Hendrik H G Hansen1, Gert Jan de Borst2, Michiel L Bots2, Frans L Moll2, Gerard Pasterkamp2, Chris L de Korte2. 1. From the Medical Ultrasound Imaging Center, Department of Radiology and Nuclear Medicine, Radboud University Medical Center, Nijmegen, The Netherlands (H.H.G.H., C.L.d.K.); and Department of Vascular Surgery (G.J.d.B., F.L.M.), Julius Center for Health Sciences and Primary Care (M.L.B.), and Laboratory of Experimental Cardiology and Laboratory of Clinical Chemistry (G.P.), University Medical Center Utrecht, The Netherlands. rik.hansen@radboudumc.nl. 2. From the Medical Ultrasound Imaging Center, Department of Radiology and Nuclear Medicine, Radboud University Medical Center, Nijmegen, The Netherlands (H.H.G.H., C.L.d.K.); and Department of Vascular Surgery (G.J.d.B., F.L.M.), Julius Center for Health Sciences and Primary Care (M.L.B.), and Laboratory of Experimental Cardiology and Laboratory of Clinical Chemistry (G.P.), University Medical Center Utrecht, The Netherlands.
Abstract
BACKGROUND AND PURPOSE: Carotid plaque rupture is a major cause of stroke. Key issue for risk stratification is early identification of rupture-prone plaques. A noninvasive technique, compound ultrasound strain imaging, was developed providing high-resolution radial deformation/strain images of atherosclerotic plaques. This study aims at in vivo validation of compound ultrasound strain imaging in patients by relating the measured strains to typical features of vulnerable plaques derived from histology after carotid endarterectomy. MATERIALS AND METHODS: Strains were measured in 34 severely stenotic (>70%) carotid arteries at the culprit lesion site within 48 hours before carotid endarterectomy. In all cases, the lumen-wall boundary was identifiable on B-mode ultrasound, and the imaged cross-section did not move out of the imaging plane from systole to diastole. After endarterectomy, the plaques were processed using a validated histology analysis technique. RESULTS: Locally elevated strain values were observed in regions containing predominantly components related to plaque vulnerability, whereas lower values were observed in fibrous, collagen-rich plaques. The median strain of the inner plaque layer (1 mm thickness) was significantly higher (P<0.01) for (fibro)atheromatous (n=20, strain=0.27%) than that for fibrous plaques (n=14, strain=-0.75%). Also, a significantly larger area percentage of the inner layer revealed strains above 0.5% for (fibro)atheromatous (45.30%) compared with fibrous plaques (31.59%). (Fibro)atheromatous plaques were detected with a sensitivity, specificity, positive predictive value, and negative predictive value of 75%, 86%, 88%, and 71%, respectively. Strain did not significantly correlate with fibrous cap thickness, smooth muscle cell, or macrophage concentration. CONCLUSIONS: Compound ultrasound strain imaging allows differentiating (fibro)atheromatous from fibrous carotid artery plaques.
BACKGROUND AND PURPOSE: Carotid plaque rupture is a major cause of stroke. Key issue for risk stratification is early identification of rupture-prone plaques. A noninvasive technique, compound ultrasound strain imaging, was developed providing high-resolution radial deformation/strain images of atherosclerotic plaques. This study aims at in vivo validation of compound ultrasound strain imaging in patients by relating the measured strains to typical features of vulnerable plaques derived from histology after carotid endarterectomy. MATERIALS AND METHODS: Strains were measured in 34 severely stenotic (>70%) carotid arteries at the culprit lesion site within 48 hours before carotid endarterectomy. In all cases, the lumen-wall boundary was identifiable on B-mode ultrasound, and the imaged cross-section did not move out of the imaging plane from systole to diastole. After endarterectomy, the plaques were processed using a validated histology analysis technique. RESULTS: Locally elevated strain values were observed in regions containing predominantly components related to plaque vulnerability, whereas lower values were observed in fibrous, collagen-rich plaques. The median strain of the inner plaque layer (1 mm thickness) was significantly higher (P<0.01) for (fibro)atheromatous (n=20, strain=0.27%) than that for fibrous plaques (n=14, strain=-0.75%). Also, a significantly larger area percentage of the inner layer revealed strains above 0.5% for (fibro)atheromatous (45.30%) compared with fibrous plaques (31.59%). (Fibro)atheromatous plaques were detected with a sensitivity, specificity, positive predictive value, and negative predictive value of 75%, 86%, 88%, and 71%, respectively. Strain did not significantly correlate with fibrous cap thickness, smooth muscle cell, or macrophage concentration. CONCLUSIONS: Compound ultrasound strain imaging allows differentiating (fibro)atheromatous from fibrous carotid artery plaques.
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