Add time:07/21/2019         Source:sciencedirect.com

One of the principal problems associated with thrombolytic therapy is rethrombosis of vessels which were initially patent. Although platelets as well as coagulation activation have been implicated in rethrombosis, the specific mechanisms leading to this complication are still unclear. Available evidence is limited to smaller studies using the current thrombolytic agents. Here we report on the multicentre SUTAMI trial comparing recombinant Saruplase (cas 99149-95-8) and urokinase in 543 patients with acute myocardial infarction, in 33 of whom early reinfarction was documented. Plasma from these patients and 33 matched patients without reinfarction was investigated for thrombin-antithrombin III complex and prothrombin activation fragments 1 + 2 as markers of activated coagulation, during 72h after starting the lytic therapy.Both drugs caused considerable systemic degradation of fibrinogen and the degree of systemic lysis was very similar. The median concentrations of both thrombin-antithrombin III complex and prothrombin fragments 1 + 2 significantly increased 3- to 6-fold after the therapy, indicating extensive activation of the coagulation system. Following heparin administration, both parameters returned towards normal in most patients. At no time points studied was there any significant difference in these coagulation parameters between the patients with and those without reinfarction. In contrast to other findings, thrombin-antithrombin III complex concentration was not a useful indicator of reinfarction in the patients studied and neither was the concentration of prothrombin activation fragments 1 + 2.

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