Ann Thorac Surg 1997;63:541-543
© 1997 The Society of Thoracic Surgeons
Case Report
Prosthetic Mitral Valve Replacement: Late Complications After Native Valve Preservation
Eduardo Esper, MD,
Francis D. Ferdinand, MD,
Solomon Aronson, MD,
Robert B. Karp, MD
Section of Cardiac Surgery, Department of Surgery, and Anesthesia and Critical Care, The University of Chicago Hospitals, Pritzker School of Medicine, Chicago, Illinois
Accepted for publication October 15, 1996.
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Abstract
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Preservation of the mitral valve leaflet and tensor apparatus during valve replacement is believed to maintain left ventricular performance. The routine use of this technique may lead to left ventricular outflow or inflow obstruction as illustrated in the present report. We recommend mobilization or excision of the anterior mitral valve leaflet and preservation of the posterior leaflet if replacement of the valve is contemplated for incompetence.
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Introduction
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Mitral valve repair with preservation of the valve and subvalvular apparatus is believed to maintain left ventricular performance [1]. Although in principle, mitral valve replacement for regurgitation or stenosis with conservation of the mitral leaflets and subvalvular apparatus preserves geometry of the left ventricle [13], caution is warranted because routine use of this technique may lead to severe left ventricular outflow tract obstruction (LVOTO) and even mitral inflow obstruction requiring reintervention [4, 5]. In the following report, we describe the physiopathologic findings of 2 patients referred for treatment of severe congestive heart failure after having undergone prosthetic mitral valve insertion with preservation of the mitral leaflets and the subvalvular apparatus.
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Case Reports
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Patient 1
A 50-year-old woman was admitted with chronic congestive heart failure. She had undergone a St. Jude Medical (St. Paul, MN) mitral valve replacement 4 years prior for rheumatic mitral stenosis and regurgitation. Subsequent transthoracic and intraoperative transesophageal echocardiography showed marked biatrial dilatation, moderate right ventricular dilatation, and normal left ventricular size. Echocardiography could not identify prosthetic valve dysfunction although there was a mean gradient across the left ventricular inlet of 20 mm Hg (Figs 1, 2
). There was also severe tricuspid regurgitation. Catheterization revealed no mitral regurgitation and confirmed a transmitral gradient of 20 mm Hg. At operation, the mitral prosthesis seemed normally positioned but the posteriorly oriented half leaflet of the St. Jude valve seemed to be impinged upon by the remaining mitral valve apparatus. After removal of the valve, it was quite clear that the anterior and posterior papillary muscles and most of the tensor and leaflet apparatus of the mitral valve had been left in place in the previous operation, which interfered with function of the posterior leaflet of the prosthesis, causing a cone-like effect to produce mitral stenosis. The remaining native mitral valve apparatus was removed and a 27-mm St. Jude valve inserted. A tricuspid ring Carpentier annuloplasty was performed. Transesophageal echocardiographic images after mitral valve replacement revealed no residual obstruction or regurgitation (see Figs 1, 2
). The patient was discharged asymptomatic after day 7.

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Fig 1. . Diastolic echocardiographic views of patient 1. In the preoperative view through the mitral valve, turbulence of flow can be seen under the prosthesis in an otherwise intact subvalvular apparatus. In the postoperative view, notice no turbulence of flow. (LA = left atrium; LV = left ventricle.)
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Fig 2. . Systolic echocardiographic views of patient 1. In the preoperative view, the arrow points to a regurgitant jet. Postoperative view only demonstrates minimal amount of regurgitant jet typical of a valvular prosthesis. (LA = left atrium.)
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Patient 2
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A 65-year-old woman was referred for treatment of exertional dyspnea, orthopnea, and a large left-sided pleural effusion. Eight weeks before admission she had undergone mitral valve replacement with a porcine bioprosthesis for severe mitral regurgitation. Subsequent surface and transesophageal echocardiograms revealed systolic anterior motion of the anterior mitral leaflet causing LVOTO with a maximum velocity by continuous Doppler echocardiography of 5 m/s and a peak gradient of 100 mm Hg. There was a perivalvular leak along the anterior and posterior mitral bioprosthesis unchanged from an early postoperative echocardiogram. The left ventricle was normal in size and contractility but had severe concentric hypertrophy. The left atrium was markedly enlarged. Right-sided chambers were grossly normal. Cardiac catheterization revealed normal coronary arteries and an ejection fraction by biplane ventriculography of 0.69. A simultaneous three-catheter left-sided waveform analysis demonstrated a 100 mm Hg gradient within the left ventricular outflow tract (Fig 3
). Intraoperative transesophageal echocardiography demonstrated LVOTO/systolic anterior motion. Viewed through a left atriotomy, the porcine mitral prosthesis was well seated with the exception of a tiny perivalvular leak anteriorly. After removal of the porcine bioprosthesis, the native mitral valve was evident in both its anterior and posterior leaflets. Both had been left untouched during the previous operation, and no leaflet, chordae, or papillary muscle resection had been done. The anterior tensor apparatus seemed positioned quite anteriorly, clearly projecting into the left ventricular outflow tract. We resected in toto the anterior and most of the posterior leaflet of the mitral valve leaving a few posterior chordal remnants. A 29-mm St. Jude mitral prosthesis was inserted. After repair, transesophageal echocardiography revealed no evidence of LVOTO. Recovery was uneventful, and the patient was sent home on postoperative day 6.

