title: Calcific degeneration of bioprosthetic aortic valves in patients receiving steroid therapy.
abstract: OBJECTIVE
  Calcification of glutaraldehyde-preserved bioprosthetic valves is a frequent long-term complication of valve replacement, although the mechanism responsible for such degeneration is not clearly understood. In the current study, we investigated the calcific degeneration of bioprosthetic aortic valves in patients who had been given steroid treatment for aortitis in order to evaluate the immune response to glutaraldehyde-preserved bioprostheses.
  
  
  METHODS
  Ten patients who had undergone aortic valve replacement with bioprosthetic valves were studied. Their mean age was 48.4 years (range: 27 to 64 years). Aortitis was due to Takayasu disease in eight patients and to Behcet aortitis in two. The bioprosthetic valves used included bovine pericardial xenografts (n = 8) and porcine aortic valves (n = 2). The mean daily dosage of prednisone was 10.1 mg (range: 2.5 to 60 mg); mean duration of therapy was 8.0 years. The mean patient follow up, using echocardiography, was 11.5 years (range: 8.5 to 16 years). The total follow up period was 115 patient-years.
  
  
  RESULTS
  During follow up, three reoperations were required because of valve detachment, aortic insufficiency due to perforation of the aortic cusp, and aortic insufficiency with coronary orifice stenosis, respectively. No reoperations were required for stenotic degeneration of the bioprosthetic valves. Seven bioprosthetic valves were still functioning between 8.5 and 16 years after implantation. Calcific degeneration in two of three bovine pericardial valves that required replacing was surprisingly minimal; separation of collagen fibers in the valves by infiltration with plasma proteins was also minimal.
  
  
  CONCLUSIONS
  These results suggest that the calcific degeneration of bioprosthetic valves may be decreased by concomitant steroid therapy for aortitis, though further research will be required to confirm this effect and to determine the mechanism(s) involved.
authors.affiliation: Department of Cardiovascular Surgery, National Cardiovascular Center, Osaka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Eishi
authors.forename: H
authors.initials: H
authors.lastname: Ishibashi-Ueda
authors.forename: K
authors.initials: K
authors.lastname: Nakano
authors.forename: Y
authors.initials: Y
authors.lastname: Kosakai
authors.forename: Y
authors.initials: Y
authors.lastname: Sasako
authors.forename: J
authors.initials: J
authors.lastname: Kobayashi
authors.forename: C
authors.initials: C
authors.lastname: Yutani
mesh_terms: D000328:Adult; D001021:Aortic Valve; D001528:Behcet Syndrome / Q000150:complications / Q000188:drug therapy; D001705:Bioprosthesis; D002114:Calcinosis / Q000209:etiology / Q000517:prevention & control*; D005260:Female; D005500:Follow-Up Studies; D006350:Heart Valve Prosthesis; D006801:Humans; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000517:prevention & control; D011241:Prednisone / Q000627:therapeutic use*; D012086:Reoperation; D013625:Takayasu Arteritis / Q000188:drug therapy / Q000601:surgery
chemical_list: D011241:Prednisone