title: Impact of recipient-related factors on structural dysfunction of xenoaortic bioprosthetic heart valves.
abstract: OBJECTIVE
  To analyze the influence of recipient-related metabolic factors on the rate of structural dysfunction caused by the calcification of xenoaortic bioprostheses.
  
  
  METHODS
  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).
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Olga
authors.initials: O
authors.lastname: Barbarash
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Natalya
authors.initials: N
authors.lastname: Rutkovskaya
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Oksana
authors.initials: O
authors.lastname: Hryachkova
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Olga
authors.initials: O
authors.lastname: Gruzdeva
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Evgenya
authors.initials: E
authors.lastname: Uchasova
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Anastasia
authors.initials: A
authors.lastname: Ponasenko
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Natalya
authors.initials: N
authors.lastname: Kondyukova
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Yuri
authors.initials: Y
authors.lastname: Odarenko
authors.affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
authors.forename: Leonid
authors.initials: L
authors.lastname: Barbarash
keywords: bioprostheses; calcification; calcium–phosphorus metabolism; inflammation
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