BACKGROUND AND PURPOSE: Intraplaque hemorrhage contributes to lipid core enlargement and plaque progression, leading to plaque destabilization and stroke. The mechanisms that contribute to the development of intraplaque hemorrhage are not completely understood. A higher incidence of intraplaque hemorrhage and thin/ruptured fibrous cap (upstream of the maximum stenosis in patients with severe [≥70%] carotid stenosis) has been reported. We aimed to noninvasively study the distribution of intraplaque hemorrhage and a thin/ruptured fibrous cap in patients with mild-to-moderate carotid stenosis. MATERIALS AND METHODS: Eighty-eight symptomatic patients with stroke (,70% carotid stenosis included in the Plaque at Risk study) demonstrated intraplaque hemorrhage on MR imaging in the carotid artery plaque ipsilateral to the side of TIA/stroke. The intraplaque hemorrhage area percentage was calculated. A thin/ruptured fibrous cap was scored by comparing pre- and postcontrast black-blood TSE images. Differences in mean intraplaque hemorrhage percentages between the proximal and distal regions were compared using a paired-samples t test. The McNemar test was used to reveal differences in proportions of a thin/ruptured fibrous cap. RESULTS: We found significantly larger areas of intraplaque hemorrhage in the proximal part of the plaque at 2, 4, and 6 mm from the maximal luminal narrowing, respectively: 14.4% versus 9.6% (P = .04), 14.7% versus 5.4% (P, .001), and 11.1% versus 2.2% (P = .001). Additionally, we found an increased proximal prevalence of a thin/ruptured fibrous cap on MR imaging at 2, 4, 6, and 8 mm from the MR imaging section with the maximal luminal narrowing, respectively: 33.7% versus 18.1%, P = .007; 36.1% versus 7.2%, P, .001; 33.7% versus 2.4%, P = .001; and 30.1% versus 3.6%, P = .022. CONCLUSIONS: We demonstrated that intraplaque hemorrhage and a thin/ruptured fibrous cap are more prevalent on the proximal side of the plaque compared with the distal side in patients with mild-to-moderate carotid stenosis.
Bibliographical noteFunding Information:
This work was supported by the Center for Translational Molecular Medicine (www. ctmm.nl), project PARISK (grant 01C-202), and the Netherlands Heart Foundation. This project has received funding from the European Union Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement No 722609. M.E. Kooi is supported by an Aspasia Grant 2018/SGw/00460457 from Nederlandse Organisatie voor Wetenschappelijk Onderzoek. J. Hendrikse received funding from the European Research Council under the European Union’s Horizon 2020 program (H2020)/European Research Council grant agreement No. 637024. F.H.B.M. Schreuder is supported by the Netherlands Heart Foundation (2019T060). Please address correspondence to M. Eline Kooi, MD, Department of Radiology and Nuclear Medicine, Maastricht University Medical Centre, PO Box 5800, 6202 AZ Maastricht, the Netherlands; e-mail: email@example.com
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