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Impact of recipient-related factors on structural dysfunction of xenoaortic bioprosthetic heart valves.

Barbarash O, Rutkovskaya N, Hryachkova O, Gruzdeva O, Uchasova E, Ponasenko A, Kondyukova N, Odarenko Y, Barbarash L - Patient Prefer Adherence (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.

ABSTRACT

Objective: To analyze the influence of recipient-related metabolic factors on the rate of structural dysfunction caused by the calcification of xenoaortic bioprostheses.

Materials and 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.

Conclusion: 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.

No MeSH data available.


Related in: MedlinePlus

Scanning electron microscopy. Primary tissue degeneration with calcification. Secondary electron imaging. Scale bar −300 microns.
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f5-ppa-9-389: Scanning electron microscopy. Primary tissue degeneration with calcification. Secondary electron imaging. Scale bar −300 microns.

Mentions: In December 2013, 113 patients (31.4% of all discharged patients) had undergone reoperation as a result of BP dysfunction. The causes of BP dysfunction were identified in 105 (93%) cases (Table 1), based on histological and electron microscopic studies. The most common cause of BP dysfunction was primary tissue degeneration with calcification (46.9%) (Figures 1–5). Prosthetic valve endocarditis occurred in 25.7% of cases (Figures 6–8). Structural degeneration caused by leaflet disruption without calcification and/or infection occurred in 12.4% of cases. Calcium deposits (crystalline and amorphous forms), as well as leukocytic/lymphocytic infiltrations and/or bacterial colonies, were present on the prosthesis leaflets in 7.1% of cases, indicating the presence of inflammation (Figure 9). It is possible that the inflammation of the BP leaflets was secondary to the structural dysfunction or it may have preceded the degenerative changes of the xenomaterial; therefore, these patients were excluded from further analysis.


Impact of recipient-related factors on structural dysfunction of xenoaortic bioprosthetic heart valves.

Barbarash O, Rutkovskaya N, Hryachkova O, Gruzdeva O, Uchasova E, Ponasenko A, Kondyukova N, Odarenko Y, Barbarash L - Patient Prefer Adherence (2015)

Scanning electron microscopy. Primary tissue degeneration with calcification. Secondary electron imaging. Scale bar −300 microns.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358689&req=5

f5-ppa-9-389: Scanning electron microscopy. Primary tissue degeneration with calcification. Secondary electron imaging. Scale bar −300 microns.
Mentions: In December 2013, 113 patients (31.4% of all discharged patients) had undergone reoperation as a result of BP dysfunction. The causes of BP dysfunction were identified in 105 (93%) cases (Table 1), based on histological and electron microscopic studies. The most common cause of BP dysfunction was primary tissue degeneration with calcification (46.9%) (Figures 1–5). Prosthetic valve endocarditis occurred in 25.7% of cases (Figures 6–8). Structural degeneration caused by leaflet disruption without calcification and/or infection occurred in 12.4% of cases. Calcium deposits (crystalline and amorphous forms), as well as leukocytic/lymphocytic infiltrations and/or bacterial colonies, were present on the prosthesis leaflets in 7.1% of cases, indicating the presence of inflammation (Figure 9). It is possible that the inflammation of the BP leaflets was secondary to the structural dysfunction or it may have preceded the degenerative changes of the xenomaterial; therefore, these patients were excluded from further analysis.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Federal State Budgetary Scientific Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.

ABSTRACT

Objective: To analyze the influence of recipient-related metabolic factors on the rate of structural dysfunction caused by the calcification of xenoaortic bioprostheses.

Materials and 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.

Conclusion: 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.

No MeSH data available.


Related in: MedlinePlus