G A J C Crombag1,2, M Aizaz1,2, F H B M Schreuder3, F Benali1, D H K van Dam-Nolen4, M I Liem5, C Lucci6, A F van der Steen7, M J A P Daemen8, W H Mess9, A van der Lugt4, P J Nederkoorn5, J Hendrikse6, P A M Hofman1, R J van Oostenbrugge2,10, J E Wildberger1,2, M E Kooi11,2. 1. From the Departments of Radiology and Nuclear Medicine (G.A.J.C.C., M.A., F.B., P.A.M.H., J.E.W., M.E.K.). 2. CARIM School for Cardiovascular Diseases (G.A.J.C.C., M.A., R.J.v.O., J.E.W., M.E.K.), Maastricht University, Maastricht, the Netherlands. 3. Department of Neurology & Donders Institute for Brain Cognition & Behaviour (F.H.B.M.S.), Radboud University Medical Center, Nijmegen, the Netherlands. 4. Departments of Radiology and Nuclear Medicine (D.H.K.v.D.-N., A.v.d.L.). 5. Departments of Neurology (M.I.L., P.J.N.). 6. Department of Radiology (C.L., J.H.), University Medical Center Utrecht, Utrecht, the Netherlands. 7. Biomedical Engineering (A.F.v.d.S.), Erasmus University Medical Center, University Medical Center Rotterdam, Rotterdam, the Netherlands. 8. Pathology (M.J.A.P.D.), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, the Netherlands. 9. Clinical Neurophysiology (W.H.M.). 10. Neurology (R.J.v.O.), Maastricht University Medical Center, Maastricht, the Netherlands. 11. From the Departments of Radiology and Nuclear Medicine (G.A.J.C.C., M.A., F.B., P.A.M.H., J.E.W., M.E.K.) eline.kooi@mumc.nl.
Abstract
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.
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.
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