Barbarash Olga, Rutkovskaya Natalya, Hryachkova Oksana, Gruzdeva Olga, Uchasova Evgenya, Ponasenko Anastasia, Kondyukova Natalya, Odarenko Yuri, Barbarash Leonid
Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
Patient Prefer Adherence. 2015 Mar 9;9:389-99. doi: 10.2147/PPA.S76001. eCollection 2015.
To analyze the influence of recipient-related metabolic factors on the rate of structural dysfunction caused by the calcification of xenoaortic bioprostheses.
We retrospectively analyzed clinical status, calcium-phosphorus metabolism, and nonspecific markers of inflammatory response in bioprosthetic mitral valve recipients with calcific degeneration confirmed by histological and electron microscopic studies (group 1, n=22), and in those without degeneration (group 2, n=48).
Patients with confirmed calcification of bioprostheses were more likely to have a severe clinical state (functional class IV in 36% in group 1 versus 15% in group 2, P=0.03) and a longer cardiopulmonary bypass period (112.8±18.8 minutes in group 1 versus 97.2±23.6 minutes in group 2, P=0.02) during primary surgery. Patients in group 1 demonstrated moderate hypovitaminosis D (median 34.0, interquartile range [21.0; 49.4] vs 40 [27.2; 54.0] pmol/L, P>0.05), osteoprotegerin deficiency (82.5 [44.2; 115.4] vs 113.5 [65.7; 191.3] pg/mL, P>0.05) and osteopontin deficiency (4.5 [3.3; 7.7] vs 5.2 [4.1; 7.2] ng/mL, P>0.05), and significantly reduced bone-specific alkaline phosphatase isoenzyme (17.1 [12.2; 21.4] vs 22.3 [15.5; 30.5] U/L, P=0.01) and interleukin-8 levels (9.74 [9.19; 10.09] pg/mL vs 13.17 [9.72; 23.1] pg/mL, P=0.045) compared with group 2, with an overall increase in serum levels of proinflammatory markers.
Possible predictors of the rate of calcific degeneration of bioprostheses include the degree of decompensated heart failure, the duration and invasiveness of surgery, and the characteristics of calcium-phosphorus homeostasis in the recipient, defined by bone resorption and local and systemic inflammation. The results confirm the hypothesis that cell-mediated regulation of pathological calcification is caused by dysregulation of metabolic processes, which are in turn controlled by proinflammatory signals.
分析受体相关代谢因素对异种主动脉生物瓣膜钙化所致结构功能障碍发生率的影响。
我们回顾性分析了经组织学和电子显微镜研究确诊为钙化性退变的生物人工二尖瓣置换患者（第1组，n = 22）以及无退变患者（第2组，n = 48）的临床状况、钙磷代谢和炎症反应的非特异性标志物。
生物瓣膜确诊钙化的患者在初次手术时更可能处于严重临床状态（第1组36%为IV级功能分级，第2组为15%，P = 0.03）且体外循环时间更长（第1组为112.8±18.8分钟，第2组为97.2±23.6分钟，P = 0.02）。与第2组相比，第1组患者表现为中度维生素D缺乏（中位数34.0，四分位间距[21.0; 49.4] vs 40 [27.2; 54.0] pmol/L，P>0.05）、骨保护素缺乏（82.5 [44.2; 115.4] vs 113.5 [65.7; 191.3] pg/mL，P>0.05）和骨桥蛋白缺乏（4.5 [3.3; 7.7] vs 5.2 [4.1; 7.2] ng/mL，P>0.05），骨特异性碱性磷酸酶同工酶显著降低（17.1 [12.2; 21.4] vs 22.3 [15.5; 30.5] U/L，P = 0.01），白细胞介素-8水平降低（9.74 [9.19; 10.09] pg/mL vs 13.17 [9.72; 23.1] pg/mL，P = 0.045），促炎标志物血清水平总体升高。
生物瓣膜钙化性退变发生率的可能预测因素包括失代偿性心力衰竭的程度、手术持续时间和侵袭性，以及由骨吸收和局部及全身炎症所定义的受体钙磷稳态特征。结果证实了以下假设，即细胞介导的病理性钙化调节是由代谢过程失调引起的，而代谢过程又受促炎信号控制。
