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In a recent editorial, Algra et al summarise the current state of knowledge of drug treatment in secondary prevention after ischaemic stroke or transient ischaemic attack (TIA).1 After a review of aspirin, ticlodipine, clopidogrel, and anticoagulation with warfarin, and a critical discussion of recent relevant clinical trials, they speculate that antagonists of the platelet fibrinogen receptor, glycoprotein 11b/111a, may also have a preventive role in cerebrovascular disease in the near future and they indicate that clinical trials are planned. Unfortunately, the authors fail to mention the promise of β-hydroxy-β-methylglutary (HMG) coenzyme A reductase inhibitors (statins) in preventing stroke and TIA in patients with established vascular disease. These are a novel group of compounds which lower serum cholesterol, and which have been shown to lower mortality in large randomised controlled clinical trials in secondary prevention in patients with known vascular disease, both with and without hypercholesterolaemia, and in primary prevention in those with hypercholesterolaemia without clinical vascular disease.2 3 In addition, these trials have demonstrated that statins reduce the risk of stroke by about 30% in patients with coronary artery disease.4 5 As well as reducing serum cholesterol, statins have been shown in various models to have a broad range of beneficial effects on vascular pathophysiology, including plaque stabilisation, and direct vasodilatatory, antithrombotic, and antiplatelet effects.5 6 Some of these drugs are currently being tested in clinical trials in patients with a history of minor stroke or TIA. As statins do not exert their beneficial effects primarily through antiplatelet mechanisms, the possibility that a statin combined with aspirin (or clopidogrel or both) could provide additive therapeutic effects is exciting and needs to be tested in patients with or at risk of cerebrovascular disease. As usual the neurological community lags behind their cardiology colleagues in managing their cerebrovascular share of the systemic disease of the endothelium known as atherosclerosis.
The authors reply:
Speculation about the results of ongoing trials was not really the purpose of our review, but we agree we might have included the use of statins in patients with cerebrovascular disease. We note that Delanty has a poor opinion of the neurovascular research community. We shall have to live with it.
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