Регистрация
Забыли свой пароль?
  1. Главная
  2. Каталог статей
  3. Креативная кардиология. 2018; 12(4)
  4. Эндогенный фибринолиз и ишемическая болезнь сердца

Эндогенный фибринолиз и ишемическая болезнь сердца

Авторы: Саввинова П.П., Калинская А.И.

Организация:
Кафедра кардиологии ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России, ул. Делегатская, 20/1, Москва, 127473, Российская Федерация

Для корреспонденции: Сведения доступны для зарегистрированных пользователей.

Тип статьи: Обзорные статьи

DOI: https://doi.org/10.24022/1997-3187-2018-12-4-341-352

УДК: 616.12-005.4:615.273.55

Для цитирования:  Саввинова П.П., Калинская А.И. Эндогенный фибринолиз и ишемическая болезнь сердца. Креативная кардиология. 2018; 12 (4): 341–52. DOI: 10.24022/1997-3187-2018-12-4-341-352

Поступила / Принята к печати:  27.09.2018/09.10.2018

Ключевые слова: эндогенный фибринолиз, острый инфаркт миокарда, спонтанная реперфузия

Скачать (Download)


 

Аннотация

Ишемическая болезнь сердца (ИБС) является одной из ведущих причин госпитализаций и смертности во всем мире. Смертность от ИБС обусловлена преимущественно острыми формами – острым коронарным синдромом, а именно острым инфарктом миокарда (ОИМ), а также его осложнениями, которые развиваются как в остром, так и в отдаленном периодах. Наиболее частый патогенетический вариант развития ОИМ – образование тромба в просвете коронарной артерии вследствие разрыва или эрозии нестабильной атеросклеротической бляшки. Сформируется ли полная или частичная окклюзия коронарной артерии, зависит от активации не только свертывающей системы, но и противо- свертывающей и фибринолитической систем. В 15,7% случаев полной окклюзии инфаркт-связанной артерии возникает спонтанное восстановление кровотока. Механизм спонтанной реперфузии до конца не ясен, важную роль в ней играет функциональное состояние эндотелия, а также активация фибринолитической системы, направленной на растворение тромба. В настоящем обзоре мы рассмотрим полученные нами и другими исследователями данные о механизме и роли активации фибринолитической системы у пациентов с ИБС, а также обсудим методы изучения фибринолиза.

