Commissural dehiscence of Carpentier-Edwards mitral bioprostheses: Explant analysis and pathogenesis

Abstract

Manufacturing factors have seldom been implicated as a direct cause of structural deterioration of valvular bioprostheses; this phenomenon has generally been considered to be of a host-dependent origin. We analyzed the clinical and pathologic data from 12 Carpentier-Edwards mitral bioprostheses removed from 12 patients because of severe dysfunction and showing detachment of the porcine aortic wall from the stent in one commissure or more. These 12 prostheses were part of a group of 92 such valves that were explanted and displayed structural deterioration. They belong to a population of 405 Carpentier-Edwards bioprostheses implanted in the mitral position in our institution between May 1978 and November 1988. The patients included three men and nine women with a mean age of 54 ± 13 years. One patient had a history of chronic renal failure, and two had systemic hypertension. Prosthesis sizes were 29, 31, and 33 mm ( n = 4 for each size). The models of the valves were 6625 ( n = 8) and 6650 ( n = 4). Mean duration of implantation of the prostheses was 99 ± 27 months (52 to 136 months) and did not differ depending on the model. There was no significant clustering of commissural detachments depending on valve size, year of implantation, or gender of the patient. No similar phenomenon was observed among 76 explanted aortic Carpentier-Edwards bioprostheses with structural deterioration from a population of 441 valves implanted during the same time frame. Native porcine aortic roots ( n = 5) and aortic Carpentier-Edwards bioprostheses explanted because of structural deterioration ( n = 4) were used as controls for comparison. Macroscopic examination showed single commissural dehiscence in 10 patients and double in two. Radiology disclosed no or mild mineralization in eight valves and no calcium in the area of aortic wall dehiscence, except for heavily calcified valves. Light microscopy evidenced a significant thinning of the aortic wall at the paracommissural level of mitral bioprostheses (351 ± 68 μm) compared with either aortic bioprostheses (526 ± 59 μm; p < 0.01) or control native porcine aortic roots (419 ± 50 μm; p < 0.01). No difference was found in terms of aortic wall thickness between detached (322 ± 42 μm) and intact (366 ± 74 μm) commissures in mitral bioprostheses. It is concluded that the dehiscence of the aortic wall from the Dacron cover of the stent in the commissural area of Carpentier-Edwards bioprostheses in the mitral position is most likely produced by its weakening, as a consequence of excessive trimming with elimination of the outer layers of the aorta, during the manufacturing process. The reason this phenomenon appears in mitral bioprostheses and in a particular commissure seems to be linked to the areas of concentration of mechanical stress. (J T HORAC C ARDIOVASC S URG 95;110:688-96)