Association between Intraplaque Hemorrhage and Vascular Remodeling in Carotid Arteries: The Plaque at RISK (PARISK) Study

Kristina Dilba, Anouk Dijk, GAJC Crombag, Ton van der Steen, MJAP Daemen, Peter Koudstaal, PJ Nederkoorn, J Hendrikse, ME Kooi, Aad van der Lugt, Jolanda Wentzel

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Abstract

Introduction: Vascular remodeling is a compensatory enlargement of the vessel wall in response to atherosclerotic plaque growth. We aimed to investigate the association between intraplaque hemorrhage (IPH), vascular remodeling, and luminal dimensions in recently symptomatic patients with mild to moderate carotid artery stenosis in which the differences in plaque size were taken into account. Materials and Methods: We assessed vessel dimensions on MRI of the symptomatic carotid artery in 164 patients from the Plaque At RISK study. This study included patients with recent ischemic neurological event and ipsilateral carotid artery stenosis <70%. The cross section with the largest wall area (WA) in the internal carotid artery (ICA) was selected for analysis. On this cross section, the following parameters were determined: WA, total vessel area (TVA), and lumen area (LA). Vascular remodeling was quantified as the remodeling ratio (RR) and was calculated as TVA at this position divided by the TVA in an unaffected distal portion of the ipsilateral ICA. Adjustment for WA was performed to correct for plaque size. Results: Plaques with IPH had a larger WA (0.56 vs. 0.46 cm2 p < 0.001), a smaller LA (0.17 vs. 0.22 cm2 p = 0.03), and a higher RR (2.0 vs. 1.9; p = 0.03) than plaques without IPH. After adjustment for WA, plaques containing IPH had a smaller LA (B = -0.052, p = 0.01) than plaques without IPH, but the RR was not different. Conclusion: After correcting for plaque size, plaques containing IPH had a smaller LA than plaques without IPH. However, RR was not different.

Original languageEnglish
Pages (from-to)94-99
Number of pages6
JournalCerebrovascular Diseases
Volume50
Issue number1
DOIs
Publication statusPublished - Feb 2021

Bibliographical note

Funding Information:
This research was performed within the framework of the Center for Translational Molecular Medicine (www.ctmm.nl), project PARISK (Plaque At RISK; Grant 01C-202) and supported by the Dutch Heart Foundation. Kristina Dilba was in part supported by STW project number 10813.

Publisher Copyright:
© 2020 S. Karger AG, Basel. Copyright: All rights reserved.

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  • EMC OR-01

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