Bulging Subaortic Septum: An Important Risk Factor for Systolic Anterior Motion After Mitral Valve Repair

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1 Bulging Subaortic Septum: An Important Risk Factor for Systolic Anterior Motion After Mitral Valve Repair Sameh M. Said, MD, Hartzell V. Schaff, MD, Rakesh M. Suri, MD, DPhil, Kevin L. Greason, MD, Joseph A. Dearani, MD, and Rick A. Nishimura, MD Divisions of Cardiovascular Surgery and Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota ADULT CARDIAC 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. (Ann Thorac Surg 2011;91: ) 2011 by The Society of Thoracic Surgeons Accepted for publication Jan 28, Address correspondence to Dr Schaff, Division of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905; schaff@mayo.edu. With modern surgical methods, systolic anterior motion (SAM) of the mitral valve anterior leaflet occurs in 4% to 8.4% of patients after mitral valve repair (MVRep), and the incidence depends in part on whether intraoperative or early postoperative echocardiography is used for diagnosis [1 4]. SAM can produce mitral valve regurgitation (MR) and left ventricular outflow tract (LVOT) obstruction, but in many cases SAM resolves with conservative management, including intravascular volume augmentation and increasing systemic vascular resistance [3, 5 7]. In some patients, however, SAM and the resulting MR (with or without LVOT obstruction) can cause recurrent symptoms and requires prompt reoperation. Several approaches to prevent or correct SAM have been reported, including complex leaflet repair and even prosthetic replacement. Systolic anterior motion of the mitral apparatus was initially described in association with hypertrophic obstructive cardiomyopathy [8]. The combination of SAM and septal hypertrophy leads to LVOT obstruction that resolves with extended left ventricular (LV) septal myectomy [9, 10]. SAM has also been described as a rare complication of mitral valve replacement with preservation of the anterior mitral valve leaflet [11]. Most techniques aimed at preventing SAM during MVRep focus on reducing excessive height of the posterior leaflet. However, SAM may occur in patients without an abnormally elongated posterior leaflet. We present a new concept that may explain the development of SAM after MVRep in some patients in whom an abnormal bulging septum predisposes them to SAM after correction of MR. This SAM can be prevented by concomitant septal myectomy. Patients, Methods, and Results Case 1 A 69-year-old man with severe MR and atrial fibrillation was referred for MVRep. Preoperative transthoracic and transesophageal echocardiography (TEE) showed bileaflet prolapse with normal LV ejection fraction and wall thickness. Intraoperatively, during preparation for bypass, he became hypotensive, with a systolic blood pressure of 60 to 65 mm Hg that did not respond to inotropic agents. The hypotension appeared to be due to SAM detected on intraoperative TEE. Before MVRep, we ex by The Society of Thoracic Surgeons /$36.00 Published by Elsevier Inc doi: /j.athoracsur

2 ADULT CARDIAC 1428 SAID ET AL Ann Thorac Surg BULGING SUBAORTIC SEPTUM AND SAM AFTER MVRep 2011;91: Fig 1. Transthoracic echocardiography (TEE) of the patient in Case 2 during first cardiac procedure. (A) Posterior mitral valve leaflet prolapse and ventricular septal bulge (white arrow). No evidence of SAM was found at time of TEE. (B) The mitral valve regurgitant jet is eccentric and anteriorly directed. plored the septum through an aortotomy and found a focal bulging septum with endocardial scar that may have been a contact lesion. A septal myectomy was performed in addition to a maze procedure and MVRep with posterior leaflet plication and posterior annuloplasty band. On postoperative echocardiography, no residual MR or LVOT obstruction was seen. Case 2 A 42-year-old man with severe MR due to prolapse of the middle scallop of the posterior leaflet (Fig 1) underwent standard repair with triangular excision of the unsupported segment of the middle scallop (P2) and insertion of a posterior annuloplasty band (length, 63 mm) [12]. Early after discontinuation of the cardiopulmonary bypass, SAM was observed on TEE. The SAM appeared to be due to decreased systemic vascular resistance and hypotension and was abolished by intravascular volume augmentation and vasopressors. The patient recovered smoothly, but postoperative echocardiography showed residual SAM with dynamic LVOT obstruction (maximal late-peaking pressure gradient, 58 mm Hg). At this time, the degree of MR was mild to moderate, and the posterolateral trajectory of the jet suggested that MR was related Fig 2. Intraoperative transthoracic echocardiography (TEE) of the patient in Case 2 during second cardiac procedure. (A) Severe systolic anterior motion (SAM) with prominent septal bulge (white arrow) before bypass. (B) Severe SAM with severe mitral valve regurgitation (MR) and severe left ventricular outflow tract (LVOT) obstruction before bypass. (C) After septal myectomy (white arrow), no evidence of SAM was found when LVOT was opened wide. (D) Postseptal myectomy TEE with no SAM, widely opened LVOT, and minimal MR.

