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J Thorac Cardiovasc Surg 2007;133:136-143
© 2007 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Division of Cardiovascular Surgery, Mayo Clinic, Rochester Minn
b Division of Anesthesiology, Mayo Clinic, Rochester Minn
c Division of Cardiovascular Medicine, Mayo Clinic, Rochester Minn
d Division of Cardiology, Exeter Hospital, Exeter, NH.
Read at the Thirty-second Annual Meeting of the Western Thoracic Surgical Association, Sun Valley, Idaho, June 21-24, 2006.
Received for publication June 19, 2006; revisions received September 2, 2006; accepted for publication September 20, 2006. * Reprint requests: Harzell V. Schaff, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. (Email: Schaff{at}mayo.edu).
| Abstract |
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METHODS: We performed a retrospective chart review and survey follow-up of all patients in whom systolic anterior motion developed intraoperatively after mitral valve repair.
RESULTS: From January 1993 to December 2002, mitral valve repair was performed in 2076 patients, and in 174 cases (8.4%) systolic anterior motion was identified on intraoperative echocardiography. These patients form the study group. Initially, patients were managed with a combination of ß-blockade, vasoconstriction with phenylephrine, and/or intravascular volume expansion. Four patients had revision of repair because of persistent systolic anterior motion, and 3 additional patients had revision of repair because of mitral regurgitation from other causes. The median follow-up of the remaining 167 patients was 5.4 years (range 0-13.2 years). There were 2 late reoperations, but none were caused by systolic anterior motion or left ventricular outflow tract obstruction. Ninety percent of patients were in New York Heart Association class I, 7% were in class II, and 3% were in class III or IV. Echocardiograms were available for review in 93 patients at a median interval of 5.4 years (range 0.2-12.2 years); 13 patients had systolic anterior motion, and 4 patients had systolic anterior motion with left ventricular outflow tract obstruction.
CONCLUSIONS: In this experience, most cases of systolic anterior motion resolved with conservative measures including ß-blockade, vasoconstriction, and fluid administration. Persistent systolic anterior motion with left ventricular outflow tract obstruction was documented in 2.3% of patients who had early systolic anterior motion, but late reoperation was not required. Furthermore, the clinical outcomes of patients with systolic anterior motion are comparable to the current norms for mitral valve repair. Ninety percent of patients were in New York Heart Association class I, 7% were in class II, and 3% were in class III or IV.
| Introduction |
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The complication of systolic anterior motion (SAM) was described in early reports of mitral valve repair.6
The degree of SAM extends along a continuous spectrum from minor chordal-only SAM to its most severe form with left ventricular outflow tract obstruction (LVOTO). Despite numerous descriptions of preventative techniques,7-10
SAM continues to occur. The management of SAM in the operating room remains controversial with some groups advocating nonsurgical management11,12
and others proposing direct surgical correction.13-15
At our clinic, patients with SAM have in general been conservatively managed with intravenous volume loading, ß-blockade, increased afterload, and limited administration of inotropic drugs. Our objectives in this study were to determine the incidence of SAM in patients with degenerative mitral valve disease, evaluate the risk of SAM with various surgical techniques, and assess the long-term outcome of nonsurgical management of SAM after mitral valve repair.
| Materials and Methods |
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A cardiologist and/or cardiac anesthesiologist performed intraoperative transesophageal echocardiography (TEE) to evaluate the mitral valve before and after repair. SAM was identified by 2-dimensional echocardiographic imaging of the mitral valve in standard views and was defined as any portion of the mitral valve leaflet or chordal structure that prolapsed into the left ventricular outflow tract (LVOT). Velocities through the LVOT were measured with pulsed and continuous-wave Doppler. The modified Bernoulli equation was used to estimate pressure gradients across the LVOT. LVOTO was considered to exist if SAM was present by 2-dimensional imaging and Doppler velocities in the LVOT were 2.0 m/sec (16 mm Hg) or greater. Mitral regurgitation was graded as none-trivial, mild, moderate, moderate-severe, and severe.
All operations were performed at Mayo Clinic in Rochester, with a standard trans-sternal approach or right anterior thoracotomy. Repair techniques varied on the basis of surgeon preference and mitral valve pathology. All operative reports were reviewed to determine the type of mitral valve repair performed.
