Systemic lytic state is not a predictor of coronary reperfusion in acute myocardial infarction

To investigate why approximately one third of patients thrombolysed with streptokinase fail to reperfuse, we assessed the lytic status, antistreptokinase antibody and non invasive parameters of reperfusion in 95 consecutive patients with acute myocardial infarction treated with streptokinase for the first time. The lytic status was assessed by Clauss fibrinogen assay and thrombin clotting time before and 2 h after streptokinase infusion. Antistreptokinase antibody was measured prior to the infusion. Reperfusion was assessed by measurement of the 24:96 h troponin-T ratio (a ratio >1 indicating reperfusion) and ST segment resolution 2 h post streptokinase. Ninety-two (97%) patients achieved a systemic lytic state with a fibrinogen titre of less than 1.0 g/l and thrombin clotting time ratio of >2.5. Despite this, 27% failed to reperfuse with a mean 24:96 h troponin-T of 0.9, SD 0.6 vs. 3.4 ± 3.2 in the reperfused group, ( P < 0.0001). 83% of the reperfused group but none of the non reperfused group had ST segment resolution. No difference was observed in the levels of fibrinogen and thrombin clotting time between the reperfused 0.25 ± 0.3 g/l; 6.9 ± 4, and the non reperfused group 0.4 ± 0.6 g/1; 7.9 ± 2.6. No difference was observed in the levels of antistreptokinase antibody between the reperfused (median = 168 U/ml and the non reperfused (median = 177 U/ml). Failure to reperfuse with Streptokinase is not due to failure to achieve a lytic state. Therefore increased or accelerated dosages of streptokinase are unlikely to increase the rate of reperfusion.