Enoxaparin > UFH for STEMI treated with fibrinolysis then PCI
In patients with acute ST-elevation myocardial infarction who receive fibrinolysis and subsequent percutaneous intervention, is enoxaparin superior to unfractionated heparin?
Patients with ST-elevation myocardial infarction (STEMI) treated with fibrinolysis and subsequent percutaneous intervention (PCI) have a reduced risk of death or recurrent myocardial infarction (MI) at 30 days when managed with enoxaparin compared with unfractionated heparin (UFH), with no increased risk of bleeding. (LOE = 1b)
Gibson CM, Murphy SA, Montalescot G, et al, for the ExTRACT-TIMI 25 Investigators. Percutaneous coronary intervention in patients receiving enoxaparin or unfractionated heparin after fibrinolytic therapy for ST-segment elevation myocardial infarction in the ExTRACT-TIMI 25 Trial. J Am Coll Cardiol 2007;49:2238-2246. [PMID:17560287]
Randomized controlled trial (double-blinded)
Inpatient (any location) with outpatient follow-up
This was one of several preplanned analyses of the ExTRACT-TIMI 25 trial, an international randomized double-blind double-dummy study that compared enoxaparin with UFH as adjunctive therapy for fibrinolysis among patients with acute STEMI. Of the 20,479 patients in ExTRACT-TIMI 25, this substudy included the 4676 patients who underwent PCI within 30 days. Patients received enoxaparin until hospital discharge (or for a maximum of 8 days), or UFH for at least 48 hours. In addition, patients undergoing PCI received either preprocedure intravenous enoxaparin or placebo if the last dose of enoxaparin had been administered more than 8 hours earlier. Patients who underwent PCI after day 8 or hospital discharge were treated with open label UFH, regardless of original treatment group. Of patients undergoing PCI, 17% were administered glycoprotein IIb/IIIa inhibitors and 68% received clopidogrel. Both groups were well matched for baseline characteristics, and results were analyzed by intention to treat. Compared with patients receiving UFH, patients receiving enoxaparin were less likely to undergo PCI and had a longer time to recurrent ischemia or infarction. The rate of the primary end point, death or nonfatal MI by 30 days, was lower in the enoxaparin group (number needed to treat [NNT] = 32; 95% CI, 20 - 81), mainly due to a decrease in recurrent MI. Stroke was also reduced in the patients receiving enoxaparin (NNT = 164; 92 - 567). There was no difference in the rates of major, minor, or intracranial bleeding. The net clinical benefit (composite end point of death, MI, or major bleeding) remained lower in the enoxaparin group (NNT = 31; 19 - 75). Of note, patients with kidney disease (creatinine level < 2.5 mg/dL for men, < 2.0 mg/dL for women) were excluded.
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