and associated regurgitation were abolished with septal myectomy. In 2 patients undergoing mitral repair, bulging septum was identified preoperatively, and prophylactic septal myectomy was performed at valve repair. One patient was referred for valve replacement because of severe mitral regurgitation due to bileaflet prolapse and associated SAM. Doppler echocardiography showed minimal resting gradient. He had a prominent subaortic septum, and mitral regurgitation seemed due to organic valve disease and dynamic outflow obstruction. He received septal myectomy and mitral valve repair with resolution of SAM and mitral regurgitation. CONCLUSIONS: Bulging subaortic septum may be a risk factor for SAM after mitral valve repair. Treatment should include septal myectomy with valvuloplasty.
BACKGROUND: The purpose of this study is to determine etiologic factors of systolic anterior motion (SAM) of the mitral valve after repair. METHODS: We describe 6 patients with mitral valve repair (MVRep) for degenerative mitral valve disease and a bulging angulated subaortic septum that seemed a risk factor for SAM. RESULTS: No patient had a hypertrophic cardiomyopathy diagnosis. All patients had an angulated septum (angle of long axis of left ventricle and aorta, >60°) with a discrete septal bulge (proximal septum, ≥1.5 cm with normal midseptal thickness). One patient had severe mitral regurgitation and became hypotensive intraoperatively, with a SAM. He had successful valve repair and septal myectomy. In 2 patients, the bulging septum was not appreciated preoperatively, and SAM developed postoperatively, causing symptomatic left ventricular (LV) outflow tract (LVOT) obstruction and recurrent mitral regurgitation. At reoperation, SAM and associated regurgitation were abolished with septal myectomy. In 2 patients undergoing mitral repair, bulging septum was identified preoperatively, and prophylactic septal myectomy was performed at valve repair. One patient was referred for valve replacement because of severe mitral regurgitation due to bileaflet prolapse and associated SAM. Doppler echocardiography showed minimal resting gradient. He had a prominent subaortic septum, and mitral regurgitation seemed due to organic valve disease and dynamic outflow obstruction. He received septal myectomy and mitral valve repair with resolution of SAM and mitral regurgitation. CONCLUSIONS: Bulging subaortic septum may be a risk factor for SAM after mitral valve repair. Treatment should include septal myectomy with valvuloplasty.