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Fig 3. . Three-catheter wave form analysis using Millar catheters in the deep portion of the left ventricle (LV), the left ventricular outflow tract (LVOT), and the aorta (Ao). There is approximately 100 mm Hg gradient between the LV and the LVOT, as well as spike and dome morphology characteristic of LVOT obstruction.
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Comment
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Results of surgical therapy of mitral valve regurgitation have favored repair over valve replacement [6]. Total excision of the mitral valve and subvalvular apparatus and replacement with a mechanical or tissue prosthesis has been in disfavor because it may interfere with the integrity of the mitral annulus and overall ventricular performance [3]. DeAnda and colleagues [7], in an elegant animal experiment, and David and associates [1], in clinical follow-up, have clearly shown that preservation of the mitral tensor apparatus improves postoperative geometric and pressure-volume relationships and ventricular ejection fraction.
The great majority of surgeons concur that chordal preservation in mitral valve operations is important in maintaining left ventricular contractile function. However, we disagree with the concept of performing prosthetic mitral valve implantations over unresected or not carefully mobilized mitral leaflets. The 2 cases reported herein clearly demonstrate this error, and illustrate two pathologic mechanisms leading to left ventricular dysfunction: inflow ventricular obstruction caused by the interference between the prosthetic valve and the subvalvular mitral apparatus, creating a situation similar to mitral stenosis in spite of echocardiographic evidence of "normal" prosthetic valve motion, and LVOTO caused by the contact of the prosthetic valve with the unresected mitral valve leaflets and subvalvular apparatus.
If implantation of a prosthetic valve for mitral regurgitation or stenosis is needed, we recommend resection of the unsupported portion of the anterior leaflet or chordal transfer to avoid LVOTO or inflow ventricular obstruction by the mechanisms previously explained. We usually preserve the posterior leaflet, thus increasing the chances of maintaining good left ventricular performance and geometry. A prosthetic mitral implantation can then be securely accomplished without the consequences of inflow or outflow obstruction.
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Footnotes
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Address reprint requests to Dr Karp, Section of Cardiac Surgery, University of Chicago Hospitals, 5841 S Maryland Ave, MC5040, Chicago, IL 60637.
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References
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- David TE, Uden TE, Strauss HD. The importance of the mitral apparatus in left ventricular function after correction of mitral regurgitation. Circulation 1983;68(Suppl 2):7682.[Free Full Text]
- Spence PA, Peniston CM, David TE, et al. Toward a better understanding of the etiology of left ventricular dysfunction after mitral valve replacement: an experimental study with possible clinical implications. Ann Thorac Surg 1986;41:36371.
- Sarris GE, Miller DC. Valvular-ventricular interaction: the importance of the mitral chordae tendineae in terms of global left ventricular systolic function. J Card Surg 1988;3:21534.[Medline]
- Kronzon I, Cohen ML, Winer HE, Colvin SB. Left ventricular outflow obstruction: a complication of mitral valvuloplasty. J Am Coll Cardiol 1984;4:8258.[Abstract]
- Bortolotti U, Milano A, Tursi V, Minarini M, Thiene G, Mazzucco A. Fatal obstruction of the left ventricular outflow tract caused by low-profile bioprosthesis in the mitral position. Chest 1993;103:12889.[Abstract/Free Full Text]
- Sand ME, Naftel DC, Blackstone EH, Kirklin JW, Karp RB. A comparison of repair and replacement for mitral valve incompetence. J Thorac Cardiovasc Surg 1987;94:20819.[Abstract]
- DeAnda A Jr, Komeda M, Nikolic SD, et al. Left ventricular function, twist and recoil after mitral valve replacement. Circulation 1995;92(Suppl 2):45866.[Abstract/Free Full Text]
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