In those cases identified with intraoperative SAM, patient records and echocardiograms were further evaluated. Patients who underwent mitral valve re-repair or replacement at the time of operation or in the immediate postoperative period for any cause were examined in detail, but their long-term results were not included with the primary group who did not have further surgical procedures. Surveys designed to assess symptoms to correlate with New York Heart Association (NYHA) functional class were sent to all patients with SAM on intraoperative TEE.
| Results |
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Intraoperatively, 174 patients demonstrated SAM early after mitral valve repair (Table 1). The ages of these patients ranged from 29 to 89 years (median 62 years), and 72% were men. The mean preoperative ejection fraction was 63% ± 6%. Fifty-seven percent of patients had isolated mitral valve repairs. Concomitant coronary artery bypass grafting was performed in 21% of patients, and other cardiac procedures were performed in 25% of patients.
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Patients in whom SAM developed intraoperatively were managed conservatively. This included discontinuing any inotropic drugs, increasing systemic vascular resistance, augmenting intravascular volume, and administering ß-blockade as tolerated.
Revision of repair or valve replacement during initial operation was undertaken in only 4 patients (Table 3). In 2 of these 4 cases, re-repair was required because of imperfect leaflet repair and not because of SAM; 1 patient underwent resection of a residual prolapsing segment of the posterior leaflet, and 1 patient had reinforcing sutures placed at the free edge of the incision in the posterior leaflet. In the other 2 patients, there was little improvement in SAM with medical management, and because of persistent SAM-related mitral regurgitation and the advanced age of the patients (81 and 83 years), the operating surgeon decided to revise the repair with removal of the band in 1 patient and mitral valve replacement in 1 patient.
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The course of the remaining 167 patients who had SAM early after valve repair is shown in Figure 2. There were a total of 165 dismissal echocardiograms performed at a median interval of 5 days postoperatively (range 2-38 days). By the time of predismissal transthoracic echocardiography, SAM had resolved in 105 patients (63%).
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Follow-up was available in 139 patients at a median interval of 4.7 years (range 1.2-11.8 years). Only 34% of patients continued to report ß-blocker use. Ninety percent of patients were in NYHA functional class I. NYHA class II symptoms were present in 7% of patients, and 3% of patients were in NYHA class III and IV.
| Discussion |
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Most patients at risk for SAM had posterior leaflet repair with leaflet plication or resection and a concomitant partial flexible annuloplasty ring (n = 966). Thus, it was not surprising that the largest number of patients with SAM (n = 121) also underwent this repair method. Although other repair techniques were used in smaller numbers of patients, the incidence of SAM was generally similar. It is notable that among 7 patients undergoing quadrangular resection with sliding annuloplasty, SAM developed in 1. With triangular resection of the posterior leaflet, the most common posterior leaflet procedure in our series, sliding annuloplasty, is unnecessary.21
The occurrence of SAM was lowest among patients undergoing anterior leaflet procedures (2 patients), and this is consistent with results from other institutions where anterior leaflet pathology is corrected by limited resection22
or insertion of chordae.8
There were few complete (n = 12) or rigid rings (n = 4) in this series, so it is not possible to correlate the development of SAM with annuloplasty methods. Other reports18,23,24
have suggested that both flexible and rigid complete rings reduce the mitro-aortic angle, thus contributing to SAM. In contrast with other studies,25,26
SAM was not observed in patients in this series who did not have prosthetic bands or ring annuloplasty.
Some authors have identified excessive reduction of annular circumference as a risk factor for SAM.18,27
Certainly, annular reduction with a ring or band seems to be a contributing factor, but our data do not allow a comparison of ring size with the development of SAM. We have, in general, preferred a uniform posterior band of 6.3 cm for most patients. This size is predicated on the normal mitral valve annular circumference of 10 cm and the 2:1 relationship between the segment of the annulus subtended by the posterior leaflet compared with that of the anterior leaflet.
