Asian Cardiovasc Thorac Ann 2002;10:248-250
© 2002 Asia Publishing EXchange Pte Ltd
Patch Enlargement of the Posterior Mitral Leaflet in Ischemic Regurgitation
Felipe Rendón, MD,
José I Aramendi, MD,
David Rodrigo, MD1,
Christian Baraldi, MD,
Pablo Martínez, MD
Division of Cardiac Surgery
1 Division of Cardiology Hospital de Cruces Barakaldo, Spain
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For reprint information contact: José I Aramendi, MD Tel: 34 94 600 6339 Fax: 34 94 600 6076 email: jiaramendi{at}hcru.osakidetza.net Division of Cardiac Surgery, Hospital de Cruces, Cruces, Barakaldo 48903, Spain.
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ABSTRACT
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We discuss our early experience in 2 patients with a patch enlargement technique for treating chronic ischemic mitral regurgitation due to restricted motion of the posterior mitral leaflet. This technique corrects the restricted motion and offers better coaptation without compromising the mitral orifice.
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INTRODUCTION
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The outlook for patients with chronic ischemic mitral regurgitation (IMR) is substantially worse than that for regurgitation from other causes1 because IMR is usually due to left ventricular (LV) dysfunction resulting from myocardial infarction. The causes of IMR include annular dilatation, abnormal annular motion, papillary muscle dysfunction, and retraction of the papillary muscle secondary to necrosis with subsequent lack of coaptation of the leaflet edges.2 The hospital mortality of mitral valve replacement in IMR cases can be as high as 15% or even more,3 but this approach is still preferred because of the apparent complexity of valve repair. Mitral valvuloplasty is an established treatment of IMR. Mitral ring annuloplasty, commissuroplasty, and Alfieri stitch have been tried with varying success.4 A frequent reason for failed surgical repair is the lack of sufficient leaflet tissue to obtain a perfect coaptation without compromising the mitral orifice.
We present our early experience in 2 patients with a recently developed method5 for treating IMR using a bovine pericardial patch to partially enlarge the posterior mitral leaflet (PML).
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CASE REPORTS
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Patient 1 was a 43-year-old woman with a body surface area of 1.49 m2, Canadian Cardiovascular Society class III angina pectoris, New York Heart Association (NYHA) functional class III heart failure, and a Euroscore of 3. Transthoracic echocardiography (Figure 1A
) showed severe mitral regurgitation (MR) secondary to restricted PML motion in systole. There was no dilatation of the left ventricle; left ventricular ejection fraction (LVEF) was 62% and end-diastolic and systolic diameters (LVEDD and LVESD) were 52 mm and 33 mm, respectively. Mild tricuspid regurgitation and a pulmonary artery pressure of 42 mm Hg were found. She underwent coronary artery bypass grafting (CABG) of the right internal thoracic artery to the right coronary artery, together with mitral plasty as described later. She was in NYHA class I and free from angina 10 months after surgery. Transesophageal echocardiography (Figure 1B) showed a good opening of the mitral orifice and normal coaptation of the mitral leaflets, with LVEF of 64%, LVEDD 52 mm, and LVESD 34 mm.
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Figure 1. (A) Preoperative echocardiogram showing restricted motion of the posterior mitral leaflet (arrow), while the anterior leaflet reached the level of the annulus. (B) Postoperative echocardiogram showing visible pericardial patch (arrow), good leaflet coaptation, and no regurgitation.
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Patient 2 was a 67-year-old man with a body surface area of 1.83 m2. He was in Canadian Cardiovascular Society class III and NYHA class III and had a Euroscore of 7. Transthoracic echocardiography showed severe MR secondary to restricted PML motion. There was apical, septal, anterior, and anterolateral dyskinesia of the ventricular walls with moderate dilatation of the left ventricle. LVEF was 37%, LVEDD 62 mm, and LVESD 42 mm. Dobutamine stress echocardiography showed improvement in ventricular contractility. He underwent sequential CABG of the saphenous vein to the posterior descending, obtuse marginal, and first diagonal arteries, together with mitral repair. He was in NYHA class I and free from angina 7 months after surgery. Transesophageal echocardiography revealed a good opening of the mitral orifice and normal coaptation of the mitral leaflets, with LVEF of 50%, LVEDD 58 mm, and LVESD 39 mm.
In both patients, a median sternotomy was performed, and cardiopulmonary bypass was established with aortic perfusion, bicaval cannulation, and venting of the left ventricle under moderate systemic hypothermia. Cold blood cardioplegia was given antegradely and retrogradely every 20 minutes, and terminal warm blood cardioplegia was infused before declamping the aorta. After performing distal coronary anastomoses, the left atrium was approached through the interatrial groove, and the mitral valve was exposed and examined. The medial half of P2, the entire P3, and the posteromedial commissural leaflet were detached from the mitral annulus (Figure 2). Mattress sutures for ring implantation were placed in the posterior mitral annulus. A patch of bovine pericardium (Edwards Lifesciences, Irvine, CA, USA) of approximately 50 x 14 mm was cut into a sickle shape and sewn in the PML defect with continuous 5/0 polypropylene sutures. Finally, a Carpentier Physioring mitral annuloplasty ring (Edwards Lifesciences, Irvine, CA, USA) of 28 mm for patient 1 and 30 mm for patient 2 was attached. Transesophageal echocardiography was performed before and at the end of cardiopulmonary bypass.
