Eishi K, Ishibashi-Ueda H, Nakano K, Kosakai Y, Sasako Y, Kobayashi J, Yutani C
Department of Cardiovascular Surgery, National Cardiovascular Center, Osaka, Japan.
J Heart Valve Dis. 1996 Nov;5(6):668-72.
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.
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.
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.
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.
尽管戊二醛保存的生物瓣膜钙化的退变机制尚不清楚，但它是瓣膜置换常见的长期并发症。在本研究中，我们调查了因大动脉炎接受类固醇治疗的患者生物人工主动脉瓣的钙化退变情况，以评估对戊二醛保存生物瓣膜的免疫反应。
对10例接受生物瓣膜主动脉瓣置换术的患者进行研究。他们的平均年龄为48.4岁（范围：27至64岁）。8例患者的大动脉炎由高安氏病引起，2例由白塞氏大动脉炎引起。使用的生物瓣膜包括牛心包异种移植物（n = 8）和猪主动脉瓣（n = 2）。泼尼松的平均每日剂量为10.1毫克（范围：2.5至60毫克）；平均治疗持续时间为8.0年。使用超声心动图对患者的平均随访时间为11.5年（范围：8.5至16年）。总随访期为115患者年。
随访期间，分别因瓣膜脱离、主动脉瓣尖穿孔导致的主动脉瓣关闭不全以及伴有冠状动脉口狭窄的主动脉瓣关闭不全进行了3次再次手术。生物瓣膜的狭窄性退变无需再次手术。7个生物瓣膜在植入后8.5至16年仍在发挥功能。3个需要更换的牛心包瓣膜中有2个的钙化退变出人意料地轻微；瓣膜中胶原纤维因血浆蛋白浸润而分离的情况也很轻微。
这些结果表明，大动脉炎的类固醇联合治疗可能会减少生物瓣膜的钙化退变，尽管需要进一步研究来证实这种效果并确定其中涉及的机制。