3 Ann Thorac Surg SAID ET AL 2011;91: BULGING SUBAORTIC SEPTUM AND SAM AFTER MVRep 1429 Fig 3. Intraoperative transesophageal echocardiography of the patient in Case 3 during first cardiac procedure. (A) Septal bulge (white arrow) before bypass. (B) Anteriorly directed mitral valve regurgitation (MR) jet and septal bulge (white arrow) but no systolic anterior motion (SAM) before bypass. (C) Severe SAM with mild LVOT obstruction noted initially after bypass. (D) Severe mitral valve regurgitation (MR). MR and left ventricular outflow tract (LVOT) obstruction improved with administration of vasopressors and fluids after bypass. ADULT CARDIAC to SAM. The patient was treated with -blockers and monitored. Neither the preoperative nor the postoperative echocardiographic evaluation was interpreted as showing LV septal hypertrophy or any other evidence of hypertrophic obstructive cardiomyopathy. The patient did well for almost 3 years but then had effort intolerance. Doppler echocardiography was repeated and showed marked SAM and a resting dynamic LVOT obstruction with a maximum instantaneous gradient of 81 mm Hg and a secondary MR that appeared moderate in severity. At reoperation, we noted a bulging subaortic septum on TEE. We did not know whether the septal bulge was an acquired form of hypertrophy of the subaortic septum or whether the patient had underlying hypertrophic cardiomyopathy before his MVRep. Because of the patient s symptoms and exercise limitation, we proceeded to relieve the LVOT obstruction using transaortic LV septal myectomy, with a possible mitral valve second repair or replacement. Before the cardiopulmonary bypass, measured resting aortic pressure was 81/52 mm Hg and LV pressure was 153/5 mm Hg, producing a gradient of 72 mm Hg. After a premature ventricular contraction (Brockenbrough-Braunwald-Morrow maneuver), the aortic pressure decreased to 65/41 mm Hg and the LV pressure rose to 212/9 mm Hg, producing a gradient of 147 mm Hg. After aortotomy, we noticed a prominent, bulging subaortic basal septum (Fig 2A) and evidence of endocardial scarring due to SAM (Fig 2B). We proceeded with an extended LV septal myectomy (Fig 2C), and nothing was done to the previous MVRep. After myectomy, the LVOT was opened wide (Fig 2D), the aortic pressure was 128/45 mm Hg, and the LV pressure was 128/15 mm Hg. There was no gradient after a premature ventricular contraction. The patient did well after the surgery, and successive echocardiography confirmed no residual LVOT obstruction. Case 3 A 58-year-old woman was referred for repair of severe MR. Intraoperative echocardiography showed prolapse of the medial (P1) and middle (P2) scallops of the posterior leaflet, with an anteriorly directed regurgitant jet (Fig 3A, 3B). Surgical inspection identified an additional perforation of the posterior leaflet, likely due to healed endocarditis. The medial half of the middle scallop and the lateral half of the medial scallop were excised, and the leaflet was repaired in two layers with 4-0 polypropylene suture. The leaflet repair was enforced with a 63-mm posterior annuloplasty band. After cardiopulmonary bypass, the patient had intermittent SAM, which produced moderate to severe MR (Fig 3C, 3D) and some degree of LVOT narrowing. However, when the systemic vascular resistance was increased, SAM improved dramatically. The patient had

4 ADULT CARDIAC 1430 SAID ET AL Ann Thorac Surg BULGING SUBAORTIC SEPTUM AND SAM AFTER MVRep 2011;91: Fig 4. Intraoperative transesophageal echocardiography of the patient in case 3 during second cardiac procedure. (A) Severe mitral valve regurgitation (MR) due to severe systolic anterior motion (SAM) with a posteriorly directed jet (white arrow) before bypass. (B) Septal bulge (white arrow) and severe SAM before bypass. (C) Postseptal myectomy with no SAM. (D) No MR and no left ventricular outflow tract (LVOT) obstruction after septal myectomy. almost no regurgitation, and the LVOT obstruction abated. Nothing further was done surgically. The patient was observed regularly, and almost a year later she was found to have severe symptomatic MR due to SAM (Fig 4A) and LVOT obstruction. At reoperation, TEE showed a prominent basal septum (Fig 4B) that, in retrospect, was determined to have been present before the initial repair. We proceeded with extended LV septal myectomy, and after repair aortic pressure was 146/70 mm Hg and LV pressure was 146/5 mm Hg. After a premature ventricular contraction, there was no gradient. We