Key result
Warfarin therapy for primary and secondary prevention in coronary artery disease is discussed in a review of its clinical evidence and mechanisms of action.
This editorial highlights the pathophysiological rationale for adding an anticoagulant like warfarin to antiplatelet therapy in acute coronary syndromes.
Accessible online at: www.karger.com/hed Plaque disruption, platelet activation and aggregation and thrombus formation are significant factors in the pathophysiology of acute coronary syndromes [1, 2]. Exposure of the subendothelial components following plaque rupture also activates the coagulation cascade, resulting in thrombin production (activation of platelets, factor V and factor VIII). Aspirin or clopidogrel, however, do not inhibit the platelet activation by thrombin. The addition of an antithrombotic drug (unfractionated heparin, low-molecular-weight heparin or direct antithrombin) has therefore been shown to be beneficial. The persistence and increased pro-coagulant activity up to 6 months following an ischaemic event [3] and the raised concentration of factor VII (associated with recurrent ischaemic events) [4] would favour the addition of an anticoagulant. In this edition of Heart Drug, Askew et al. [5] have reviewed the evidence regarding the use of warfarin for both primary and secondary prevention in coronary artery disease and have described the possible mechanisms for its actions.
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Manoharan et al. (2002) conducted an editorial in Acute Coronary Syndromes. Warfarin was evaluated. Warfarin therapy for primary and secondary prevention in coronary artery disease is discussed in a review of its clinical evidence and mechanisms of action.
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