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(Circulation. 2006;114:1344-1346.)
© 2006 American Heart Association, Inc.

Editorial

Small-Molecule Glycoprotein IIb/IIIa Antagonists and Bleeding Risk in Women

Too Much of a Good Thing?

Jane A. Leopold, MD

From the Cardiology Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Jane A. Leopold, MD, Brigham and Women’s Hospital, 77 Ave Louis Pasteur, NRB 0630K, Boston, MA 02115. E-mail jleopold@partners.org

Key Words: Editorials • anticoagulants • hemorrhage • kidney • women

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

Initial treatment strategies for patients who present with non–ST-segment–elevation acute coronary syndromes (NSTE ACSs) recommend early administration of both antiplatelet and antithrombotic therapies. Clinical trials have borne out the efficacy of upstream use of small-molecule glycoprotein IIb/IIIa (GP IIb/IIIa) antagonists in high-risk patients identified by positive cardiac serum markers and ST-segment ECG changes. In troponin-positive patients, these agents were found to be equally efficacious in men and women.¹ The magnitude of risk reduction is significant; a meta-analysis has demonstrated an 9% relative reduction in the odds of death or myocardial infarction at 30 days in patients treated with GP IIb/IIIa antagonists.¹

Article p 1380

Despite these clinical benefits, the decision to treat with a GP IIb/IIIa antagonist must consider, and adjust for, the increased risk of major bleeding inherent with the use of these agents. Meta-analyses have found a 32% increased risk of moderate to major bleeding in GP IIb/IIIa antagonist–treated patients, with an increased incidence of adverse hemorrhagic events in women compared with men (3.0% versus 2.2%).^1,2 It is of particular interest that female gender has been identified consistently as a risk factor for hemorrhagic events.³ In women, the increased incidence of bleeding after GP IIb/IIIa antagonist administration has been attributed to advanced age at presentation, higher-risk clinical characteristics, and smaller body surface area (BSA) compared with their male counterparts, as well as altered platelet function and gender-specific differences in pharmacokinetic and pharmacodynamic effects.^4–6 Although these risk factors were suggested by clinical trial results, "real-world" experience often differs significantly.⁷ . . . [Full Text of this Article]

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