Литература

  1. Sakakura K., Nakano M., Otsuka F., Ladich E., Kolodgie F.D., Virmani R. Pathophysiology of atherosclerosis plaque. Hear. Lung Circ. 2013; 22 (6): 399–411. DOI: 10.1016/j.hlc.2013.03.001
  2. Virmani R., Kolodgie F.D., Burke A.P., Farb A., Schwartz S.M. Lessons from sudden coronary death: a comprehensive morphological classification scheme. Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1262–75. DOI: 10.1161/01.ATV.20.5.1262
  3. Fernandez-ortiz A., Badimon J.J., Falk E., Fuster V., Meyer B., Mailhac A. Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. J. Am. Coll. Cardiol. 1994; 23 (7) 1562–9. DOI: 10.1016/0735-1097 (94)90657-2
  4. Owens A.P., Mackman N. Tissue factor and thrombosis: the clot starts here thromb. Haemost. 2010; 104 (3): 432–9. DOI: 10.1160/TH09-11-0771
  5. Freynhofer M.K., Bruno V., Wojta J., Huber K. The role of platelets in athero-thrombotic events. Cur. Pharm. Design. 2012; 18: 5197–214. DOI: 10.2174/138161212803251899
  6. Tahler T., Fu Y., Wagner G., Goodman S., Fresco C., Granger C. et al. aborted myocardial infarction in patients with ST-Segment elevation. J. Am. Coll. Cardiol. 2004; 44 (1): 38–43. DOI: 10.1016/j.jacc.2004.03.041
  7. DeWood M., Spores J., Hensley G. Coronary arteriographic findings in acute transmural myocardial infarction. Circulation. 1983; 68: 139–49.
  8. Stone G.W., Cox D., Garcia E., Brodie B.R., Morice M.C. et al. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction analysis from the primary angioplasty in myocardial infarction trials. Circulation. 2001; 104 (6): 636–41. DOI: 10.1161/hc3101.093701
  9. Werf F., Ross A., Granger C., Diaz R. Aylward P., Huber K. et al. Primary versus tenecteplase-facilitated percutaneous coronary intervention in patients with ST-segment elevation acute myocardial infarction (ASSENT-4 PCI): randomised trial. Lancet. 2006; 367 (9510): 569–78. DOI: 10.1016/S0140-6736 (06)68147-6
  10. Fefer P., Hod H., Hammerman H., Boyko V., Behar S., Matetzky S. Relation of clinically defined spontaneous reperfusion to outcome in ST-elevation myocardial infarction. Am. J. Cardiol. 2009; 103 (2): 149–53. DOI: 0.1016/j.amjcard.2008.08.050 11. Miles L., Greengard J., Griffin J. A comparison of the abilities of plasma kallikrein, beta-Factor XIIa, Factor XIa and urokinase to activate plasminogen. Thromb Res. 1983; 29 (4): 407–17.
  11. Sakamoto T., Ogawa H., Takazoe K., Yoshimura M., Shimomura H., Moriyama Y. et al. Effect of activated protein c on plasma plasminogen activator inhibitor activity in patients with acute myocardial infarction treated with alteplase. J. Am. Coll. Cardiol. 2003; 42 (8): 1389–94. DOI: 10.1016/S0735-1097 (03)01059-3
  12. Collen D., Lijnen H.R. Basic and clinical aspects of fibrinolysis and thrombolysis. Blood. 1991; 78 (12): 3114–24.
  13. Lucas M.A., Fretto L.J., Mckee A. The binding of human plasminogen to fibrin and fibrinogen. J. Biol. Chem. 1983; 258 (7): 4249–56.
  14. Stricker R.B., Wong D., Shiu D.T., Reyes P.T., Shuman M.A. Activation of plasminogen by tissue plasminogen activator on normal and thrombasthenic platelets: effects on surface proteins and platelet aggregation. Blood. 1986; 68 (1): 275–80. DOI: 0006-4971/86/6801-004303.00/0.
  15. Wiman B., Collen D. On the mechanism of the reaction between human α2-antiplasmin and plasmin. J. Biol. Chem. 1979; 254 (18): 9291–7.
  16. Braunwald E., Bonow R.O., Mann D., Zipes D., Libby P. Braunwald heart disease. Elsevier; 2011.
  17. Booyse F.M., Bruce R., Dolenak D., Grover M., Casey L.C. et al. Rapid release and deactivation of plasminogen activators in human endothelial cell cultures in the presence of thrombin and lonophore A23187. Sem. Thromb. Hemost. 1986; 12 (3): 10–2. DOI: 10.1055/s-2007-1003558
  18. Singh I., Burnand K.G., Collins M., Luttun A., Collen D., Boelhouwer B. et al. Failure of thrombus to resolve in urokinase-type plasminogen activator gene-knockout mice. Circulation. 2003; 107: 869–75. DOI: 10.1161/01.CIR.0000050149.22928.39
  19. Gurewich V., Pannell R. Synergism of tissuetype plasminogen activator (t-PA) and singlechain urokinase-type plasminogen activator (scu-PA) on clot lysis in vitro and a mechanism for this effect. J. Thromb. Haemost. 1987; 57: 372–3.
  20. Wiman B., Chmielewska J., Rinbyt M., Ranby M. Inactivation of tissue plasminogen activator in plasma. J. Biol. Chem. 1984; 259 (6): 3644–7.
