Recombinant tissue plasminogen activator treatment for COVID-19 associated ARDS and acute cor pulmonale
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01.03.2021 |
Kosanovic D.
Yaroshetskiy A.I.
Tsareva N.A.
Merzhoeva Z.M.
Trushenko N.V.
Nekludova G.V.
Schermuly R.T.
Avdeev S.N.
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International Journal of Infectious Diseases |
10.1016/j.ijid.2020.12.043 |
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© 2020 The Author(s) Existing literature highlights the fact that patients with COVID-19 exhibit alterations in the coagulation process and are associated with respiratory and cardiovascular diseases, including acute respiratory distress syndrome and acute cor pulmonale. In this report, we describe the effects of systemic thrombolysis on acute cor pulmonale in a patient suffering from COVID-19. We demonstrated that systemic thrombolysis successfully improved the hemodynamics of our patient and resulted in a prominent reduction in hypercapnia, alveolar dead space, and ventilatory ratio.
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Effects of tranexamic acid, factor XIII, and fibrinogen on clot formation and lysis in the model of hyperfibrinolysis induced by tissue- vs urokinase-type plasminogen activator
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01.01.2018 |
Budnik I.
Morozova O.
Tsymbal A.
Shenkman B.
Einav Y.
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Gematologiya i Transfusiologiya |
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© 2018 Izdatel'stvo Meditsina. All rights reserved. Aim of the study. To compare the effects of tranexamic acid (TXA), factor XIII concentrate (FXIII) and fibrinogen concentrate on clot formation and fibrinolytic resistance in the in vitro model of hyperfibrinolysis induced by tissue-(tPA) vs urokinase-type (uPA) plasminogen activators. Materials and methods. Citrated whole blood from 28 adult healthy volunteers was supplemented with 10 μg/ mL TXA, 2 lU/mL FXIII, or 3 mg/mL fibrinogen concentrate. Hyperfibrinolysis was induced by spiking the blood with PA or uPA at their half-maximal effective concentrations (90 and 33 lU/mL, respectively). Clotting was induced by recalcification and addition of tissue factor and monitored using rotation thromboelastometry. Results. The use of TXA increased maximal clot firmness in the presence of tPA and markedly inhibited clot lysis in the presence of any of the plasminogen activators. Supplementation of blood with FXIII significantly increased clot firmness and improved fibrinolytic resistance in the presence of either PA or uPA. Supplementation with fibrinogen concentrate elicited a strikingly different effect on clot formation and lysis depending on the type of plasminogen activator. In the presence of tPA, fibrinogen concentrate significantly increased clot firmness and attenuated clot lysis. In contrast, in the presence of uPA, the use of fibrinogen markedly reduced clot firmness and promoted clot lysis. Similar effects of fibrinogen concentrate were observed in platelet-rich and microparticles-free plasma. Conclusion. In hyperfibrinolysis, effect of the hemostatic drugs significantly depends on the type of plasminogen activator used. Therefore, mechanisms of hyperfibrinolysis should be taken into consideration while administering hemostatic drugs.
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