administered sodium nitroprusside to decrease the systemic vascular resistance, and this medical therapy did not produce an LVOT gradient or MR (Fig 4C, 4D). The patient recovered uneventfully. Case 4 A 70-year-old woman underwent MVRep with insertion of artificial chordae to the anterior leaflet and a posterior annuloplasty band for correction of severe MR. The preoperative echocardiogram showed severe MR, LV enlargement, and normal ventricular wall thickness. Intraoperative TEE showed focal basal septal thickening with no LVOT obstruction. Because this septal bulge appeared to be the anatomic substrate for LVOT obstruction after repair, we elected to perform septal myectomy to prevent SAM, in addition to MVRep. At the conclusion of the cardiopulmonary bypass procedure, there was no MR and no SAM or LVOT obstruction. The patient recovered well, and follow-up echocardiography showed a similar good result. Case 5 The fifth patient was a 49-year-old woman with Barlow s disease and severe MR due to bileaflet prolapse. In addition, preoperative transthoracic echocardiography showed LV enlargement with normal wall thickness and an ejection fraction of 63%. Although not previously reported, a distinct septal bulge was noted at preoperative surgical review and was confirmed on intraoperative TEE. There was no resting gradient before repair, but isoproterenol infusion produced SAM and LVOT obstruction with a maximum instantaneous gradient of 67 mm Hg. The patient underwent transaortic septal myectomy and MVRep with triangular resection of the middle scallop of the posterior leaflet and insertion of a 63-mm posterior annuloplasty band. Postoperative echocardiography showed no SAM and only trace MR. Case 6 A 54-year-old man was referred with severe MR due to bileaflet mitral valve prolapse. However, his major symptom was exertional chest pain, not shortness of breath, and transthoracic echocardiography showed basal septal

5 Ann Thorac Surg SAID ET AL 2011;91: BULGING SUBAORTIC SEPTUM AND SAM AFTER MVRep Table 1. Echocardiographic Features of Patients With Bulging Septum Patient No. Basal Septal Thickness (cm) Midventricular Septal Thickness (cm) Basal Septal Thickness to Midventricular Septal Thickness Ratio Angle Between Left Ventricular and Aortic Long Axes degrees degrees degrees degrees degrees degrees 1431 ADULT CARDIAC prominence with dynamic LVOT obstruction (peak gradient with Valsalva maneuver, 34 mm Hg). The left ventricle was enlarged, but wall thickness was normal. Cardiac catheterization was performed to assess hemodynamics. In the baseline state, aortic pressure was 96/57 mm Hg and LV pressure was 118/0 mm Hg with enddiastolic pressure of 12 mm Hg. There was a dynamic LVOT gradient, which increased to 80 mm Hg after premature ventricular contraction. This LVOT gradient was found to be associated with SAM on echocardiography. Also, a left ventriculogram showed moderate to severe MR that was clearly worse with vasodilatation due to contrast injection. With phenylephrine infusion (peak dose, 0.8 g/kg/min), the LVOT gradient decreased to 0 mm Hg. No SAM was observed on echocardiography during phenylephrine infusion. A repeated left ventriculogram done at this time showed only mild MR. Overall, the catheterization showed that the MR was dynamic and improved with treatment of the LVOT gradient. The patient was treated with -blockade and underwent septal myectomy combined with MVRep. During operation, the posterior leaflet was repaired with triangular excision of the unsupported portion of the posterior leaflet without ring annuloplasty. The patient had a smooth postoperative recovery with improvement in his symptoms; on follow-up echocardiography, only mild residual MR was detected, and no evidence of SAM of the mitral valve or LVOT obstruction was seen. Comment SAM of the mitral valve is the term that describes anterior motion of one or both mitral valve leaflets during systole. The resulting narrowing or obstruction of the LVOT may be accompanied by MR. SAM was described in early reports of MVRep [13]. In clinical practice, a spectrum of SAM severity is seen, extending from minor, chordalonly SAM to the most severe form with LVOT obstruction. Initially, the LVOT obstruction was thought to be the result of septal hypertrophy producing a Venturi effect that would suck the mitral valve leaflet in the LV cavity [14], but the occurrence is more complex than this. It has been shown that the mitral leaflets are being pushed into the LVOT by a drag