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Inverse association between size of the lipid-rich necrotic core and vascularization in human carotid plaques

Journal article
Authors Ola Hjelmgren
L. Johansson
Ulrica Prahl
Caroline Schmidt
Göran Bergström
Published in Clinical Physiology and Functional Imaging
Volume 38
Issue 2
Pages 326-331
ISSN 1475-0961
Publication year 2018
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 326-331
Language en
Links dx.doi.org/10.1111/cpf.12418
Keywords atherosclerotic disease, atherosclerotic plaque, carotid artery, contrast media, magnetic resonance, contrast-enhanced ultrasound, intraplaque neovascularization, atherosclerotic plaques, high-resolution, artery plaques, stenosis, events, mri, Physiology
Subject categories Physiology

Abstract

Purpose To study the relationship between the size of the lipid-rich necrotic core measured by MRI (magnetic resonance imaging) and the level of plaque vascularization measured by contrast-enhanced ultrasound, in human carotid plaques. Further, to compare the size of lipid-rich necrotic core from MRI to plaque echogenicity. Methods Thirty-one subjects with carotid plaques underwent standard B-mode ultrasound, contrast-enhanced ultrasound and MRI. The lipid-rich necrotic core was quantified using MRI. Contrast-enhanced ultrasound was used to measure carotid plaque vascularization. Standard B-mode ultrasound was used to measure plaque echogenicity as greyscale median. Results The amount of lipid-rich necrotic core correlated inversely with the degree of plaque vascularization (r = -0.40, P = 0.03). There were no correlations between the degree of plaque vascularization and the amount of fibrous tissue or calcifications. There were no correlations between greyscale median and the lipid-rich necrotic core, fibrous tissue or calcifications. Conclusions We show that more dense plaque vascularization is associated with a lower plaque content of lipid-rich necrotic core. A large lipid-rich necrotic core and high plaque vascularization are both proposed as predictors of vulnerability, and our finding is therefore odds with some earlier observations. Our finding can be explained by the fact that the necrotic core of the plaque contains no viable tissue and therefore less of the plaque can be vascularized if the lipid-rich necrotic core is large. Our study suggests that the true relation between plaque vascularization and other indices of vulnerability is more complex than initially thought.

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