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I agree that, for secondary prevention of ischaemic stroke, alternatives to aspirin have to be identified,1not only because the scope for aspirin related therapeutic benefit is limited by the fact that aspirin blocks only one of at least eight potential pathways for activation of platelet aggregation,2 but also because some patients, initially responsive to the inhibitory affect of aspirin on platelet aggregation, subsequently escape from this effect,3 with consequent risk of recurrence of ischaemic stroke. Glycoprotein IIb/IIIa receptor blockers might superficially seem to be the final solution to this problem, as they block the final common pathway of platelet aggregation, but enthusiasm for their use should be tempered by the acknowledgement that acute profound thrombocytopaenia (platelet count< 20 000/mm3) may be an occasional side effect,2 with the consequence (at least in theory) of clinically significant intracranial haemorrhage in elderly patients who have ischaemic stroke coexisting with the type of small vessel disease predisposing to silent intracerebral microhaemorrhages,4 or coexisting with cerebral amyloid angiopathy, itself a risk factor for intracranial haemorrhage.5
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