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(Stroke. 2002;33:1723.)
© 2002 American Heart Association, Inc.

Emerging Therapies

Warfarin-Aspirin Recurrent Stroke Study (WARSS) Trial

Is Warfarin Really a Reasonable Therapeutic Alternative to Aspirin for Preventing Recurrent Noncardioembolic Ischemic Stroke?

Graeme J. Hankey, MBBS, MD, FRCP, FRCP(Edin), FRACP

From the Department of Neurology, Royal Perth Hospital, Perth, Western Australia.

Correspondence to Clinical Prof Graeme J. Hankey, Consultant Neurologist and Head of Stroke Unit, Department of Neurology, Royal Perth Hospital, Wellington Street, Perth, Western Australia 6001. E-mail gjhankey@cyllene.uwa.edu.au

Section Editor: Marc Fisher MD

Key Words: anticoagulants • aspirin • clinical trials • stroke, ischemic

Eleven years ago, on June 1, 1991, Dr J.P. Mohr addressed delegates of the International Conference on Stroke, Geneva, about anticoagulants as a therapeutic strategy in stroke. He bemoaned the fact that heparin and warfarin had the "bad luck" to be manufactured initially in the post-World War II period, before drugs were evaluated by controlled clinical trials. As a consequence, clinicians judged their effectiveness on the basis of theory and compared their personal experience with historical controls and with those found in the literature. With the passage of time, the drug patents expired, the views and practices of clinicians became polarized, and any commercial and scientific motive to conduct controlled clinical trials of anticoagulation in secondary stroke prevention, once called for, disappeared. Dr Mohr sadly concluded that "there are no [reliable] data really" for anticoagulation after ischemic stroke. This was probably the platform from which he planned, with colleagues, the Warfarin-Aspirin Recurrent Stroke Study (WARSS).¹

What Was the Rationale for Comparing the Effectiveness of Warfarin and Aspirin in Noncardioembolic Ischemic Stroke?

Noncardioembolic ischemic stroke underpins 60% of all first-ever and recurrent strokes. The major causes are (1) thrombotic occlusion of large and medium-sized arteries that is due to in situ atherothrombosis or atherothromboembolism and (2) thrombotic occlusion of small perforating intracerebral arteries affected by microatheroma/lipohyalinosis.

The formation of thrombus on the subendothelial tissue of arteries depends on the initial formation of a platelet plug (by means of platelet adhesion, activation, and aggregation) and the generation of a meshwork of fibrin (by means of the coagulation cascade). Antiplatelet drugs are designed to prevent the formation of the . . . [Full Text of this Article]

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