PLASMA MARKERS OF THROMBIN ACTIVITY DURING CORONARY THROMBOLYTIC THERAPY WITH SARUPLASE OR UROKINASE - NO PREDICTION OF REINFARCTION

One of the principal problems associated with thrombolytic therapy is rethrombosis of vessels which were initially patent. Although platelet s as well as coagulation activation have been implicated in rethrombos is, the specific mechanisms leading to this complication are still unc lear. Available evidence is limited to smaller studies using the curre nt thrombolytic agents. Here we report on the multicentre SUTAMI trial comparing recombinant saruplase and urokinase in 543 patients with ac ute myocardial infarction, in 33 of whom early reinfarction was docume nted. Plasma from these patients and 33 matched patients without reinf arction was investigated for thrombin-antithrombin III complex and pro thrombin activation fragments 1+2 as markers of activated coagulation, during 72 h after starting the lytic therapy. Both drugs caused consi derable systemic degradation of fibrinogen and the degree of systemic lysis was very similar. The median concentrations of both thrombin-ant ithrombin III complex and prothrombin fragments 1+2 significantly incr eased 3- to 6-fold after the therapy, indicating extensive activation of the coagulation system. Following heparin administration, both para meters returned towards normal in most patients. At no time points stu died was there any significant difference in these coagulation paramet ers between the patients with and those without reinfarction. In contr ast to other findings, thrombin-antithrombin III complex concentration was not a useful indicator of reinfarction in the patients studied an d neither was the concentration of prothrombin activation fragments 12.