Ann Thorac Surg 2004;77:1443-1445
© 2004 The Society of Thoracic Surgeons
Case report
Immediate structural valve deterioration of 27-mm Carpentier-Edwards aortic pericardial bioprosthesis
Arlen G. Fleisher, MDa*,
Rocco J. Lafaro, MDa,
Richard A. Moggio, MDa
a Department of Surgery, Division of Cardiothoracic Surgery, Westchester Medical Center, New York Medical College, Valhalla, New York, USA
Accepted for publication April 25, 2003.
* Address reprint requests to Dr Fleisher, Department of Surgery, Division of Cardiothoracic Surgery, Westchester Medical Center, Macy Pavilion, Rm W128, Valhalla, NY 10595, USA
e-mail: fleishera{at}wcmc.com
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Abstract
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We describe two cases of immediate structural valve deterioration of the 27-mm Carpentier-Edwards pericardial valve. Tissue characteristics of bovine pericardium and the possible mechanism of failure are discussed.
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Introduction
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Structural valve deterioration is defined as any change in valve function resulting from an intrinsic abnormality leading to either stenosis or regurgitation. Factors associated with structural valve dysfunction include changes intrinsic to the valve including wear, calcification, leaflet tear, and stent creep [1]. These changes usually occur over time. The following is a report of two patients, each with a 27-mm Carpentier-Edwards Perimount Pericardial bioprosthesis Model 2700, who developed immediate significant aortic valve insufficiency requiring explantation.
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Case reports
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Patient 1
A 43-year-old man was admitted to another hospital for the treatment of severe aortic valve stenosis with insufficiency. He had a trileaflet valve with severe calcification involving primarily the leaflets. He underwent an aortic valve replacement using a 27-mm Carpentier-Edwards Perimount Pericardial valve Model 2700 using pledgeted 2-0 mattress sutures. He tolerated the procedure well, but a murmur consistent with aortic insufficiency was noted on the first postoperative day. A transthoracic echocardiography demonstrated mild aortic insufficiency. He was asymptomatic and discharged home.
Over the next 2.5 years the patient had shortness of breath with minimal exertion. He was evaluated with transthoracic echocardiography, which revealed a dilated left ventricle with normal left ventricular systolic function. Aortic insufficiency was moderate to severe. A cardiac catheterization showed severe prosthetic aortic valve regurgitation with normal coronary arteries. He was referred to our institution for reoperation. At surgery, intraoperative transesophageal echocardiography showed the central regurgitation through the valve leaflets. Examination of the valve before explantation showed an elongated cusp with prolapse and central regurgitation as a result of the lack of coaptation of the leaflets. There was no evidence of any other structural deformity or a paravalvular leak (Figs 1 and 2).
The valve was replaced with a 25-mm mechanical valve.
Patient 2
An 83-year-old man was admitted to our institution with severe aortic valve stenosis and regurgitation. He had a severely calcified trileaflet aortic valve. An aortic valve replacement was performed using a 27-mm Carpentier-Edwards Perimount Pericardial valve Model 2700 using 2-0 pledgeted mattress sutures. Routine postoperative transthoracic echocardiography performed on postop day 3 showed moderate-to-severe bioprosthetic aortic insufficiency. The regurgitant jet was seen to arise from the junction of the right and noncoronary cusps of the bioprosthesis. There was normal leaflet mobility. A reoperation was performed a few days later. Before explant the valve was observed to be well seated in the supraannular position. The suture line was intact around the sewing ring of the valve. A prolapsed cusp was identified that resulted in a lack of coaptation of the leaflets causing aortic insufficiency. As in the other patient (Figs 1 and 2) no tears or other structural defects were found apart from apparent stretching of the tissue of one cusp causing maladaptation and prolapse. The valve was replaced with a 25-mm porcine bioprosthesis.
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Comment
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The Carpentier-Edwards Perimount pericardial valve Model 2700 was introduced to clinical use in 1981 and approved for use in the United States in 1991. It has been associated with excellent long-term clinical results [2–4]. Structural valve deterioration is one of the main complications of tissue valves that result in reoperation. Structural valve deterioration includes changes intrinsic to the valve including wear, calcification, leaflet tear, and stent creep but excludes infected or thrombosed valves as determined at explantation [1]. In most patients calcification was the cause of structural valve dysfunction requiring explantation [5].
