Augmented Plasma Protein C Activity after Coronary Thrombolysis with Urokinase in Patients with Acute Myocardial Infarction

Goto, Shinichi; Handa, Shunnosuke; Kawai, Yohko; Watanabe, Kazuhiro; Abe, Sumihisa; Takáhashi, Eiichi; Hori, Shingo; Ikeda, Yasuo

doi:10.1159/000175010

Cited by 5 publications

(2 citation statements)

References 5 publications

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“…A rapid decrease of protein C inhibitor has been reported in patients with acute deep vein thrombosis during heparin treatment, but without change in protein C activity itself (14). Our results are consistent with a report of an increase of protein C activity in patients with acute myocardial infarction and thrombolysis by urokinase (16). It is apparent from our data, that protein C can be determined in the acute phase of a thrombosis.…”

Section: Discussionsupporting

confidence: 92%

Parameters of Haemostasis during Acute Venous Thrombosis

et al. 1995

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SummaryUnderlying disorders of the coagulation system such as inhibitor deficiencies or decreased fibrinolysis are common in patients suffering from venous thrombosis. They may lead to the necessity of a lifelong prophylaxis. Prompt diagnosis is obviously to the patients benefit. We investigated 22 patients suffering from venous thromboses for the inhibitors antithrombin III (ATIII), protein C, and protein S during the first 8 to 12 days after admission to hospital and in addition after withdrawal from anticoagulant treatment after several months. At the day of admission ATIII and protein C levels were comparable to those several months later, but after 2 days they shifted downward or upward, respectively. Protein S did not shift during the period of hospitalisation, but was initially slightly lower than several months later. For inhibitors the day of admission to hospital is most suitable to take the samples. About 50% of the patients still had elevated activation markers (prothrombin fragments F1+2, thrombin-antithrombin complex TAT, and D-dimers) after several months.

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Section: Discussionsupporting

confidence: 92%

Parameters of Haemostasis during Acute Venous Thrombosis

et al. 1995

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“…Me|utim, sama aktivnost proteina C kod bolesnika koji nisu postigli reperfuziju mo`e biti smanjena, verovatno zbog zna~ajne aktivacije inhibitora ovog sistema (71). Fibrinoliti~ka terapija dovodi do izrazite aktivacije proteina C tokom i neposredno nakon primene (72,73). Mogu}e je da je ovaj efekat fibrinoliti~ke terapije vrlo bitan za odr`anje prolaznosti infarktne arterije.…”

Section: Antikoagulantni Sistem U Akutnom Infarktu Miokardaunclassified

Haemostasis in acute myocardial infarction

Obradovic

Mandić-Radić²,

Dinčić

et al. 2003

Jugoslav Med Biohem

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Kratak sadr`aj: Akutni infarkt miokarda uzrokovan je lokalizovanom arterijskom trombozom koja dovodi do ishemije i nekroze mi{i}nog tkiva. Ovaj doga|aj ima za posledicu reakciju samog sr~anog mi{i}a (akinezija i diskinezija ishemi~nih delova srca, poreme}aji sr~anog ritma i hemodinamike), ali i vrlo izra`enu sistemsku reakciju (aktivacija neuroendokrinog sistema i pokretanje inflamatornog odgovora). Iz pomenutog je jasno da su pore-me}aji hemostaze koji se mogu na}i u akutnom infarktu miokarda delimi~no posledica lokalne aktivacije hemostaze u tromboziranoj epikardnoj arteriji, delimi~no ih uzrokuje aktivacija hemostaznih procesa zbog poreme}enog toka krvi kroz sr~ane {upljine (aritmije i diskinezija) i zbog poreme}ene hemodinamike, a delimi~no su odraz sistemske reakcije organizma (fibrinogen i von-Willebrand-ov faktor su proteini akutne faze). Brojni terapijski postupci tako|e zna~ajno uti~u na hemostazu, od postavljanja poveske za va|enje krvi, venepunkcija, pa do primene lekova od kojih su u akutnom infarktu miokarda klju~ni ba{ oni koji deluju na procese hemostaze. Na koagulacione parametre u trenutku akutnog infarkta uti~u zna~ajno i premorbidna stanja (pu{enje, hipertenzija, dijabetes, hiperlipoproteinemije, hroni~ni inflamatorni procesi) kao i pridru`ene bolesti.

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Serial Changes in Coagulant Activities After Thrombolytic Therapy for Acute Myocardial Infarction

et al. 1994

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Early reocclusion and bleeding complications are still unresolved problems in thrombolytic therapy for acute myocardial infarction (AMI). In the present study, 16 patients treated with either fibrin-specific tissue-type plasminogen activator (t-PA) or nonspecific urokinase (UK) were studied to determine the effects of thrombolytic therapy on serial hemostatic states. Hemostatic states of each patient were estimated by measuring various plasma markers at one- to two-hour intervals during the first six hours of therapy, daily during the next three days, and subsequently on day 7. Two markers of plasma thrombin generation, thrombin antithrombin III complex (TAT) and prothrombin fragment 1 + 2 (F 1 + 2), showed an activated coagulant state immediately after thrombolytic therapy. The amount of thrombin generation indicated by these markers showed significant positive correlation with direct markers of fibrinolysis such as fibrin degradation products (FDP), while it did not show any correlation with the markers for plasmin generation. The potential for coagulation as indicated by prothrombin time (%) decreased with thrombolysis using fibrin nonselective agents, owing perhaps to destruction of coagulant factors by free plasmin. Fibrinolytic activity induced by thrombolytic therapy for AMI caused transient activation of the coagulant system, which could contribute to early reocclusion. Fibrin nonselective agents decreased the potential for coagulation by destroying clotting factor through the generation of free plasmin. These data provide theoretical support for simultaneous administration of anticoagulant therapy with fibrin-specific thrombolytic agents.

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Augmented Plasma Protein C Activity after Coronary Thrombolysis with Urokinase in Patients with Acute Myocardial Infarction

Cited by 5 publications

References 5 publications

Parameters of Haemostasis during Acute Venous Thrombosis

Parameters of Haemostasis during Acute Venous Thrombosis

Haemostasis in acute myocardial infarction

Serial Changes in Coagulant Activities After Thrombolytic Therapy for Acute Myocardial Infarction

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