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Ann Thorac Surg 2005;80:179-182
© 2005 The Society of Thoracic Surgeons

Original article: Cardiovascular

Prevention of Systolic Anterior Motion After Repair of the Severely Myxomatous Mitral Valve With an Anterior Leaflet Valvuloplasty

Robert L. Quigley, MD, PhD*

Albert Einstein Medical Center, Jefferson Health System, Philadelphia, Pennsylvania

Accepted for publication January 7, 2005.

* Address reprint requests to Dr Quigley, Division of Cardiothoracic Surgery, Albert Einstein Medical Center-Jefferson Health System, 5501 Old York Rd, Levy 3 East, Philadelphia, PA19141 (Email: quigleyr{at}einstein.edu).

Presented at the Fifty-first Annual Meeting of the Southern Thoracic Surgical Association, Cancun, Mexico, Nov 2–4, 2004.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Comment
 Discussion
 References
 
BACKGROUND: Systolic anterior motion after mitral valve repair of severely myxomatous valves is due to excess tissue or anterior displacement, or both, of the leaflet coaptation point. Our series of anterior leaflet valvuloplasty, an alternative to the sliding leaflet technique to prevent systolic anterior motion, is presented.

METHODS: Between January 1, 1996 and January 6, 2003, we performed elliptical excisions of the base of the anterior leaflet in 47 patients with a mean age of 66 years (range, 29 to 86). All patients had an anterior leaflet height of 3.0 cm or more and an annular diameter of 4.0 cm or more. Repairs included posterior leaflet (37; 80%), and anterior leaflet (28; 61%) resections, with occasional transposition flaps (9; 19%). All 47 (100%) had an annuloplasty ring (9, Physio; 37, Seguin). Four (8%) included tricuspid repair, 6 (13%) aortic valve replacement, and 9 (19%) coronary artery bypass. Follow-up was between 2 months and 8 years.

RESULTS: There was no systolic anterior motion or in-hospital (30-day) mortality. Postoperative echocardiography revealed an average anterior leaflet height of 2.2 ± 0.3 cm, with an annular diameter of 3 ± 0.2 cm. The anterior/posterior leaflet ratio decreased from 1.6 ± 0.2 to 1.4 ± 0.1 cm while the coaptation point–annular plane distance decreased from 1.2 ± 0.2 to 0.9 ± 0.1 cm. There were 4 late noncardiac deaths. Two patients have required mitral valve replacement owing to progressive disease and 6 patients were lost to follow-up. The 35 patients remaining have trace-mild mitral regurgitation.

CONCLUSIONS: Our anterior mitral valve leaflet valvuloplasty, regardless of the ring, results in a decrease in surface area and excursion of the anterior leaflet without systolic anterior motion.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Comment
 Discussion
 References
 
The incidence of systolic anterior motion (SAM) after repair of the myxomatous mitral valve ranges from 2% to 16% [1]. Although multiple theories have been proposed relating SAM to abnormalities of the mitral valve (MV) apparatus, ultimately it was suggested that a relatively large posterior mitral valve leaflet (PMVL) may coapt with the anterior mitral valve leaflet (AMVL) closer to its base and cause both an anterior shift of the coaptation point and an increase in the amount of redundant leaflet tissue in the left ventricular outflow tract (LVOT) [2]. Consequently, the traditional surgical approach to prevent SAM and LVOT obstruction has focused on a PMVL sliding valvuloplasty and an oversize of the annuloplasty ring [3, 4]. Unfortunately, these techniques do not consistently eliminate SAM after mitral valve repair (MVR).

Grossi and colleagues [5] were the first to challenge this theory and proposed triangular resection of the AMVL to reduce the incidence of SAM in this context. The hypothesis of a large redundant AMVL as the primary etiology of SAM has more recently been supported by Shah and Raney [6], who recommend reduction of the AMVL height to prevent SAM.

