2015


To access this material please log in or register

Register Authorize
2015/№6

Evaluation of proinflammatory status in recipients of biological prosthetic heart valves

Rutkovskaya N. V., Ponasenko A. V., Stasev A. N., Kuzmina O. K., Barbarash L. S.
Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases” at the Siberian Branch of the Russian Academy of Medical Sciences, Sosnovy Bulvar 6, Kemerovo 650002

Keywords: bioprosthetic valve incompetence, calcification, heart valve prosthetic replacement, systemic inflammation

DOI: 10.18087/rhj.2015.6.2096

Background. Dystrophic mineralization can be considered a result of dysregulated metabolic processes controlled by specific proinflammatory signals. However, the relationship between the intensity of inflammation in the body of a biological prosthetic heart valve (BPHV) recipient and the presence of its dysfunction is still unclear. Aim. To study the relationship between parameters characterizing the proinflammatory status of BPHV recipients and the presence of structural BPHV dysfunction induced by calcification. Materials and methods. Two groups of recipients with different condition of BPHV, preserved function (n=47), and signs of calcinosis (n=19) in the remote postoperative period. IL-6, IL-8, IL-10, and TNF-α were studied. Results. In patients with clinically pronounced dysfunction, the development of BPHV calcium degeneration was associated with a significant decrease in concentration of IL-8 with a general increase in activities of proinflammatory serum markers. Conclusion. Based on the obtained results, we suggested that the activity of local and systemic inflammation can be designated as a factor influencing the rate of formation of BPHV structural dysfunction.
  1. Yu PJ, Skolnick A, Ferrari G, Heretis K, Mignatti P, Pintucci G et al. Correlation between plasma osteopontin levels and aortic valve calcification: potential insights into the pathogenesis of aortic valve calcification and stenosis. J Thorac Cardiovasc Surg. 2009 Jul;138: (1);196–9.
  2. Aronow WS. Osteoporosis, osteopenia and atherosclerotic vascular disease. Arch Med Sci. 2011 Feb;7 (1):21–6.
  3. New SE, Aikawa E. Molecular imaging insights into early inflammatory stages of arterial and aortic valve calcification. Circ Res. 2011 May 27;108 (11):1381–91.
  4. Mahjoub H, Mathieu P, Senechal M, Larose E, Dumesnil J, Despres JP, Pibarot P. ApoB / ApoA ratio is associated with increased risk of bioprosthetic valve degeneration. J Am Coll Cardiol. 2013 Feb 19;61 (7):752–61.
  5. Thiene G, Valente M. Anticalcification strategies to increase bioprosthetic valve durability. J Heart Valve Dis. 2011 Jan;20 (1):37–44.
  6. Рутковская Н. В., Савостьянова Ю. Ю., Барбараш О. Л. Факторы риска развития атеросклероза в формировании дисфункций биопротезов клапанов сердца. Кардиология. 2014;54 (6):76–80.
  7. Chen JH, Simmons CA. Cell-matrix interactions in the pathobio­logy of calcific aortic valve disease: critical roles for matricellular, matricrine, and matrix mechanics cues. Circ Res. 2011 Jun 10;108 (12):1510–24.
  8. New SE, Aikawa E. Cardiovascular сalcification: an inflammatory disease. Circ J. 2011;75 (6):1305–13.
  9. Barbarash OL, Rutkovskaya NV, Hryachkova ON, Gruzdeva OV, Uchasova EG, Ponasenko AV et al. Impact of recipient-related factors on structural dysfunction rates of xenoaortic bioprothetic heart valve. Patient Preference Adherence. 2015 Mar 9;9:389–99.
  10. Hjortnaes J, Butcher J, Figueiredo JL, Riccio M, Kohler RH, Kozloff KM et al. Arterial and aortic valve calcification inversely correlates with osteoporotic bone remodelling: a role for inflammation. Eur Heart J. 2010 Aug;31 (16):1975–84.
  11. Yu Z, Seya K, Daitoku K, Motomura S, Fukuda I, Furukawa K. Tumor necrosis factor-α accelerates the calcification of human aortic valve interstitial cells obtained from patients with calcific aortic valve stenosis via the BMP2‑Dlx5 pathway. J Pharmacol Exp Ther. 2011 Apr;337 (1):16–23.
  12. Cote C, Pibarot P, Despres JP, Mohty D, Cartier A, Arsenault BJ et al. Association between circulating oxidized low-density lipoprotein and fibrocalcific remodelling of the aortic valve in aortic stenosis. Heart. 2008 Sep;94 (9):1175–80.
  13. Shetty R, Pibarot P, Auget A, Janvier R, Dagenais F, Perron J et al. Lipid-mediated inflammation and degeneration of bioprosthetic heart valves. Eur J Clin Invest. 2009 Jun;39 (6):471–80.
  14. Rafrafi А, Chahed В, Kaabachi S, Kaabachi W, Maalmi H, Hamzaoui K, Sassi FH. Association of IL-8 gene polymorphisms with non small cell lung cancer in Tunisia: A case control study. Hum Immunol. 2013 Oct;74 (10):1368–74.
  15. Raaz-Schrauder D, Klinghammer L, Baum C, Frank T, Lewczuk P, Achenbach S et al. Association of systemic inflammation mar­kers with the presence and extent of coronary artery calcification. Cytokine. 2012 Feb;57 (2):251–7.
  16. Thampi P, Nair D, R L, N V, Venugopal S, Ramachandra U. Pathological effects of processed bovine pericardial scaffolds – a comparative in vivo evaluation. Artif Organs. 2013 Jul;37 (7):600–5.
  17. Wilhelmi MH, Mertsching H, Wilhelmi M, Leyh R, Haverich A. Role of inflammation in allogeneic and xenogeneic heart valve degeneration: immunohistochemical evaluation of inflammatory endothelial cell activation. J Heart Valve Dis. 2003 Jul;12 (4):520–6.
Rutkovskaya N. V., Ponasenko A. V., Stasev A. N., Kuzmina O. K., Barbarash L. S. Evaluation of proinflammatory status in recipients of biological prosthetic heart valves. Russian Heart Journal. 2015;14 (6):411–416

To access this material please log in or register

Register Authorize
Ru En