English Polski
Tom 12, Nr 3 (2017)
Artykuł przeglądowy
Opublikowany online: 2016-09-13

dostęp otwarty

Wyświetlenia strony 1107
Wyświetlenia/pobrania artykułu 9357
Pobierz cytowanie

Eksport do Mediów Społecznościowych

Eksport do Mediów Społecznościowych

Markery włóknienia w niewydolności serca

Bożena Karolko, Monika Przewłocka-Kosmala
Folia Cardiologica 2017;12(3):245-253.

Streszczenie

Niewydolność serca (HF) jest najczęstszą przyczyną zgonu z przyczyn sercowo-naczyniowych. Liczba zachorowań wzrasta, mimo postępu w dziedzinie farmakologii i medycyny interwencyjnej. Pociąga to za sobą ogromne nakłady finansowe na leczenie. Od lat prowadzone są badania nad wprowadzeniem do diagnostyki kardiologicznej nowych markerów biochemicznych wspomagających ustalenie rozpoznania, monitorowanie odpowiedzi na leczenie oraz prognozowanie ryzyka. Biomarkery są wykładnikiem patologicznych procesów zachodzących w niewydolnym mięśniu sercowym. Na szczególną uwagę zasługują biomarkery włóknienia — jednego z kluczowych patofizjologicznych mechanizmów wpływających na rozwój HF. Biomarkery włóknienia dają możliwość monitorowania postępu choroby i oceny stopnia niekorzystnych zmian. W niniejszej pracy przedstawiono zarówno dobrze już poznane, jak i nowe markery włóknienia oraz ich przydatność w diagnostyce HF.

