Jjml. Hoffmann et al., PLASMA MARKERS OF THROMBIN ACTIVITY DURING CORONARY THROMBOLYTIC THERAPY WITH SARUPLASE OR UROKINASE - NO PREDICTION OF REINFARCTION, Fibrinolysis, 7(5), 1993, pp. 330-334
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.