期刊
FRONTIERS IN NEUROLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fneur.2021.719329
关键词
stroke; carotid stenosis; carotid plaque; biomarkers; atherosclerosis
资金
- Canadian Institutes of Health Research (CIHR)
- Heart and Stroke Foundation
- University Hospital Foundation
- Canada Foundation for Innovation (CFI)
- National Institutes of Health (NIH)
- Faculty of Medicine and Dentistry Motyl Graduate Studentship in Cardiac Sciences
- Alberta Innovates Graduate Student Scholarship
- Ballermann Translational Research Fellowship
- Izaak Walton Killam Memorial Scholarship
There is evidence supporting a potential causal relationship between ESUS and non-stenotic carotid plaques. However, the coexistence of other potential etiologies of stroke, such as atrial fibrillation and intracranial atherosclerosis, makes it challenging to confirm the causal link between non-stenotic plaques and ESUS. Ongoing studies are exploring the use of select protein and RNA biomarkers to facilitate the reclassification of some ESUS cases and optimize secondary prevention strategies.
Embolic stroke of unknown source (ESUS) represents one in five ischemic strokes. Ipsilateral non-stenotic carotid plaques are identified in 40% of all ESUS. In this narrative review, we summarize the evidence supporting the potential causal relationship between ESUS and non-stenotic carotid plaques; discuss the remaining challenges in establishing the causal link between non-stenotic plaques and ESUS and describe biomarkers of potential interest for future research. In support of the causal relationship between ESUS and non-stenotic carotid plaques, studies have shown that plaques with high-risk features are five times more prevalent in the ipsilateral vs. the contralateral carotid and there is a lower incidence of atrial fibrillation during follow-up in patients with ipsilateral non-stenotic carotid plaques. However, non-stenotic carotid plaques with or without high-risk features often coexist with other potential etiologies of stroke, notably atrial fibrillation (8.5%), intracranial atherosclerosis (8.4%), patent foramen ovale (5-9%), and atrial cardiopathy (2.4%). Such puzzling clinical associations make it challenging to confirm the causal link between non-stenotic plaques and ESUS. There are several ongoing studies exploring whether select protein and RNA biomarkers of plaque progression or vulnerability could facilitate the reclassification of some ESUS as large vessel strokes or help to optimize secondary prevention strategies.
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