Referencje

  1. Colucci WS, Braunwald E. Pathophysiology of heart hailure. In: Braunwald WS, Zippes DP, Libby P. ed. Heart disease. Ed. 6. WB Saunders Company, Philadelphia 2001: 503–533.
  2. Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC Committee for Practice Guidelines (CPG), ESC Committee for Practice Guidelines (CPG). ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J. 2008; 29(19): 2388–2442.
  3. Karasek D, Kubica A, Sinkiewicz W, et al. Epidemiologia niewydolności serca — problem zdrowotny i społeczny starzejących się społeczeństw Polski i Europy. Folia Cardiol Excerpta. 2008; 5: 242–248.
  4. Gierczyński J, Gryglewicz J, Karczewicz E, Zalewska H. ed. Niewydolność serca — analiza kosztów ekonomicznych i społecznych. Uczelnia Łazarskiego, Warszawa 2013.
  5. Swedberg K, Cleland J, Dargie H, et al. Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J. 2005; 26(11): 1115–1140.
  6. Yancy C, Jessup M, Bozkurt B, et al. Writing Committee Members, American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation . 2013; 128(16): e240–e327.
  7. Thygesen K, Mair J, Mueller C, et al. Study Group on Biomarkers in Cardiology of the ESC Working Group on Acute Cardiac Care. Recommendations for the use of natriuretic peptides in acute cardiac care: a position statement from the Study Group on Biomarkers in Cardiology of the ESC Working Group on Acute Cardiac Care. Eur Heart J. 2012; 33(16): 2001–2006.
  8. Iqbal N, Wentworth B, Choudhary R, et al. Cardiac biomarkers: new tools for heart failure management. Cardiovasc Diagn Ther. 2012; 2(2): 147–164.
  9. Passino C, Barison A, Vergaro G, et al. Markers of fibrosis, inflammation, and remodeling pathways in heart failure. Clin Chim Acta. 2015; 443: 29–38.
  10. Beręsewicz A, Duda M, Klemenska E. Patofizjologia niewydolności serca. Centrum Medyczne Kształcenia Podyplomowego, Warszawa 2010: 40–43.
  11. Weber KT, Pick R, Jalil JE, et al. Patterns of myocardial fibrosis. J Mol Cell Cardiol. 1989; 21(Suppl 5): 121–131.
  12. Berk BC, Fujiwara K, Lehoux S. ECM remodeling in hypertensive heart disease. J Clin Invest. 2007; 117(3): 568–575.
  13. López B, González A, Querejeta R, et al. Alterations in the pattern of collagen deposition may contribute to the deterioration of systolic function in hypertensive patients with heart failure. J Am Coll Cardiol. 2006; 48(1): 89–96.
  14. Kong P, Christia P, Frangogiannis NG. The pathogenesis of cardiac fibrosis. Cell Mol Life Sci. 2014; 71(4): 549–574.
  15. López B, González A, Díez J. Circulating biomarkers of collagen metabolism in cardiac diseases. Circulation. 2010; 121(14): 1645–1654.
  16. Dobaczewski M, Chen W, Frangogiannis NG. Transforming growth factor (TGF)-β signaling in cardiac remodeling. J Mol Cell Cardiol. 2011; 51(4): 600–606.
  17. Lipka: D, Boratyński J. Metaloproteinazy MMP. Struktura i funkcja . Post Hig Med Dośw. 2008; 62: 328–336.
  18. Sundström J, Evans JC, Benjamin EJ, et al. Relations of plasma matrix metalloproteinase-9 to clinical cardiovascular risk factors and echocardiographic left ventricular measures: the Framingham Heart Study. Circulation. 2004; 109(23): 2850–2856.
  19. Martos R, Baugh J, Ledwidge M, et al. Diagnosis of heart failure with preserved ejection fraction: improved accuracy with the use of markers of collagen turnover. Eur J Heart Fail. 2009; 11(2): 191–197.
  20. Frantz S, Störk S, Michels K, et al. Tissue inhibitor of metalloproteinases levels in patients with chronic heart failure: an independent predictor of mortality. Eur J Heart Fail. 2008; 10(4): 388–395.
  21. Zile MR, Desantis SM, Baicu CF, et al. Plasma biomarkers that reflect determinants of matrix composition identify the presence of left ventricular hypertrophy and diastolic heart failure. Circ Heart Fail. 2011; 4(3): 246–256.
  22. Zannad F, Alla F, Dousset B, et al. Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure: insights from the randomized aldactone evaluation study (RALES). Rales Investigators. Circulation. 2000; 102(22): 2700–2706.
  23. Zannad F, Dousset B, Alla F. Treatment of congestive heart failure: interfering the aldosterone-cardiac extracellular matrix relationship. Hypertension. 2001; 38(5): 1227–1232.
  24. Cheng JM, Akkerhuis KM, Battes LC, et al. Biomarkers of heart failure with normal ejection fraction: a systematic review. Eur J Heart Fail. 2013; 15(12): 1350–1362.
  25. López B, González A, Ravassa S, et al. Circulating biomarkers of myocardial fibrosis: the need for a reappraisal. J Am Coll Cardiol. 2015; 65(22): 2449–2456.
