Key result
A review of phase 2 and 3 trials highlights the mechanisms and efficacy of heparin, low molecular weight heparins, and direct anti-thrombins in managing acute coronary syndromes.
This review summarizes the mechanisms of action and phase 2/3 trial evidence for heparins and direct anti-thrombins in acute coronary syndromes.
Provides no new data to alter ACS management; leaves open optimal antithrombin selection for future trials.
The generation of thrombin and the formation of platelet rich intra-coronary thrombus in response to atherosclerotic plaque rupture is pathognomonic of acute coronary syndromes. An understanding of the process of thrombin generation and the unique relationship between the structure and function of thrombin is essential to developing more effective anti-thrombotic strategies than the use of standard unfractionated heparin in the acute coronary syndromes. The mechanisms of action of heparin, low molecular weight heparins (LMWHs) and the newer direct anti-thrombins, recombinant hirudin and Hirulog, are reviewed. Evidence from the currently available phase 2 and 3 trials of these drugs regarding their efficacy in the acute coronary syndromes is also reviewed.
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Phil Tideman (1999) conducted a review in Acute coronary syndromes. Antithrombins (heparin, LMWHs, recombinant hirudin, Hirulog) was evaluated. A review of phase 2 and 3 trials highlights the mechanisms and efficacy of heparin, low molecular weight heparins, and direct anti-thrombins in managing acute coronary syndromes.
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