Secondary prevention of stroke and the expanding role of the neurologist

Abstract

Stroke is the leading cause of adult disability and dependency in western society. Following stroke, the risk of myocardial infarction (MI) is increased by a factor of around 2-3 compared with baseline. Indeed, after the first 30 days, stroke survivors are more likely to die from a cardiac event than from a cerebrovascular event. In patients with atherothrombotic stroke, preventing subsequent manifestations of the underlying disease is therefore an important therapeutic goal. A number of options have been shown to reduce the risk of stroke. Aggressively controlling stroke risk factors, such as hypertension, diabetes and smoking, should provide significant benefit in reducing stroke risk; however, it is difficult to realize the full potential of these approaches in routine clinical practice. A number of classes of medication can reduce the risk of stroke and other vascular events, including antiplatelet agents, anticoagulants, angiotensin-converting enzyme inhibitors and statins. Several antiplatelet agents are approved to reduce the risk of recurrent stroke, although only clopidogrel and acetylsalicylic acid (ASA) are approved for the reduction of both stroke and MI in such patients. In the CAPRIE study, clopidogrel showed a statistically significant relative risk reduction of 8.7% (p = 0.043) compared with ASA for the composite endpoint of ischaemic stroke, MI or vascular death. Evidence from animal studies, ex vivo models in humans, and patients undergoing coronary stent insertion or patients with unstable angina/non-Q-wave MI clearly demonstrates the synergistic antiplatelet effect of using clopidogrel with ASA. In summary, most patients with an ischaemic stroke should be treated with an antiplatelet agent to reduce their risk of recurrent stroke, MI, or vascular death. The use of aggressive antiplatelet therapy has the potential to become a new paradigm for managing patients with vascular disease due to atherothrombosis.