Abstract Number ‐ 267: The Role of Non‐stenosing Carotid Artery Plaques in ESUS, is it a Silent Offender?

Introduction The secondary prevention of Acute ischemic stroke (AIS)varies based on the root cause of the initial event; thus, determining the cause of an individual AIS is critical for implementing effective care. The well‐described TOAST classification is used to classify stroke etiology, and according to this paradigm, the presence of large vessel disease is considered a high risk for subsequent stroke only if >50% carotid artery stenosis is present. Cryptogenic strokes represent around 30% of all AIS and Embolic stroke of unknown source (ESUS) is a subcategory of the cryptogenic strokes and is characterized as a non‐lacunar ischemic stroke presumed to be of an embolic origin with no evidence of an obvious source of emboli. Here we discuss the most important and latest evidence on the relationship between ESUS and high‐risk plaque features not causing significant stenosis per NASCET criteria. Methods N/A Results The Relationship Between ESUS and Non‐stenosing Carotid Artery Plaques is mainly illustrated in the following points: Plaque vulnerability Researchers have described the following high‐risk features of plaques that may lead to stroke (Table). Plaque vulnerability is a plaque’s susceptibility to rupture and is a proposed determinant of high risk for superimposed thrombosis. According to a meta‐analysis conducted by Kamtchum‐Tatuene et al, high‐risk plaque features were three times more prevalent in patients with symptomatic versus asymptomatic carotid stenosis.3 Laterality of cartid plaques and stroke A meta‐analysis of 8 studies that assessed 323 patients with ESUS showed that mild carotid stenosis with high‐risk plaque features was more commonly located ipsilateral to the stroke side (32.5%) versus being contralaterally located (4.6%).4 Knight‐Greenfield et al evaluated plaque features by CTA in patients with AIS who did not have hemodynamic stenosis. It was also found that ESUS patients had a higher total plaque thickness ipsilateral to the stroke side when compared to the contralateral stroke‐free hemisphere.5 Clot composition and stroke etiology Fibrin/platelet component was dominant in cardioembolic thrombi and cryptogenic stroke, while red blood cells were seen more frequently in non‐cardioembolic thrombi. This supports the hypothesis that plaque histological features play a major role in causing large vessel occlusion despite the absence of significant stenosis.8 Conclusions Despite the evidence that high‐risk plaque features can predict a recurrent stroke, adoption of this principle and its integration into the medical guidelines have not yet been established. This reflects a lack of clinical trials that have utilized detailed plaque characterization for assessing risk of stroke.