As early as 1995, we recognized the significance of the AMVL in postrepair SAM in 3 patients with severely myxomatous valves, and subsequently defined a simple AMVL valvuloplasty to reduce AMVL height and eliminate postrepair SAM precluding mitral valve replacement [7]. Using previously described echocardiographic morphologic determinants of SAM, in this report, we objectively evaluate the efficacy of this procedure in a cohort of patients with complex floppy mitral valves [1].


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Comment
 Discussion
 References
 
Patients
Between January 1996 and June 2003, 296 MVR were performed at our institutions for the correction of mitral insufficiency. Etiologies included myxomatous degeneration, endocarditis, ischemia, and rheumatic valve disease. Forty-seven (16%) of these patients had complex floppy mitral valves (Barlows), the definition of which is provided in Figure 1. The characteristics of this cohort are listed in Table 1 [8].



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  		Fig 1. The complex floppy mitral valve (Barlows). Anterior mitral valve leaflet ≥ 2.7 cm; posterior mitral valve leaflet ≥ 1.5 cm; annular diameter ≥ 3.2 cm.

 

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  		Table 1. Patient Characteristics
 
Surgical Procedures
All 47 patients, considered to be at risk for postoperative SAM, underwent elliptical excisions at the base of the AMVL (Fig 2). Preoperatively, at end diastole, the AMVL height (distance from the anterior annular plane to the leading edge or rough zone) was measured (AMVL-A). After intraoperative exposure of the mitral valve, the complete AMVL surface was exposed and measured with the use of two nerve hooks secured at the rough zone (AMVL-B). The maximum height of the eliptical excision was determined by subtracting AMVL-A from AMVL-B. Simply closing this incision (which on average consumes 6 minutes of cross-clamp time) primarily, with a double-layer 5-0 Prolene stitch (Ethicon, Somerville, NJ) reduces the AMVL height by approximately 5 mm. This site on the body of the AMVL was selected as it is invariably void of any secondary chordal attachments.



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  		Fig 2. Elliptical excision at base of anterior mitral valve leaflet (left atrial view).

 
Each case included an annuloplasty ring, the size of which was selected on the surface area of the AMVL (after reduction) rather than the intertrigonal distance. The surface area corresponded to the "sizers" provided by the manufacturer. The semiflexible rings were either Physio (9; 19% [Baxter Edwards, Irvine, California]) or Seguin (38; 81% [St. Jude Medical, St. Paul, Minnesota]). In addition to the ring and the elliptical excision of the base of the AMVL, 37 patients (80%) had a quadrangular resection of the PMVL, 28 (61%) a triangular resection of their AMVL for small flail segments, and 9 (19%) transposition flaps (competent PMVL segments transposed to the atrial surface of large flail AMVL segments that could not be resected with triangular resections). After quadrangular resection of the PMVL, none of the reconstructions included leaflet advancement (sliding plasty) in this cohort. The PMVL was reconstructed at the annular level with two pledgetted horizontal mattress nonabsorbable 4-0 sutures and at the leaflet level with both simple and running nonabsorbable 5-0 sutures. Similarly, plication of the annulus was not performed.

Echocardiography
The mitral valve was assessed both preoperatively and postoperatively using transesophageal echocardiography from the transverse five-chamber views, as described by Lee and coworkers [9], at the end of diastole. The preoperative and postoperative severity of mitral regurgitation was quantified, and the postoperative presence of SAM evaluated [10]. Preoperatively, the anatomic defect responsible for the mitral regurgitation was identified with multiplane transesophageal echocardiography, as were the dimensions of the subvalvular apparatus (AMVL, PMVL, and CPAD [the distance between the leaflet coaptation point and the annular plane]). The leaflets were measured in the coaptive position (annulus to coaptation edge). After implantation of the ring, the annular diameter was made from the inner aspects of this prosthesis.

