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Circulation. 2009;119:1186-1188
Published online before print February 23, 2009, doi: 10.1161/CIRCULATIONAHA.108.845552
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(Circulation. 2009;119:1186-1188.)
© 2009 American Heart Association, Inc.


Editorial

Anticoagulation for ST-Segment Elevation Myocardial Infarction

John W. Eikelboom, MD; Jeffrey I. Weitz, MD

From the Departments of Medicine (J.W.E., J.I.W.) and Biochemistry and Medical Sciences (J.I.W.), McMaster University and Henderson Research Centre, Hamilton, Ontario, Canada.

Correspondence to John Eikelboom, Thrombosis Service, Hamilton General Hospital, 237 Barton St E, Hamilton, Ontario, L9K 1H8, Canada. E-mail eikelbj@mcmaster.ca


Key Words: Editorials • anticoagulants • heparin • myocardial infarction


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Adjunctive anticoagulant therapy reduces the risk of recurrent infarction and death in patients with ST-segment elevation myocardial infarction (STEMI) receiving fibrinolytic therapy.1–5 Unfractionated heparin (UFH), the first anticoagulant evaluated for this indication,1 continues to be used because of its predominantly nonrenal clearance, short half-life, reversibility, and the familiarity of clinicians with the drug. However, the anticoagulant response to UFH is unpredictable, which necessitates coagulation monitoring, and the time to achieve a therapeutic anticoagulant effect can vary from patient to patient. This is problematic because failure to achieve a therapeutic anticoagulant effect with UFH has been associated with an increased risk of recurrent ischemic events.6

Article p 1195

In this edition of Circulation, Cheng and colleagues report the results of their study exploring the clinical predictors of initial nontherapeutic anticoagulation with UFH in a subset of 6055 patients with STEMI enrolled in the Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment-Thrombolysis in Myocardial Infarction (ExTRACT-TIMI)–25 trial.7 In this patient subset, UFH was given as an initial bolus dose of 60 U/kg (maximum 4000 U) followed by an intravenous infusion of 12 U/hr (maximum 1000 U/hr) according to the American College of Cardiology/American Heart Association (ACC/AHA)-recommended weight-based nomogram.8,9 Subsequent UFH dose adjustments, which were standardized via a central interactive voice response system, were based on the results of the activated partial thromboplastin time (aPTT). The trial protocol mandated continuation of UFH for a minimum of 48 hours. Patients in whom the UFH infusion was interrupted before the first aPTT measurement . . . [Full Text of this Article]