Non-Stenotic Ruptured Atherosclerotic Plaque Causing Thrombo-Embolic Stroke

Recently there has been much debate about the appropriateness of surgery for carotid atherosclerotic disease, as the surgical risk may outweigh the long-term benefi t conferred [1, 2] , particularly if surgery is delayed [3] . Carotid endarterectomy (CEA) is currently offered to recently symptomatic patients with severe internal carotid artery (ICA) stenosis [4, 5] . Additionally, selected symptomatic patients with moderate ICA stenosis may also benefi t from surgical therapy [6] . Currently used risk stratifi cation parameters, luminal stenosis, although a good refl ector of the haemodynamic consequence of ICA stenosis [7] may not refl ect the true burden of disease as outward expansion of the vessel wall can disguise large in situ plaques [8] . This process of remodelling suggests that despite cerebrovascular perfusion being preserved, luminal patency may not adequately refl ect risk of subsequent ischaemic stroke [9] , which is now thought to be more accurately refl ected by plaque burden and composition [10] . Rupture of so-called ‘vulnerable’ plaques, which are often non-stenotic [8] is thought to be the primary event leading to thrombo-embolism [11] . There exists a population of symptomatic patients with non-severe ICA stenosis who may not be offered defi nitive treatment despite being at high risk of further cerebral ischaemic events. This report describes how noninvasive MRI may improve risk stratifi cation in this group of patients by identifying so-called vulnerable/ruptured plaques in vivo, and thereby selecting a sub-group of patients at high risk of further ischaemic events, despite adequate luminal patency. Copyright © 2005 S. Karger AG, Basel