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Medical management of intracranial atherosclerosis: current state of the art.

Noncardioembolic ischemic stroke accounts for at least 60% of all strokes due to atherothrombosis or thromboembolism involving the large cervicocephalic vessels, the medium intracranial vessels, or the small perforating vessels. In the intracranial vasculature, the proposed mechanisms of an acute vascular event include plaque rupture and thrombotic occlusion or thromboembolism due to platelet adhesion/activation/aggregation and subsequent cross-linking with fibrin. Theoretically, both antiplatelet and oral anticoagulant therapies should be effective in preventing these events. However, most clinical trials assessing the efficacy of antithrombotic therapies have focused on the index event (such as transient ischemic attack [TIA], reversible ischemic neurologic deficit, minor or moderate stroke) or the involved vascular territory (carotid vs vertebrobasilar) as a starting point without much analysis beyond excluding those subtypes that require anticoagulation (atrial fibrillation, recent myocardial infarction [MI], prosthetic valve) or that require surgical therapy (severe symptomatic carotid stenosis). As a result, the most frequently cited clinical trials, including most of the aspirin trials, the Ticlopidine-Aspirin Stroke Study (TASS), the European Stroke Prevention Study (ESPS-2), and the Clopidogrel vs Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial, do not allow for subset analyses devoted to patients with intracranial atherosclerosis. Without adequate identification of stroke subtypes or knowledge of the differences in stroke subtype mix among the studies, it is also impossible to make meaningful indirect efficacy comparisons among the various antithrombotic therapy trials. These factors are largely responsible for the ongoing controversy regarding optimal therapy for patients with cerebrovascular disease due to causes other than atrial fibrillation or carotid stenosis.