Ann Thorac Surg 2001;72:1386-1387
© 2001 The Society of Thoracic Surgeons
Case report
Congenital mitral regurgitation from absence of the anterolateral papillary muscle
Kazuhiro Hashimoto, MDa,
Motohiro Oshiumi, MDa,
Hiromitsu Takakura, MDa,
Tatsuumi Sasaki, MDa,
Katsuhisa Onoguchi, MDa
a Department of Cardiovascular Surgery, Saitama Cardiovascular and Respiratory Center, Saitama, Japan
Accepted for publication September 25, 2000.
Address reprint requests to Dr Hashimoto, Department of Cardiovascular Surgery, Saitama Cardiovascular and Respiratory Center, 1696 Itai, Konan-machi, Osato-gun, Saitama, 360-0105, Japan
e-mail: drs-hashimoto{at}mti.biglobe.ne.jp
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Abstract
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A 21-year-old woman had congenital mitral regurgitation. Echocardiography showed absence of the anterolateral papillary muscle and corresponding marginal chordae. This rare abnormality was corrected by anterolateral commissural annuloplasty and insertion of artificial chordae to prevent prolapse of the anterior leaflet. Postoperatively, there was no regurgitation, and an appropriate mitral valve area was achieved.
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Introduction
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Absence of one papillary muscle for the mitral valve is rare. In patients with this condition, all of the chordae tendineae are usually inserted into a single papillary muscle, ie, the so-called parachute mitral valve [1–3]. The absence of one papillary muscle with normal positioning of the other is a different, but rare, mitral deformity [4, 5].
A 21-year-old woman had a ventricular septal defect (with spontaneous closure) and mitral regurgitation as a child. She was referred to our hospital for detailed examination. Transthoracic and transesophageal echocardiography showed massive anterolateral mitral regurgitation. The posteromedial papillary muscle was positioned normally and controlled the posteromedial half of both leaflets. Protrusions on the anterolateral ventricular wall were not a papillary muscle and became indistinct during scanning, particularly during diastole (Fig 1). The corresponding half of the anterior leaflet prolapsed heavily, and no chordae were visible (Fig 1). Cardiac catheterization showed severe grade 4 mitral regurgitation with normal left ventricular function. Although the patient was asymptomatic, she had an operation because of the severity of regurgitation and because she hoped to become pregnant later.
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Fig 1. Preoperative transesophageal echocardiograms. (AL = anterior leaflet; ALC = anterolateral commissure; PL = posterior leaflet; PMC = posteromedial commissure; PMPM = posteromedial papillary muscle.)
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The right lateral wall of the left atrium was incised through a median sternotomy under normothermic cardiopulmonary bypass. The posteromedial part of the mitral valve apparatus (papillary muscle, chordae, and leaflets) was normal in shape and position, but the anterolateral papillary muscle and the marginal chordae for this part of both leaflets were absent. The anterolateral portion of the anterior leaflet lacked support by the chordae and showed severe prolapse. The posterior leaflet had basal chordae, which prevented apparent prolapse, and was not attached to the left ventricular wall (Fig 2). The anterolateral part of the commissure was moderately fused. The corresponding half of both the anterior and posterior leaflets was thickened but normal in size. Two artificial chordae were created from CV4 polytetrafluoroethylene sutures and placed between the edge of the anterior leaflet and the posteromedial papillary muscle (Fig 2). Anterolateral commissural annuloplasty was also done to reduce the enlarged annulus to a diameter of 27 mm. No valve ring was inserted because of the unusual architecture of the mitral valve and the subvalvular apparatus. The patient’s recovery was uneventful. Echocardiography at 11 months postoperatively showed no recurrence of mitral regurgitation, and the mitral valve area was 3.2 cm2 (Fig 3).
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Fig 2. Surgical findings and procedures. (AC = artificial chordae; AL = anterior leaflet; PL = posterior leaflet; PMPM = posteromedial papillary muscle.)
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Fig 3. Postoperative transesophageal echocardiograms. (AL = anterior leaflet; ALC = anterolateral commissure; PL = posterior leaflet; PMC = posteromedial commissure.)
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Comment
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Our patient had a congenitally abnormal mitral valve, which was classified as type 3 (subvalvar, papillary muscle) agenesis according to the congenital heart surgery nomenclature of The Society of Thoracic Surgeons [6]. The type 3 defect is characterized by the absence of a papillary muscle, usually agenesis of the anterolateral papillary muscle, as reported previously [4]. The so-called parachute mitral valve, in which all of the chordae are attached to a single papillary muscle arising from the posterior ventricular wall, is also classified as type 3 but is actually regarded as a separate category. In a postmortem series of 49 cases of congenital mitral stenosis, Ruckman and Van Praagh [3] reported that 4 patients had a single papillary muscle categorized as a parachute mitral valve. The anterolateral papillary muscle is usually missing, and the arrangement of the solitary papillary muscle varies [1, 2]. Because of the uncertainty of previous classifications of parachute valve or solitary papillary muscle (either from fusion of the two papillary muscles or an actual solitary muscle) and the variable location of the single papillary muscle in the ventricle, the true incidence of this abnormality remains unknown. Becker and Anderson [4] described cases similar to ours, in which a single papillary muscle was grossly hypoplastic and displaced to the parietal ventricular wall, so its commissure was attached more or less directly to the ventricular anterolateral free wall. Although we could not identify a rudimentary papillary muscle, their cases and ours are similar. In a report on surgical cases of congenital mitral malformation, Carpentier and associates [5] included two cases of papillary muscle agenesis. In one case, the patient had an absent posteromedial papillary muscle with direct insertion of the chordae into the posteromedial ventricular wall. The abnormal chordae and posterior leaflet were resected, followed by approximation of the leaflets. In the other patient, both papillary muscles were absent, and numerous chordae arose from the myocardial wall. That patient had prosthetic valve replacement. Our patient had no papillary muscle and no marginal chordae on one side of the commissure with pure mitral regurgitation, a unique situation. Torn chordae occasionally disappear eventually, which can be difficult to differentiate from agenesis, but we believe that our patient actually had agenesis. The creation of a new commissure and suspension of the leaflets from the posteromedial papillary muscle by inserting artificial chordae shifted the unusual orifice posteromedially (Fig 3) but achieved precise coaptation and a nonstenotic orifice.
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References
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Shone J.D., Sellers R.D., Anderson R.C., Adams P., Jr, Lillehei C.W., Edwards J.E. The developmental complex of "parachute mitral valve," supravalvular ring of left atrium, subaortic stenosis, and coarctation of aorta. Am J Cardiol 1963;11:714-725.[Medline]
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Rosenquist G.C. Congenital mitral valve disease associated with coarctation of the aorta. A spectrum that includes parachute deformity of the mitral valve. Circulation 1974;49:985-993.[Abstract/Free Full Text]
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Ruckman R.N., Van Praagh R. Anatomic types of congenital mitral stenosis: report of 49 autopsy cases with consideration of diagnosis and surgical implication. Am J Cardiol 1978;42:592-601.[Medline]
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Becker A.E., Anderson R.H. Atrioventricular valve malformations. In: Becker A.E., Anderson R.H., eds. Pathology of congenital heart disease. London: Butterworths, 1981:140-152.
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Carpentier A., Branchini B., Cour J.C. Congenital malformation of the mitral valve in children. Pathology and surgical treatment. J Thorac Cardiovasc Surg 1976;72:854-866.[Abstract]
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Society of Thoracic Surgeons. Congenital heart surgery. Nomenclature and database project. Mitral valve disease. Ann Thorac Surg 2000;69:S132-S146.[Abstract/Free Full Text]
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