Role of soluble Fas ligand in myocardial remodeling, severity and outcomes of chronic heart failure


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Abstract

Aim. To reveal the specific features of Fas ligand-mediated ischemic myocardial remodeling and those of chronic heart failure (CHF) development during a 12-month prospective follow-up. Subjects and methods. A total of 94 patients with ischemic CHF were examined and divided into 3 groups according to NYHA Functional Class (FC): 1) FC II CHF in 35 patients; 2) FC III CHF in 31; 3) FC IV CHF in 28. According to the results of the 12-month follow-up, the patients were randomized into 2 groups: A) 49 patients with a favorable course of cardiovascular disease and B) 45 patients with its poor course. Serum soluble Fas ligand (sFas-L) levels were measured by enzyme immunoassay. Results. In the patients with CHF, the baseline sFas-L levels substantially exceeded that in the control group by 3—6 times (p<0.01). In the men with the poor course of CHF, the baseline serum sFAS-L levels (85.94±4.14 pg/ml) were significantly higher than that in the favorable CHF group (107.33±5.13 pg/ml; р=0.0015). ROC analysis of the sensitivity and specificity of cardiovascular risk stratification according to sFAS-L levels revealed the high prognostic value of this marker — ROC-Area±S.E. was 0.75±0.05 (95% confidence interval, 0.60 to 0.81; p=0.0005). There was a statistically significant moderate correlation of left ventricular (LV) ejection fraction with sFAS-L concentrations and a moderate direct correlation between serum sFAS-L concentrations and LV remodeling parameters. Conclusion. The serum level of sFas-L determines the development of ischemic LV remodeling and the severity of CHF, by increasing in proportion to the degree of disease progression. The determination of serum sFas-L levels assists in objectively estimating the severity of apoptosis and may be an important prognostic test to assess the course of CHF in patients with coronary heart disease.

References

  1. Бузиашвили Ю.И., Ключников И.В., Мелконян А.М., Иноземцева Е.В., Коваленко О.А., Мамаев Х.К. Ишемическое ремоделирование левого желудочка (определение, патогенез, диагностика, медикаментозная и хирургическая коррекция). Кардиология. 2002;10:88-95.
  2. Maytin M, Colucci WS. Molecular and cellular mechanisms of myocardial remodeling. J NuclCardiol. 2002;9(3):319-327. doi: 10.1067/mnc.2002.123207
  3. Takemura G, Kanoh M, Minatoguchi S, Fujiwara H. Cardiomyocyte apoptosis in the failing heart — a critical review from definition and classification of cell death. Int J Cardiol. 2013;16(6):2373-2386. doi: 10.1016/j.ijcard.2013.01.163
  4. Ярилин А.А. Апоптоз. Природа феномена. Его роль в целостном организме. Патологическая физиология и экспериментальная терапия. 1998;2:43-48.
  5. Mughal W, Dhingra R, Kirshenbaum LA. Striking a balance: autophagy, apoptosis, and necrosis in a normal and failing heart. Cur Hypertension Reports. 2012;14(6):540-547. doi: 10.1007/s11906-012-0304-5
  6. Kwak HB. Effects of aging and exercise training on apoptosis in the heart. J Exercise Rehabilitation. 2013;9(2):212-219. doi: 10.12965/jer.130002
  7. Хлапов А.П., Вечерский Ю.Ю., Рязанцева Н.В., Калюжин В.В., Мустафина Л.Р., Шипулин В.М., Новицкий В.В. Роль апоптоза кардиомиоцитов в механизмах ишемического ремоделирования миокарда. Бюллетень сибирской медицины. 2008; 3:33-37.
  8. Angelini A, Maiolino, G, La Canna G, Ceconi C, Calabrese F, Pettenazzo E, Valente M, Alfieri O, Thiene G, Ferrari R. Relevance of apoptosis in influencingrecovery of hibernating myocardium. Eur J Heart Fail. 2007:9:377-383. doi: 10.1016/j.ejheart.2006.09.012
  9. Bing OH. Hypothesis: apoptosis may be a mechanism for the transition to heart failure with chronic pressure overload. J Mol Cell Cardiol. 1994;26:943-948. doi: 10.1006/jmcc.1994.1115
  10. Залесский В.Н., Поливода С.Н. Апоптоз кардиомиоцитов, сердечная недостаточность и постинфарктное ремоделирование (проблемы и перспективы). Запорожский медицинский журнал. 2003;5:55-58.
  11. Lee Y, Gustafsson AB. Role of apoptosis in cardiovascular disease. Apoptosis. 2009;14(4):536-548. doi: 10.1007/s10495-008-0302-x
  12. Garg S, Narula J, Chandrashekhar Y. Apoptosis and heart failure: clinical relevance and therapeutic target. J Mol Cell Cardiol. 2005;38:73-79. doi: 10.1016/j.yjmcc.2004.11.006
  13. Бойчук С.В., Мустафин И.Г. Fas-рецептор и его роль при атопических заболеваниях. Иммунология. 2001;3:24-29.
  14. Gang L, Huhua L, Liangming W. Serum levels of soluble Fas ligand and soluble Fas receptor in patients with chronic congestive heart failure. Chinese Med Scie J. 2002;17(4):258.
  15. Москалева Е.Ю., Севрин С.Е. Возможные механизмы адаптации клетки к повреждениям, индуцирующих программированную гибель. Связь с патологией. Патологическая физиология и экспериментальная терапия. 2006;2:2-16.
  16. Venkataraman K, Khurana S, Tai TC. Oxidative stress in aging-matters of the heart and mind. Int J Mol Scie. 2013;14(9):17897-17925. doi: 10.3390/ijms140917897
  17. Albina JE, Cui S, Mateo RB, Reichner JS. Nitric oxide-mediated apoptosis in murine peritoneal macrophages. J Immunol. 1993;150(11):5080-5085. doi: 10.1016/0169-4758(93)90226-6
  18. Nakano K, Vousden KH. PUMA, a novel proapoptotic gene, is induced by p53. Mol Cell. 2001;7(3):683-694. doi: 10.1016/S1097-2765(01)00214-3
  19. Matute-Bello G, Wurfel MM, Lee JS, Park DR, Frevert CW, Madtes DK, Shapiro SD, Martin TR. Essential role of MMP-12 in Fas-induced lung fibrosis. Am J Respir Cell Mol Biol. 2007;372:210-221. doi: 10.1165/rcmb.2006-0471OC
  20. Kasama S, Furuya M, Toyama T, Ichikawa S, Kurabayashi M. Effect of atrial natriuretic peptide on left ventricular remodelling in patients with acute myocardial infarction. Eur Heart J. 2008;29(12):1485-1494. doi: 10.1093/eurheartj/ehn206
  21. Balsam LB, Kofidis T, Robbins RC. Caspase-3 inhibition preserves myocardial geometry and long-term function after infarction. J Surg Res. 2005;124(2):194-200. doi: 10.1016/j.jss.2004.09.017
  22. Yang B, Ye D, Wang Y. Caspase-3 as a therapeutic target for heart failure. Expert Opin Ther Targets. 2013;17(3):255-263. doi: 10.1016/j.jss.2004.09.017
  23. Yue TL, Ma XL, Wang X, Romanic AM, Liu GL, Louden C, Gu JL, Kumar S, Poste G, Ruffolo RR, Feuerstein GZ. Possible involvement of stress-activated protein kinase signaling pathway and Fas receptor expression in prevention of ischemia/reperfusion-induced cardiomyocyte apoptosis by carvedilol. Circul Res. 1998;82(2):166-174. doi: 10.1161/01.res.82.2.166

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