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Low-Molecular-Weight Heparin for Acute STEMI

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Low-Molecular-Weight Heparin for Acute STEMI
Background: Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases, with acute ST-segment elevation myocardial infarction (STEMI) showing a higher mortality rate than non-ST-segment elevation myocardial infarction (NSTEMI). There is evidence that low-molecular-weight heparin (LMWH) shows greater efficacy than unfractionated heparin (UFH). This open-label, single-centre, randomised study was conducted to compare the efficacy and safety of parnaparin sodium, a LMWH, with UFH in patients with STEMI.
Patients and Methods: Patients with STEMI were randomised to receive either parnaparin sodium (4250IU aXa subcutaneously every 12 hours for 7 days, initiated 12 hours after thrombolysis) or UFH (100 U/kg intravenous bolus, initiated 12 hours after thrombolytic therapy, followed by 1000 U/hour as a continuous infusion for 3 days, then 7500U subcutaneously every 12 hours for 4 days). Patients were followed up for 45 days (≥14 days in hospital).
Results: In total, 186 patients were randomised to receive parnaparin sodium (n = 96) or UFH (n = 90). A significantly greater reduction in the composite primary endpoint (sum of all deaths, first occurrence of recurrent MI, and first occurrence of emergency revascularisation) was seen with parnaparin sodium compared with UFH at day 45 (27.08% vs 42.22%; p = 0.03). A lower incidence of composite endpoint was seen as early as day 2 with parnaparin sodium, but this did not reach significance versus UFH. The rate of individual endpoint events (death, first occurrence of non-fatal recurrent MI and first occurrence of emergency revascularisation) was lower in the parnaparin sodium group than the UFH group at 2, 7, 14 and 45 days, but the differences were not statistically significant. At day 7, the incidences of any bleeding and heparin-induced thrombocytopenia were also lower in the parnaparin sodium group compared with the UFH group (3.13% vs 10.0%; p = 0.06 and 0% vs 3.33%; p = 0.07, respectively).
Conclusion: The results of this study indicate that parnaparin sodium is more effective than UFH in reducing composite cardiac events in patients with STEMI following thrombolytic therapy. There was also a lower incidence of bleeding and heparin-induced thrombocytopenia with parnaparin sodium than with UFH. In view of these findings, parnaparin sodium represents an effective, convenient and well tolerated alternative to UFH.

Acute myocardial infarction (AMI) is one of the most serious cardiovascular diseases. It is divided into acute ST-segment elevation myocardial infarction (STEMI) and acute non-ST-segment elevation myocardial infarction (NSTEMI), of which STEMI has the higher mortality rate. The standard anticoagulation therapy in these patients is unfractionated heparin (UFH) and aspirin, but in clinical practice we find that low-molecular-weight heparin (LMWH) is more effective than UFH and improves patient outcome. Parnaparin sodium has been shown to have potent anticoagulant effects in haemodialysis patients and in patients with thromboembolic disorders. In a recent study in patients with unstable angina, parnaparin sodium was better tolerated and more effective than UFH. However, specific data in AMI are limited.

This open-label, single-centre study was designed to compare the efficacy and safety of UFH and parnaparin sodium in patients with acute STEMI undergoing thrombolytic therapy. Findings from this study have previously been published in China.

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