Six RCTs (6,069 patients) were included. Three trials used streptokinase, two used tenecteplase, and one used t-PA as the thrombolytic agent.
There was a non significant reduction in mortality in patients treated with enoxaparin compared with control (OR 0.86, 95% CI: 0.69, 1.09, P=0.19).
Treatment with enoxaparin reduced the rates of AMI (5 studies, OR 0.58, 95% CI: 0.44, 0.75, P=<0.001), refractory ischaemia or angina (3 studies, OR 0.69, 95% CI: 0.54, 0.88, P=0.003), and the combined end points (refractory ischaemia, death or AMI: OR 0.68, 95% CI: 0.58, 0.80, P=<0.001; death or AMI: OR 0.73, 95% CI: 0.61, 0.87, P=<0.001).
There was a significant increase in minor bleeding with enoxaparin (OR 1.29, 95% CI: 1.12, 1.41, P=<0.001). The overall results for major bleeding showed a trend towards increased risk with enoxaparin (OR 1.36, 95% CI: 0.98, 1.88, P=0.06) and no significant difference for intracranial bleeding (OR 0.97, 95% CI: 0.54, 1.73, P=0.92). When one trial that used placebo as control was excluded, the OR for major bleeding was 1.34 (95% CI: 0.97, 1.87, P=0.08). Major bleeding was more frequent with t-PA or tenecteplase than with streptokinase (OR 1.44, P=0.032).
Angiographic outcomes (3 trials) showed no significant difference in early TIMI grade 2 and 3 flow between the enoxaparin and control groups. However, there was a significant improvement in flow during late angiography (TIMI grade 2-3, OR 1.90, 95% CI: 1.35, 2.68, P<0.001).
Apart from bleeding outcomes, there was little difference between outcomes when the trials were grouped by those that used t-PA and tenecteplase versus those that used streptokinase. The other results were reported in the paper.
Except for angiography late TIMI 2-3 (P=0.06), tests for analyses showed no significant heterogeneity.