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Systemic lytic state is not a predictor of coronary reperfusion in acute myocardial infarction
N el Gaylani1, S Davies, J Tovey
1Department of Cardiology, University Hospital of Wales, Heath Park, Cardiff, UK.
Insights
Many patients treated with streptokinase for heart attacks do not achieve reperfusion. This failure is not due to insufficient lytic status, suggesting higher streptokinase doses won't improve outcomes.
Area of Science:
- Cardiology
- Thrombolytic Therapy
Background:
- Approximately one-third of patients receiving streptokinase for acute myocardial infarction fail to achieve reperfusion.
- Understanding the reasons for treatment failure is crucial for optimizing patient outcomes.
Purpose of the Study:
- To investigate the factors contributing to reperfusion failure in patients treated with streptokinase for the first time.
- To determine if failure to achieve a systemic lytic state or the presence of antistreptokinase antibodies are responsible for reperfusion failure.
Main Methods:
- Assessed lytic status (fibrinogen, thrombin clotting time) before and after streptokinase infusion in 95 patients.
- Measured antistreptokinase antibodies prior to treatment.
- Evaluated reperfusion using 24:96 h troponin-T ratio and ST segment resolution post-infusion.
Main Results:
- 97% of patients achieved a systemic lytic state.
- Despite achieving a lytic state, 27% of patients failed to reperfuse.
- No significant differences were observed in fibrinogen levels, thrombin clotting time, or antistreptokinase antibody levels between reperfused and non-reperfused groups.
Conclusions:
- Failure to reperfuse with streptokinase is not caused by an inability to achieve a sufficient lytic state.
- Increasing streptokinase dosage or infusion rate is unlikely to improve reperfusion rates in patients who do not respond initially.
Abstract:
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/l; 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.