force that is produced by the accelerated flow around the hypertrophied septum [15]. Despite numerous descriptions of preventive techniques [16 19], SAM continues to occur in a small percentage of patients undergoing MVRep. Assessment for SAM is an integral part of echocardiographic evaluation after MVRep. A previous review from our institution of 2,076 patients having MVReps indicated that postoperative SAM was seen mainly in patients with degenerative mitral valve disease who had an annuloplasty ring placed as part of their reconstruction [3]. Medical management, including volume loading, vasoconstriction, and -blockade, often eliminated SAM in the early postoperative period, and frequency of SAM diminished further with ventricular remodeling in many patients. Reoperation for SAM late after MVRep is rare [5 7]. Many techniques have been described to manage this problem, including sliding plasty of the posterior leaflet, posterior leaflet shortening, and even prosthetic replacement. Carpentier identified various features as risk factors for SAM, including excess tissue, high posterior leaflet, hyperkinetic heart, extensive quadrangular resection of the posterior leaflet, closed aortic-mitral angle, an undersized annuloplasty ring, incorrect orientation of the ring, and a bulging septum [1]. The present series of cases represent 0.6% of 948 isolated MVReps performed between May 2001 and December This experience is similar to the report published by Civelek and associates [20], in which the authors identified 5 of 358 patients (1.4%) over a 2-year period with SAM that occurred after operation and was relieved by septal myectomy. The experience emphasizes the importance of a bulging septum in the pathophysiologic factors of SAM in some patients. Understanding this mechanism and the potential for treatment with transaortic septal myectomy may help preserve the patient s native valve and avoid some of the complex techniques that have been described to treat SAM that may decrease the repair s long-term durability. In contrast to patients with hypertrophic obstructive cardiomyopathy, the cases we describe had little additional hypertrophy in the distal septum and LV free wall, none had significant SAM preoperatively, and none had a family history of hypertrophic cardiomyopathy. Also, no patient had a contact lesion on the septal endocardium indicating preexisting SAM. Hypertrophic cardiomyopathy in elderly patients may be associated with obstruction when septal hypertrophy is combined with

6 ADULT CARDIAC 1432 SAID ET AL Ann Thorac Surg BULGING SUBAORTIC SEPTUM AND SAM AFTER MVRep 2011;91: anterior displacement of the mitral valve (sigmoid septum). Our patients appear to be distinct because only 2 were elderly (69 years and 70 years) and systemic hypertension was not a prominent feature. Also, SAM and LVOT gradients in elderly patients with sigmoid septa tend to be associated with very narrow outflow tracts, anterior displacement of the entire mitral valve apparatus, and a large area of contact between the mitral valve leaflet and the septum. Morphologic features of the septem may differ considerably. Table 1 lists the quantitative measures of the bulging septa in our patients. Of note, the maximum thickness ranged from 1.5 cm to 2.0 cm. We found that the ratio between the basal septal thickness and the midseptum was at least 1.3, and, interestingly, contact was abnormally close between the anterior mitral valve leaflet and the interventricular septum in diastole. Also, the angle between the long axis of the left ventricle and that of the aorta was at least 60 degrees. When the septum in the immediate subaortic area appears unusually thick in a patient undergoing MVRep, the surgeon should consider concomitant subaortic myectomy or additional maneuvers to clarify whether the finding may lead to SAM after repair. In such situations, we perform simultaneous measurement of LV and aortic pressures and stimulate the heart through pharmacologic means (isoproterenol or sodium nitroprusside) or a Brockenbrough maneuver. As illustrated in Cases 2 and 3, it is important to evaluate the subaortic area carefully in patients who manifest SAM early after mitral repair. Identification and treatment with myectomy may eliminate any need for revision of the repair or valve replacement. Conclusion A bulging subaortic septum without dynamic LVOT obstruction can predispose to the development of SAM after MVRep. 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