  21. Vaughan D.E. PAI-1 and atherothrombosis. Thromb. Haemost. 2005; 3: 1879–83. DOI: 10.1111/j.1538-7836.2005.01420.x
  22. Wiman B., Andersson T., Hallqvist J., Reuterwall C., Ahlbom A. Plasma levels of tissue plasminogen activator/plasminogen activator inhibitor- 1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study. Arterioscler. Thromb. Vasc. Biol. 2000; 20 (8): 2019–23. DOI: 10.1161/01.ATV.20.8.2019
  23. Tregouet D.A., Schnabel R., Alessi M., Godefroy T., Declerck P.J., Nicaud V. et al. Activated thrombin activatable fibrinolysis inhibitor levels are associated with the risk of cardiovascular death in patients with coronary artery disease: the AtheroGene study. J. Thromb. Haemost. 2009; 7 (1): 49–57. DOI: 10.1111/j.1538-7836.2008.03221.x
  24. Leenaerts D., Bosmans J.M., van der Veken P., Sim Y., Lambeir A. M., Hendriks D. Plasma levels of carboxypeptidase U (CPU, CPB2 or TAFIa) are elevated in patients with acute myocardial infarction. J. Thromb. Haemost. 2015; 13 (12) 2227–32. DOI: 10.1111/jth.13135
  25. Shaukat S., Lipinski B. Purification and partial characterization of a single-chain high-form of urokinase from human urine affinity chromatography a previously described technique for isoshown to consist of two subunits linked by is believed to be derived from the HMW urokinase by proteolytic degradation fibrinogen. Arch. Biochem. Biophys. 1983; 220 (1): 31–8.
  26. Xu J., Li W., Bao X., Ding H., Chen J., Zhang W. et al. Association of putative functional variants in the PLAU gene and the PLAUR gene with myocardial infarction. Clin. Sci. 2010; 119 (8): 353–9. DOI: 10.1042/CS20100151
  27. Yamamoto J., Inoue N., Otsui K., Ishii H., Gorog D.A. Global Thrombosis Test (GTT) can detect major determinants of haemostasis including platelet reactivity , endogenous fi brinolytic and thrombin generating potential. Thromb. Res. 2014; 133 (5): 919–26. DOI: 10.1016/j.thromres.2014.02.018
  28. Saraf S., Christopoulos C., Salha I.B., Stott D.J., Gorog D.A. Impaired endogenous thrombolysis in acute coronary syndrome patients predicts cardiovascular death and nonfatal myocardial infarction. J. Am. Coll. Cardiol. 2010; 55 (19): 2107–15. DOI: 10.1016/j.jacc.2010.01.033
  29. Zamani P., Schwartz G.G., Olsson A.G., Rifai N.W., Libby P. et al. Inflammatory biomarkers, death, and recurrent nonfatal coronary events after an acute coronary syndrome in the MIRACL study. J. Am. Heart Assoc. 2013; 2 (1): 1–8. DOI: 10.1161/JAHA.112.003103
  30. May M., Lawlor D., Patel R., Rumley A., Lowe G., Ebrahim S. Associations of von Willebrand factor, fibrin D-dimer and tissue plasminogen activator with incident coronary heart disease: British Women’s Heart and Health cohort study. Eur. J. Cardiovasc. Prev. Rehabil. 2007; 14 (5): 638–45. DOI: 0.1097/HJR.0b013e3280e129d0
  31. Tofler G.H., Massaro J., O'Donnell C.J., Wilson P.W.F., Vasan R.S., Sutherland P.A. et al. Plasminogen activator inhibitor and the risk of cardiovascular disease: The Framingham Heart Study. Thromb. Res. 2016; 140: 30–5. DOI: 10.1016/j.thromres.2016.02.002
  32. Abd T.A., Rezk E.N. A. Relation of PAI-1 and TPA genes polymorphisms to acute myocardial infarction and its outcomes in egyptian patients. Cell. Biochem. Biophys. 2015; 71 (1): 227–34. DOI: 10.1007/s12013-014-0188-x
  33. Olofsson B.O., Dahlén G., Nilsson T.K. Evidence for increased levels of plasminogen activator inhibitor and tissue plasminogen activator in plasma of patients with angiographically verified coronary artery disease. Eur. Heart J. 1989; 10 (1): 77–82.
  34. Itakura H., Sobel B.E., Boothroyd D., Leung L.L. Do plasma biomarkers of coagulation and fibrinolysis differ between patients who have experienced an acute myocardial infarction versus stable exertional angina? Am. Heart J. 2007; 154 (6): 1059–64. DOI: 10.1016/j.ahj.2007.09.01
  35. Pineda J., Marín F., Marco P., Roldán V., Valencia J., Ruiz-Nodar J.M. et al. Premature coronary artery disease in young (age < 45) subjects: Interactions of lipid profile, thrombophilic and haemostatic markers. Int. J. Cardiol. 2008; 136 (2): 222–5. DOI: 10.1016/j.ijcard.2008.04.020
  36. Bespalko I.A., Vasilieva E.Y., Sobolev K.E., Lyaginsky A.V., Radzevich A.E. Change of tissue plasminogen level and activation in patients with coronary artery disease. Kardiologia. 1995; 3: 9–11.