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Figure 2. Operative image at the completion of repair with a pericardial patch (arrow), showing good leaflet coaptation. The ventricle is filled with saline.
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DISCUSSION
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Some degree of MR is found in approximately 30% of patients with coronary artery disease who are considered for CABG. In most cases, MR is mild; but in the small percentage with severe MR (3% in one large series), the prognosis is poor.2
Three types of anatomical lesions can be found in MR of ischemic origin: rupture of the head of the papillary muscle, which causes acute MR that is not amenable to surgical repair; and annular dilatation and restricted motion in systole of the PML in chronic IMR. Annular dilatation is due to LV dilatation in long-term ischemic cardiomyopathy and is easily corrected with ring annuloplasty, as in any other causes of LV dilatation. Restricted motion constitutes the genuine type of IMR and poses a real challenge to the surgeon. When inspected, the valve looks essentially normal: the annulus is not dilated, and the leaflets and chordae are normal with no elongation or prolapse. The main feature is the dilatation of the inferior wall secondary to myocardial infarction or, more rarely, ischemia affecting the posteromedial papillary muscle (PPM). The PPM moves away from the annular plane pulling the chordae in systole, thus restricting leaflet motion. The free edge of half of the PML corresponding to P2 and P3 does not reach the annular plane, and this produces asymmetrical coaptation, resulting in severe regurgitation. The anterior mitral leaflet is not affected, nor the P1 portion of the PML, whose chordae run from the anterior papillary muscle.
An annuloplasty ring alone cannot restore valvular competence in this type of lesion. Repairing valves with this asymmetric geometry requires readjustment of the leaflet excursion with respect to the papillary muscle–annulus relationship. One way to achieve this is to detach the PPM from the LV wall and reattach it more proximally to the annulus in the LV free wall, as reported by Carpentier.6 This technique is seldom reproducible, except in very expert hands, as it is difficult to ascertain the exact place to reimplant the PPM and the muscle-to-muscle suture is highly friable. Another is to increase the posterior leaflet surface area using extension plasty with the pericardium.7 By enlarging the leaflet area by 1 cm, the deviation of the PPM from the valvular plane is compensated for, bringing the leaflet edges closer together, thereby allowing coaptation to occur more readily.
Patch enlargement of the PML in IMR may restore both the normal extent of the mitral leaflet coaptation and PML motion. We selected the bovine pericardial patch instead of an autologous pericardium as the material of choice because it is easier to handle, shrinks less, and provides durable and predictable repair.7 Because the area affected is localized in the medial half of P2 and the entire P3, while the rest of the leaflet is normal, the pericardial patch was designed to enlarge just this area. The length is dictated by the distance between the midpoint of the posterior mitral annulus and the right fibrous trigone (usually about 50 mm). Following Dobre and colleagues,5 we selected a width of 14 mm to provide an enlargement of about 10 mm, taking into account a loss of about 2 mm of the patch on either side of the suture line. The annuloplasty ring is mandatory in all cases for it restores the shape of the orifice and prevents further annular dilatation.
Although our experience with patch enlargement in IMR is still short, we are convinced that this technique is easy to reproduce and applicable in the majority of patients with restricted leaflet motion. Most series that used repair techniques could not show any improvement mainly because there was no reliable and reproducible technique that provides an anatomic and physiologic correction of the restricted motion of the PPM.1,8 The patch enlargement repair technique, coupled with the use of a mitral annuloplasty ring, offers an excellent alternative to valve replacement, and we think it could become in the future the technique of choice to resolve the complex problem that causes IMR.
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REFERENCES
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- Cohn LH, Rizzo RJ, Adams DH, Couper GS, Sullivan TE, Collins JJ Jr, et al. The effect of pathophysiology on the surgical treatment of ischemic mitral regurgitation: operative and late risks of repair versus replacement. Eur J Cardio-thorac Surg
1995;9:568–74.[Abstract]
- Tcheng JE, Jackman JD Jr, Nelson CL, Gardner LH, Smith LR, Rankin JS, et al. Outcome of patients sustaining acute ischemic mitral regurgitation during myocardial infarction. Ann Intern Med
1992;117:18–24.
- Akins CW, Hilgenberg AD, Buckley MJ, Vlahakes GJ, Torchiana DF, Daggett WM, et al. Mitral valve reconstruction versus replacement for degenerative or ischemic mitral regurgitation. Ann Thorac Surg
1994; 58:668–76.[Abstract]
- David TE. Techniques and results of mitral valve repair for ischemic mitral regurgitation. J Card Surg
1994;9 (Suppl 2):274–7.[Medline]
- Dobre M, Koul B, Rojer A. Anatomic and physiologic correction of the restricted posterior mitral leaflet motion in chronic ischemic mitral regurgitation. J Thorac Cardiovasc Surg
2000;120:409–11.[Free Full Text]
- Deloche A, Jebara VA, Relland JY, Chauvaud S, Fabiani JN, Perier P, et al. Valve repair with Carpentier techniques. The second decade. J Thorac Cardiovasc Surg
1990;99:990–1002.[Abstract]
- Ng CK, Nesser J, Punzengruber C, Pachinger O, Auer J, Franke H, et al. Valvuloplasty with glutaraldehyde-treated autologous pericardium in patients with complex mitral valve pathology. Ann Thorac Surg
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- Dion R, Benetis R, Elias B, Guennaoui T, Raphael D, Van Dyck M, et al. Mitral valve procedures in ischemic regurgitation. J Heart Valve Dis
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ABSTRACT
INTRODUCTION