Results
All 47 patients were successfully weaned from cardiopulmonary bypass with trace or mild mitral regurgitation and no SAM. Table 2 compares the preoperative and postoperative echocardiographic morphologic variables that were quantified. There were no perioperative myocardial infarctions or deaths within 30 days. The mean cardiopulmonary bypass time was 91 ± 26 minutes with a mean cross-clamp time of 76 ± 14 minutes. There were no clinically significant gradients across the mitral valve after the repair. All patients were followed up annually with echocardiography, and to date, only 2 have required reoperation for symptomatic recurrent mitral regurgitation. Six patients were lost to follow-up, however, and 4 have died from unrelated medical conditions.


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  		Table 2. Echocardiographic Morphologic Variables
 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Comment
Discussion
 References
 
In our experience with MVR, we analyzed the mitral valve anatomy of those 3 patients in whom intraoperative postrepair SAM and LVOT developed. Although the incidence was less than 5%, we noted that all had elongated AMVL (≥ 2.7 cm), elongated PMVL (≥ 1.5 cm), and annular dilatation (≥ 3.2 cm). Those 3 affected patients diagnosed with SAM intraoperatively after repair, and who were refractory to fluid challenges or inotrope withdrawal, underwent revision of their MVR with an elliptical AMVL valvuloplasty. In all such cases, intraoperative transesophageal echocardiography not only revealed resolution of SAM, but also of the associated mitral regurgitation. There were no cases of SAM diagnosed postoperatively after exit from the operating room. In this study, 47 patients with the described mitral valve characteristics prospectively had this AMVL valvuloplasty in addition to their repair, and none experienced SAM postoperatively. Coincidentally, none of the other 249 MVR cases performed during this same period experienced postrepair SAM.

Although there is some controversy in the literature as to the exact mechanism of SAM and LVOTO after MVR, most authors concur that a postoperative increase in the CPAD increases the likelihood of this complication [1, 2]. As indicated in this report, this increase in the CPAD is related predominately to AMVL length [5, 6, 11] and to a lesser extent to PMVL [9, 12].

Mihaileanu and colleagues [4] have suggested that the etiology of LVOTO after MVR is multifactorial and may include narrowing of the mitroaortic angle. It is interesting that some of our patients who experienced LVOTO after MVR, before this study, did have a dilated cardiomyopathy and by definition widened mitroaortic angles. The LVOTO observed in these cases was after a significant reduction annuloplasty. This observation justified our prophylactic AMVL elliptical valvuloplasty, even in those patients with depressed left ventricle function and coincidental left ventricular dilatation.

The results of this study suggest that transesophageal echocardiography analysis of the mitral valve apparatus can identify patients who have a severely myxomatous mitral valve, likely to develop SAM/LVOTO after MVR. Furthermore, a simple elliptical excision at the base of the AMVL, at least in this series, not only eliminated the need for the time-consuming and sometimes complicated sliding posterior leaflet procedure previously thought to be indicated in this clinical scenario, but also avoided mitral valve replacement. Finally, this technique eliminates SAM without compromising flow across the mitral valve apparatus, which can occur with the Alfieri stitch recently proposed for the same purpose [13].


   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Comment
 Discussion
References
 
DR JOHN D. OSWALT (Austin, TX): I enjoyed your paper very much and actually have spoken with Aidan Raney about this technique, as he has also described it or had a paper on it there in California. I am a little bit surprised that we have had to go to finding another technique to avoid SAM. There are the previous techniques that we have learned with the sliding plasty making sure we reduce the height of the posterior leaflet and measurement of the height of the anterior leaflet and proper ring size selection.

In our practice, we basically don’t see SAM at all. So I am interested in knowing is there something else that is missing there to produce this higher incidence of SAM that would make you develop a new technique to avoid it?

DR QUIGLEY: Your point is well taken. I want to emphasize that the historic or traditional thinking has been that the etiology of SAM, particularly in this subset of patients with severely myxomatous floppy mitral valves, is a high-riding posterior leaflet. In my primitive mind, I kept having difficulty with that concept, even though I was reprimanded by Professor Carpentier when I challenged his theory, because it was his original theory. I kept thinking that it is the anterior leaflet that actually obstructs the outflow tract, and so if I could somehow modify the surface area and the excursion of the anterior leaflet, I could then avoid doing the sliding plasty, which I used to do in my earlier career.