Although we could not determine which, if any, particular technique was a factor in patients outcomes, it is clear that SAM and SAM with LVOTO can occur with a variety of repair techniques. There was no particular identifiable ring or band, rigid or flexible, or size that seemed to greatly influence the outcome. It is likely a combination of patient factors, including the cause of mitral regurgitation and hemodynamic status, and surgical factors, including both repair technique and annuloplasty, that leads to the development of SAM.
Because of the retrospective nature of this study, we cannot access surgical decisions that may have been made to attempt to "prophylactically" eliminate SAM. However, the surgical practice at our clinic has been to conservatively manage patients in whom SAM develops immediately after mitral valve repair with intravenous volume loading, ß-blockade, increased cardiac afterload, and limited use of inotropic drugs.11,12
We have not commonly used methods that others have recommended to prevent SAM, including the sliding leaflet technique,7
transfer of posterior chordae to the anterior leaflet,8
anterior leaflet valvuloplasty,22
the Pomeroy procedure,13
and "edge-to-edge" repair.14,15
The rationale for not using more complex methods to prevent or treat SAM is the clinical observation that SAM improves with hemodynamic manipulation and subsequent ventricular remodeling in most patients. Indeed, among the 174 patients who manifested SAM early after mitral valve repair, only 2 had valve re-repair or replacement because of a lack of significant improvement of the degree of SAM and mitral regurgitation. Age was a factor in deciding to readdress the repair, because 2 patients were aged more than 80 years.
An additional 2 patients required reoperation within 3 weeks for postoperative SAM and LVOTO; 1 patient had associated hemolysis, and 1 patient had moderate-severe mitral regurgitation. It is important to note that SAM improved initially after repair in both patients. Both patients had severe myxomatous disease, and during reoperation 1 patient underwent successful re-repair.
There were no patients in this series who required late reoperation for SAM or SAM with LVOTO. In a recent case report by Zegdi and colleagues,28
redo mitral valve repair was performed 8 years later for SAM and LVOTO causing moderate regurgitation. The rarity of late re-repair in this study supports our clinical impression that SAM with or without LVOTO improves with time and late ventricular remodeling.
Notably, there were no perioperative or postoperative deaths among patients with SAM, and only 2 late deaths were attributable to a cardiac cause. Furthermore, on follow-up, 90% of patients were in NYHA class I. Thus, nonsurgical management was safe and yielded excellent results even among the few patients who had minor degrees of residual SAM or SAM with LVOTO.
Carpentiers group28
have expressed concerns that some repair methods designed to eliminate SAM, such as those that focus on reduction of the height anterior leaflet, are of unproven durability. Indeed, there are few late follow-up studies of such techniques.29
It should be noted that most patients in this series with prolapse of the midportion of the posterior leaflet had repair with triangular resection of the area, and this method, as in quadrangular resection with sliding annuloplasty, reduces the height of the posterior leaflet. Two patients in our series required mitral valve revision during the follow-up period, and 5 patients had moderate-severe or severe mitral valve regurgitation. This is comparable to previously reported late results of our mitral valve repairs for degenerative disease.30
Patients who have SAM after mitral valve repair need consistent cardiology follow-up and medical treatment with ß-blockade and avoidance of afterload-reducing medications that could further worsen SAM and any associated mitral valve regurgitation. We recheck echocardiograms 1 month after dismissal to evaluate the degree of SAM, LVOTO, and/or mitral regurgitation. Patients who have persistent LVOTO should be followed closely until the obstruction resolves. Patients do not generally require lifelong ß-blocker therapy. If LVOTO resolves, ß-blockers may be weaned with follow-up echocardiograms 3 months later. Those who have SAM without LVOTO may be followed clinically at the discretion of a cardiologist unless there is a change in the patients functional status or a new or changing murmur develops, at which point a repeat echocardiogram would be prudent.
SAM is an important cause of mitral regurgitation early after valve repair. Identification and proper treatment with ß-blockade and avoidance of afterload-reducing medications are usually successful, and re-repair is rarely necessary. However, if medical management fails to improve mitral regurgitation, surgeons must be willing to undertake operative revision of the mitral valve repair.
The late outcomes in this series (no mortality and 90% of patients in NYHA class I at late follow-up) support the strategy of nonsurgical treatment of SAM with or without LVOTO.
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