Objective: Aortic homografts offer many advantages over prosthetic valves. However, homograft dysfunction due to degeneration or infection may lead to reoperation. Aortic valve replacement in patients who have undergone previous aortic root replacement with an aortic homograft remains a technical challenge. To assess reoperation events a retrospective review was conducted. Materials and methods: From January 2000 to October 2006, 20 consecutive patients (38.8 AE 14.9 years old) underwent repeat surgery for aortic homograft failure. Results: Reoperation was performed 7.2 AE 3.5 years after implantation of the aortic homograft as a root. Indication was homograft degeneration (n = 18 [90%]) and endocarditis (n = 2 [10%]). In patients with major homograft wall calcifications or endocarditis, nine aortic root reconstructions were performed (Bentall procedure n = 7; homograft implantation n = 2). Each homograft was dissected with electrical cauterization and removed 'en-bloc' sparing the coronary buttons. In case of flexible homograft wall, stented prostheses (mechanical n = 10, bioprosthesis n = 1) were implanted along the homograft annulus. Additional procedures consisted of mitral valve replacements (n = 8), tricuspid repairs (n = 4), Konno procedure (n = 1) and coronary bypass (n = 5). Perioperative complications occurred in seven (35%) patients: sternal re-entry accident (n = 2); reoperations for mediastinitis (n = 1) or bleeding (n = 2); renal insufficiency (n = 1); total heart block (n = 1). No association was found between operative procedures and postoperative complications (Fisher's exact test). Two patients (10%) died from multiorgan failure in the early postoperative period. In total, 94.4% of the survivors remained free from reoperation at 74 months. Conclusion: Reoperation on patients with an aortic homograft as a root presents a relatively high perioperative morbidity. The surgical strategy depends on the degree of homograft wall calcification. #
Reapproximating the papillary muscles has an immediate effect on mitral leaflet mobility by suppressing the tethering resulting from displacement of the papillary muscles. It has an effect in preventing recurrent mitral regurgitation by avoiding further papillary muscle displacement. In this cohort of severely disabled patients, reverse remodeling can be expected with the double-level repair.
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