The Perimount valve has been biomechanically engineered to optimize hemodynamics and durability while also providing consistent coaptation during closure. The shape and geometry of the leaflets are designed for optimal valve opening while minimizing closing stresses. Using a computer-generated design the leaflets and stent are engineered for a precise fit, which ensures uniform and consistent valve opening and closing.
All prosthetic valves exhibit some amount of regurgitation during closure. The flow pattern as visualized during echocardiography will vary based on stent design. In the Perimount valve due to the low stent profile the leaflets are shorter and straighter at the free edges compared with a porcine valve. The combination of this leaflet geometry and the wider opening area results in a higher closing volume, leading to a larger color flash along the coaptation edge during valve closure when seen under echo Doppler. Edwards Lifesciences refers to this in their educational material as the "signature flow pattern."
In addition to the shape and geometry of the leaflets the tissue characteristics of the bovine pericardium are critical for the durability and function of the valve. Tissue variability of the pericardial tissue includes the thickness of the pericardium and its stress-strain properties (the amount that the pericardium will stretch under a given pressure load).
Edwards Lifesciences was contacted and confirmed that reports such as these are extremely rare and unusual. Even in the few cases that have been reported, the event was normally explained by stent distortion, mechanical disruption, or in some cases suture tail abrasion. Despite the very low rate of occurrence, Edwards Lifesciences did indicate that it has a number of continuous improvement programs intended to improve valve manufacturability. Two of these programs relate directly to the pericardial tissue, specifically an automated thickness mapping process (Peri-Mapping), and a deflection characterization test that allows precise matching of tissue based on how the leaflets deflect under a given load (Michael Scott, PhD, personal communication, 6/19/02, written letter).
In the two cases reported here we observed none of the above-mentioned causes. Interestingly, in both cases a smaller valve was implanted at the second operation. This size change can be explained by the differences in specifically numbered sizers among different valve prostheses. In our cases we observed no differences between the sizers of the 25-mm porcine and mechanical valve versus the 27-mm pericardial valve.
We have reported an extremely rare occurrence that we believe was a result of a mismatch of pericardium of different extensile properties in our patients. Recently developed technology has allowed for quantification of deflection that can adequately match leaflet properties (Michael Scott, PhD, personal communication, 6/19/02, written letter). Edwards engineers indicated that the potential for mismatched tissue should be virtually eliminated with these enhanced manufacturing processes. Subsequent to the valve implantations detailed in this report, Edwards completed implementation of both Peri-Mapping and leaflet deflection technologies on Perimount aortic and mitral valves.
Although the second patient had an echocardiography report of mild regurgitation, this finding may have been misinterpreted or underestimated because he had a significant murmur and postoperative clinical course consistent with significant aortic regurgitation. These patients should probably have an intraoperative transesophageal echocardiography after implantation to assess baseline valve function. Excessive regurgitation should be addressed at the original operation. In addition close follow-up with serial echocardiographic scans can be obtained with some caution in dismissing early aortic insufficiency on clinical or echocardiography examination as normal.
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References
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- Edmunds L.H., Jr, Clark R.E., Cohn L.H., Grunkemeier G.L., Miller D.C., Weisel R.D. Guidelines for reporting morbidity and mortality after cardiac valvular operations. Ann Thorac Surg 1996;62:932-935.[Abstract/Free Full Text]
- Frater R.W.M., Furlong P., Cosgrove D.M., et al. Long-term durability, and patient functional status of the Carpentier-Edwards perimount pericardial bioprosthesis in the aortic position. J Heart Valve Dis 1998;7:48-53.[Medline]
- Poirier N.C., Pelletier L.C., Pellerin M., Carrier M. 15-Year experience with the Carpentier-Edwards pericardial bioprosthesis. Ann Thorac Surg 1998;66:557-561.[Abstract/Free Full Text]
- Neville P.H., Aupart M.R., Diemont F.F., Sirinelli A.L., Lemoine E.M., Marchand M.A. Carpentier-Edwards pericardial bioprosthesis in aortic or mitral position: a 12-year experience. Ann Thorac Surg 1998;66(Suppl):S143-147.
- Banbury M.K., Cosgrove D.M., White J.A., Blackstone E.H., Frater R.W., Okies J.E. Age and valve size effect on the long-term durability of the Carpentier-Edwards pericardial bioprosthesis. Ann Thorac Surg 2001;72:753-757.[Abstract/Free Full Text]
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Abstract
Introduction
