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J Am Coll Cardiol, 2003; 41:70-78
© 2003 by the American College of Cardiology Foundation
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The evolving role of direct thrombin inhibitors in acute coronary syndromes

John Eikelboom, MBBS, MSc, FRACP, FRCPA*,*, Harvey White, MB, ChB, DSc, FRACP, FACC{dagger} and Salim Yusuf, MBBS, Dphil, FRCP (UK), FRCPC, FACC{ddagger}

* Department of Medicine, University of Western Australia and Department of Haematology, Royal Perth Hospital, Perth, Australia
{dagger} Cardiology Department, Green Lane Hospital, Auckland, New Zealand
{ddagger} Division of Cardiology, Department of Medicine, McMaster University, and Population Health Institute, Hamilton Health Sciences Corporation, McMaster University, Hamilton, Ontario, Canada



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  		Figure 1 Schematic demonstrating the antithrombin activity of heparin compared with direct thrombin inhibitors. Both heparin and direct thrombin inhibitors block circulating thrombin, but only direct thrombin inhibitors block tissue-bound thrombin. Tissue-bound thrombin remains enzymatically active, promoting further platelet and coagulation activation and thrombin generation.

 


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  		Figure 2 Indirect comparison of the relative efficacy and safety of direct thrombin inhibitors versus heparin with glycoprotein (GP) IIb/IIIa inhibitors versus heparin in trials of patients with acute coronary syndrome. Direct thrombin inhibitor and GP IIb/IIIa data are adapted from references 50 and 53, respectively. CI = confidence interval; DTI = direct thrombin inhibitor; MI = myocardial infarction; OR = odds ratio. Reprinted with permission from Elsevier Science (Lancet 2002:359;294–302 and Lancet 2002:359;189–98).

 




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