Associations Between Features of Nonstenosing Carotid Plaque on Computed Tomographic Angiography and Ischemic Stroke Subtypes. Issue 24 (17th December 2019)

• Record Type: Journal Article
• Authors: Knight‐Greenfield, Ashley; Quitlong Nario, Joel Jose; Vora, Amar; Baradaran, Hediyeh; Merkler, Alex; Navi, Babak B.; Kamel, Hooman; Gupta, Ajay
• Is Part Of: Journal of the American Heart Association. Volume 8:Issue 24(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-12-17
• Subjects: acute stroke -- carotid artery -- computed tomography angiography -- plaque; Heart -- Diseases -- Periodicals; Cardiovascular system -- Diseases -- Periodicals; Cerebrovascular disease -- Periodicals; Cardiology -- Periodicals; 616.1
• DOI: 10.1161/JAHA.119.014818
• Languages: English
• ISSNs: 2047-9980

Abstract

Abstract : Background: Thromboembolism from nonstenosing carotid plaques may be an underrecognized cause of embolic strokes of undetermined source (ESUS). We evaluated the association between features of nonstenosing atherosclerotic plaque on computed tomographic angiography and ESUS. Methods and Results: We identified consecutive acute ischemic stroke patients from 2011 to 2015 who had unilateral anterior territory infarction on brain magnetic resonance imaging and a neck computed tomographic angiography. We included ESUS cases and as controls, cardioembolic strokes. Patients with ≥50% internal carotid artery atherosclerotic stenosis ipsilateral to the stroke were excluded from this analysis. Reviewers blinded to infarct location and stroke cause retrospectively evaluated computed tomographic angiography studies for specific plaque features including thickness of the total, soft, and calcified plaque; presence of ulceration; and perivascular fat attenuation. Paired t tests and McNemar's test for paired data were used to compare plaque features ipsilateral versus contralateral to the side of infarction. Ninety‐one patients with ESUS or cardioembolic stroke were included in this study. Total plaque thickness was greater on the infarcted side (2.1±2.0 mm) than the contralateral side (1.2±1.5 mm) ( P =0.006) among ESUS cases, but not among cardioembolic cases (1.9±1.6 mm versus 1.8±1.6 mm) ( P =0.32). Conclusions: Among ESUS cases, total plaque thickness was greater ipsilateral to the side of infarction than on the contralateral, stroke‐free side. No such side‐to‐side differences were apparent in cardioembolic strokes. Our findings suggest that nonstenosing large‐artery atherosclerotic plaques represent one underlying mechanism of ESUS.