  26. López B, Querejeta Q, González A. Collagen cross-linking but not collagen amount associates with elevated filling pressures in hypertensive patients with stage C heart failure: potential role of lysyl oxidase. Hypertension . 2012; 60(3): 677–683.
  27. Zibadi S, Vazquez R, Moore D, et al. Myocardial lysyl oxidase regulation of cardiac remodeling in a murine model of diet-induced metabolic syndrome. Am J Physiol Heart Circ Physiol. 2009; 297(3): H976–H982.
  28. López B, Querejeta R, González A, et al. Impact of treatment on myocardial lysyl oxidase expression and collagen cross-linking in patients with heart failure. Hypertension. 2009; 53(2): 236–242.
  29. López B, Ravassa S, González A, et al. Myocardial collagen cross-linking is associated with heart failure hospitalization in patients with hypertensive heart failure. J Am Coll Cardiol. 2016; 67(3): 251–260.
  30. de Jong S, van Veen TAB, de Bakker JMT, et al. Biomarkers of myocardial fibrosis. J Cardiovasc Pharmacol. 2011; 57(5): 522–535.
  31. Yang RY, Rabinovich GA, Liu FT. Galectins: structure, function and therapeutic potential. Expert Rev Mol Med. 2008; 10: e17.
  32. Shah RV, Chen-Tournoux AA, Picard MH, et al. Galectin-3, cardiac structure and function, and long-term mortality in patients with acutely decompensated heart failure. Eur J Heart Fail. 2010; 12(8): 826–832.
  33. de Boer RA, Yu L, van Veldhuisen DJ. Galectin-3 in cardiac remodeling and heart failure. Curr Heart Fail Rep. 2010; 7(1): 1–8.
  34. Lok DJA, Van Der Meer P, de la Porte PWA, et al. Prognostic value of galectin-3, a novel marker of fibrosis, in patients with chronic heart failure: data from the DEAL-HF study. Clin Res Cardiol. 2010; 99(5): 323–328.
  35. de Boer RA, van Veldhuisen DJ, Gansevoort RT, et al. The fibrosis marker galectin-3 and outcome in the general population. J Intern Med. 2012; 272(1): 55–64.
  36. Grandin EW, Jarolim P, Murphy SA, et al. Galectin-3 and the development of heart failure after acute coronary syndrome: pilot experience from PROVE IT-TIMI 22. Clin Chem. 2012; 58(1): 267–273.
  37. de Boer RA, Lok DJA, Jaarsma T, et al. Predictive value of plasma galectin-3 levels in heart failure with reduced and preserved ejection fraction. Ann Med. 2011; 43(1): 60–68.
  38. Lin YH, Lin LY, Wu YW, et al. The relationship between serum galectin-3 and serum markers of cardiac extracellular matrix turnover in heart failure patients. Clin Chim Acta. 2009; 409(1-2): 96–99.
  39. Gullestad L, Ueland T, Kjekshus J, et al. CORONA Study Group. Galectin-3 predicts response to statin therapy in the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA). Eur Heart J. 2012; 33(18): 2290–2296.
  40. Zamora E, Lupón J, de Antonio M, et al. Renal function largely influences Galectin-3 prognostic value in heart failure. Int J Cardiol. 2014; 177(1): 171–177.
  41. AbouEzzeddine OF, Haines P, Stevens S, et al. Galectin-3 in heart failure with preserved ejection fraction. A RELAX trial substudy (Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Diastolic Heart Failure). JACC Heart Fail. 2015; 3(3): 245–252.
  42. Carthew RW, Sontheimer EJ. Origins and mechanisms of miRNAs and siRNAs. Cell. 2009; 136(4): 642–655.
  43. Weber JA, Baxter DH, Zhang S, et al. The microRNA spectrum in 12 body fluids. Clin Chem. 2010; 56(11): 1733–1741.
  44. Tijsen AJ, Pinto YM, Creemers EE. Non-cardiomyocyte microRNAs in heart failure. Cardiovasc Res. 2012; 93(4): 573–582.
  45. Thum T. Noncoding RNAs and myocardial fibrosis. Nat Rev Cardiol. 2014; 11(11): 655–663.
  46. Roy S, Khanna S, Hussain SRA, et al. MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue. Cardiovasc Res. 2009; 82(1): 21–29.
  47. Liang H, Zhang C, Ban T, et al. A novel reciprocal loop between microRNA-21 and TGFβRIII is involved in cardiac fibrosis. Int J Biochem Cell Biol. 2012; 44(12): 2152–2160.
  48. Villar AV, García R, Merino D, et al. Myocardial and circulating levels of microRNA-21 reflect left ventricular fibrosis in aortic stenosis patients. Int J Cardiol. 2013; 167(6): 2875–2881.
  49. van Rooij E, Sutherland LB, Thatcher JE, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci U S A. 2008; 105(35): 13027–13032.
  50. Roncarati R, Viviani Anselmi C, Losi MA, et al. Circulating miR-29a, among other up-regulated microRNAs, is the only biomarker for both hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2014; 63(9): 920–927.
  51. Goren Y, Kushnir M, Zafrir B, et al. Serum levels of microRNAs in patients with heart failure. Eur J Heart Fail. 2012; 14(2): 147–154.