Thrombolytic therapy activates the contact system, and
factor XII activation may activate the coagulation cascade and
inflammation. It is not known whether an early inflammatory response is induced by
thrombolytic therapy in patients with acute
myocardial infarction (AMI). We prospectively measured the plasma levels of
activated factor XII, cleaved
kininogen,
prothrombin fragment 1 + 2 (as indexes of the contact phase and coagulation activation), and
interleukin-6 and
C-reactive protein (CRP) (as indexes of
inflammation) in 39 patients hospitalized for AMI within 12 hours of symptom onset: 26 receiving
thrombolytic therapy and 13
heparin alone. Blood samples were collected at baseline and after 90 minutes and 24 hours. Patients undergoing thrombolysis had a significant early increase in
activated factor XII (from 2.2 ng/ml at baseline to 4.7 ng/ml after 90 minutes; p = 0.0001), cleaved
kininogen (from 26% to 37%; p = 0.001), and fragment 1 + 2 (from 1.4 to 2.1 nmol/L; p = 0.0001), whereas the 24-hour levels were similar to baseline levels. The levels of
interleukin-6 significantly increased during the first 90 minutes (from 3.9 to 6.3 microg/ml; p = 0.001), and were even higher after 24 hours (11.9 ng/ml, p = 0.0001). CRP levels increased only after 24 hours (p = 0.0001). There were no changes in these parameters in patients receiving
heparin alone, except for a 24-hour increase in
interleukin-6 and CRP levels. Thus, in patients with AMI receiving
thrombolytic therapy, early activation of
inflammation parallels the activation of the contact system and the coagulation cascade, which might contribute to microvascular obstruction and
reperfusion injury.