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J Thorac Cardiovasc Surg 2006;132:401-406
© 2006 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Structural deterioration of the Freestyle aortic valve: Mode of presentation and mechanisms

Department of Cardiac Surgery, Laval Hospital, Québec City, Québec, Canada.

Received for publication December 22, 2005; accepted for publication March 23, 2006.

^_* Address for reprints: Francois Dagenais, Department of Cardiac Surgery, Laval Hospital, 2725 chemin Sainte-Foy, Sainte-Foy, Québec, Canada, G1V 4G5. (Email: francois.dagenais{at}chg.ulaval.ca).

BACKGROUND: Structural valve deterioration is the major cause of bioprosthetic valve failure. Because of the unique design features and anti-calcification treatment of the Freestyle (Medtronic Inc, Minneapolis, Minn) stentless bioprosthesis, development of structural valve deterioration may differ in comparison with other bioprosthetic valves. This study evaluates the mechanisms and clinical presentation of structural valve deterioration in the Freestyle stentless bioprosthesis.

METHODS: Between January 1993 and August 2005, 608 patients underwent aortic valve replacement with a Freestyle stentless bioprosthesis. The implantation technique was subcoronary in 475 patients and a root replacement in 133 patients. Mean overall follow-up was 5.6 ± 3.4 years. Follow-up was complete in all patients. Clinical and echocardiographic follow-ups were conducted prospectively.

RESULTS: Freedom from structural valve deterioration was 95.8% at 10 years. Twelve patients showed evidence of structural valve deterioration and underwent reoperation for aortic regurgitation (n = 10) or aortic stenosis (n = 2). The mean age of patients with structural valve deterioration was significantly lower than patients without structural valve deterioration (62.6 ± 8.2 years vs 68.6 ± 8.3 years, P = .02). The median time between implantation and explantation was 8.7 years (range: 1.9-13.3 years). Eleven structural valve deteriorations occurred after subcoronary implantation, and 1 structural valve deterioration occurred after root implantation (P = .4). The mechanisms of structural valve deterioration were leaflet tears in 10 patients (6 in the left coronary cusp and 4 in the right coronary cusp), severe valve calcification in 1 patient, and cusp fibrosis in 1 patient. The interval between onset of symptoms and reoperation was acute or subacute in 10 patients.

CONCLUSION: At 10 years, the Freestyle stentless bioprosthesis shows excellent freedom from structural valve deterioration. Structural valve deterioration in the Freestyle stentless bioprosthesis relates to leaflet tear with minimal calcification in the majority of cases. Because of the fast onset of symptoms with leaflet tear, patients with a Freestyle stentless bioprosthesis should be informed of the preferential mode of failure and time-frame of symptoms.

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