I found, as I mentioned at the beginning of the talk, that it was somewhat laborious, and in that particular subset of patients, we weren’t getting a hundred percent prevention of SAM. Even one case of SAM can be devastating, and that was the reason why this particular procedure was undertaken and then prospectively evaluated over an 8-year period.

DR JOHN H. CALHOON (San Antonio, TX): I enjoyed your presentation. I probably didn’t fully understand it. It was pretty complex. My question is how often did you see SAM in this group, or did you just adopt this technique so that you would no longer see SAM? What was your percentage of SAM before you did this, for instance?

DR QUIGLEY: Our incidence of SAM in that population of patients, and we were seeing a lot of that population of patients in the mid to late 1990s, was less than 10%; it was somewhere between 6% and 8%. In the presentation I included one of the original cases on video. It was the original preoperative video, then in the immediate postrepair video there was SAM, and then that same case, after we had left the ring intact and done our elliptical excision the SAM and outflow tract obstruction resolved along with the associated mitral regurgitation. After having several of these patients, it was then we decided to proactively go ahead and do this procedure on all of the patients who met those criteria that I previously discussed.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Comment
 Discussion
 References
 

  1. Maslow AD, Regan MM, Haering JM, et al. Echocardiographic predictors of left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease J Am Coll Cardiol 1999;34:2096-2104.[Abstract/Free Full Text]
  2. He S, Hopmeyer J, Lefebvre XP, et al. Importance of leaflet elongation in causing systolic anterior motion of the mitral valve J Heart Valve Dis 1997;6:149-159.[Medline]
  3. Carpentier A. The sliding leaflet technique Le Club Mitral Newsletter. 1998August.
  4. Mihaileanu S, Marino JP, Chauvaud S, et al. Left ventricular obstruction after mitral valve repair (Carpentier’s technique)proposed mechanisms of disease. Circulation 1998;78(Suppl 1):78-84.
  5. Grossi EA, Steinberg EM, LeBoutillier M, et al. Decreasing incidence of systolic anterior motion after mitral valve reconstruction Circulation 1994;90:195-197.[Abstract/Free Full Text]
  6. Shah PM, Raney AA. Echocardiographic correlates of left ventricular outflow obstruction and systolic anterior motion following mitral valve repair J Heart Valve Dis 2001;10:320-326.[Medline]
  7. Quigley RL, Stagl RD. Alternative approach to the repair of a floppy anterior mitral valve leaflet J Heart Valve Dis 1995;4:208-210.[Medline]
  8. Freed LA, Levy D, Levine RA, et al. Prevalence and clinical outcome of mitral valve prolapse N Engl J Med 1999;34:1-7.
  9. Lee KS, Stewart WJ, Lever HM, et al. Mechanisms of outflow tract obstruction causing failed mitral valve repair Circulation 1993;88:4-29.[Free Full Text]
  10. Grigg LE, Wigle ED, Williams WG, et al. Transesophageal Doppler echocardiography in obstructive hypertrophy cardiomyopathyclarification of pathophysiology and importance in intra-operative decision making. J Am Coll Cardiol 1992;20:42-52.[Abstract]
  11. Reed MK, Iverson LIG. Simplified correction of outflow obstruction after mitral valve repair Ann Thorac Surg 1992;54:985-986.[Abstract]
  12. Jebara VA, Mihaileanu S, Acar C, et al. Left ventricular outflow tract obstruction after mitral valve repair Circulation 1993;88:30-34.
  13. Gillinov AM, Amedira NG, Shiota T. Use of the Alfieri edge-to-edge technique to eliminate left ventricular outflow tract obstruction caused by mitral systolic anterior motion Ann Thorac Surg 2004;78:1484-1485.[Abstract/Free Full Text]



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