Thrombosis due to “unstable” atherosclerotic plaque is the main mechanism underlying acute coronary syndromes, and vascular research has focused mostly on this model. Plaque also causes a substantial proportion of ischaemic stroke, although multiple mechanisms are involved and “stable” plaque is sometimes responsible. For example, in the basilar and proximal middle cerebral arteries, stroke can result from occlusion of a small branch vessel by slow growth of otherwise “stable” plaque in the parent vessel. Slowly growing but stable plaque can also cause cerebral ischaemia due to stenosis and hypoperfusion without thromboembolism. Recent evidence, however, suggests that the predominant mechanism of stroke, at least in patients with carotid stenosis, is similar to the coronary model and involves mainly unstable plaque.123 This observation has implications for the way we manage and prevent strokes.

Carotid plaques are typically slow growing or quiescent for long periods but may suddenly develop ruptures, fissures, or endothelial erosions, triggering platelet aggregation and formation of thrombus, which leads to local occlusion or embolisation to more distal vessels. Recent studies have correlated histology of the plaque with time since last symptoms in patients with symptomatic stenosis undergoing endarterectomy.23 Spagnoli and colleagues studied 187 symptomatic plaques and reported that the frequency of thrombotically active plaque was greater after stroke than after transient ischaemic attack, and that …