  37. Takazoe K., Ogawa H., Yasue H., Sakamoto T., Soejima H., Miyao Y. et al. Increased plasminogen activator inhibitor activity and diabetes piedict suhequent coronary events in patients with angina pectoris. Ann. Med. 2001; 33 (3): 206–12. 39. Gori A.M., Prisco D., Abbate R., Gensini G.F. PAI-1 and homocysteine, but not lipoprotein (a) and thrombophilic polymorphisms, are independently associated with the occurrence of major adverse cardiac events after successful coronary stenting. Heart. 2006; 92 (3): 377–81. DOI: 10.1136/hrt.2005.061895
  38. Cagliyan C.E., Yuregir O.O., Balli M., Tekin K., Akilli R.E., Bozdogan S.T. et al. Plasminogen activator inhibitor-1 5G/5G genotype is associated with early spontaneous recanalization of the infarct-related artery in patients presenting with acute ST-elevation myocardial infarction. Coron. Artery Dis. 2013; 24 (3): 196–200. DOI: 10.1097/MCA.0b013e32835d7633
  39. Falco C., Espan F., Osa A., Zorio E., Castello R. Thrombin-activatable fibrinolysis inhibitor in young patients with myocardial infarction and its relationship with the fibrinolytic function and the protein C system. Br. J. Haematol. 2003; 122 (6): 958–65. DOI: 10.1046/j.1365-2141.2003.04549.x
  40. De Bruijne E.L., Gils A., Guimara~es A.H., Dippel D.W., Deckers J.W., van den Meiracker A.H. et al. The role of thrombin activatable fibrinolysis inhibitor in arterial thrombosis at a young age: the ATTAC study. J. Thromb. Haemost. 2008; 7 (6): 919–27. DOI: 10.1111/j.1538-7836.2009.03350.x
  41. Segev A., Hegele R.A., Lau H.K., Sparkes J.D., Teitel J.M., Chisholm R.J. et al. Thr325Ile polymorphism of the TAFI gene is related to TAFI antigen plasma levels and angiographic restenosis after percutaneous coronary interventions. Thromb. Res. 2004; 114 (2): 137–41. DOI: 10.1016/j.thromres.2004.06.003
  42. Chatteriee T., Schoeder V., Windecker S., Mehta H., Pham T., Devantay N. Thrombin Activatable Fibrinolysis Inhibitor (TAFI) levels in patients with coronary artery disease investigated by angiography. Thromb. Haemost. 2002; 88 (6): 1020–5.
  43. Erqou S., Kaptoge S., Perry P.L., Di Angelantonio E., Thompson A., White I.R. et al. Lipoprotein (a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA. 2009; 302 (4): 412–23. DOI: 10.1001/jama.2009.1063
  44. Kim J.W., Seo H.S., Suh S.Y., Choi C.U., Kim E.J., Rha S.W. et al. Relationship between lipoprotein (a) and spontaneous recanalization of infarctrelated arteries in the early phase of acute myocardial infarction. Clin. Cardiol. 2008; 31 (5): 211–6. DOI: 10.1002/clc.20143
  45. Sagastagoitia J.D., Vacas M., Saez Y., Sáez de Lafuente J.P., Santos M., Lafita M. et al. Lipoprotein (a), D-Dimer and apolipoprotein A1 as markers of presence and severity of coronary disease. Med. Clin. (Barc). 2009; 132 (18): 689–94. DOI: 10.1016/j.medcli.2008.11.037
  46. Sagastagoitia J.D., Vacas M., Saez Y., Sáez de Lafuente J.P., Santos M., Lafita M. et al. Predictive value of lipoprotein (a) and apolipoprotein A1 in patients with angiographycally evaluated coronary stenosis. Med. Clin. (Barc.). 2007; 128 (16): 601–4
  47. Wang J., Zhang C., Meng Y., Han A., Gong J., Li K. Elevated concentrations of oxidized lipoprotein (a) are associated with the presence and severity of acute coronary syndromes. Clin. Chim. Acta. 2009; 408 (1–2): 79–82. DOI: 10.1016/j.cca.2009.07.013
  48. Cushman M., Lemaitre R.N., Kuller L.H., Psaty B.M., Macy E.M., Sharrett A.R. et al. Fibrinolytic activation markers predict myocardial infarction in the elderly the cardiovascular health study. ATVB. 2015; 19 (3): 493–8. DOI: 10.1161/01.ATV.19.3.493
  49. Kallel C., Cohen W., Saut N., Blankenberg S., Schnabel R., Rupprecht H.J. Association of soluble endothelial protein C receptor plasma levels and PROCR rs867186 with cardiovascular risk factors and cardiovascular events in coronary artery disease patients: the Athero Gene study. BMC Med. Genet. 2012; 13: 103. DOI: 10.1186/1471-2350-13-103

Об авторах

  • Саввинова Полина Павловна, аспирант, orcid.org/0000-0001-8596-5212;
  • Калинская Анна Ильинична, доцент, канд. мед. наук, orcid.org/0000-0003-2316-4238

Электронная подписка

Для получения доступа к тексту статей журнала воспользуйтесь услугой «Электронная подписка»:

Оформить подписку Подробнее об электронной подписке

Главный редактор

Лео Антонович Бокерия, академик РАН и РАМН

Лео Антонович Бокерия, доктор медицинских наук, профессор, академик РАН и РАМН, президент


Сортировать по


 Если вы заметили опечатку, выделите текст и нажмите alt+A