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Symptomatic carotid plaques demonstrate less leaky plaque microvasculature compared with the contralateral side: a dynamic contrast-enhanced magnetic resonance imaging study

  • Geneviève A.J.C. Crombag
  • , Raf H.M. van Hoof
  • , Robert J. Holtackers
  • , Floris H.B.M. Schreuder
  • , Martine T.B. Truijman
  • , Tobien A.H.C.M.L. Schreuder
  • , Narender P. van Orshoven
  • , Werner H. Mess
  • , Paul A.M. Hofman
  • , Robert J. van Oostenbrugge
  • , Joachim E. Wildberger
  • , M. Eline Kooi (Corresponding author)

Research output: Contribution to journal › Article › Academic › peer-review

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Abstract

Background: Rupture of a vulnerable carotid atherosclerotic plaque is an important underlying cause of ischemic stroke. Increased leaky plaque microvasculature may contribute to plaque vulnerability. These immature microvessels may facilitate entrance of inflammatory cells into the plaque. The objective of the present study is to investigate whether there is a difference in plaque microvasculature (the volume transfer coefficient Ktrans) between the ipsilateral symptomatic and contralateral asymptomatic carotid plaque using noninvasive dynamic contrast-enhanced magnetic resonance imaging. Methods and Results: Eighty-eight patients with recent transient ischemic attack or ischemic stroke and ipsilateral >2 mm carotid plaque underwent 3 T magnetic resonance imaging to identify plaque components and to determine characteristics of plaque microvasculature. The volume transfer coefficient Ktrans, indicative for microvascular density, flow, and permeability, was calculated for the ipsilateral and asymptomatic plaque, using a pharmacokinetic model (Patlak). Presence of a lipid-rich necrotic core, intraplaque hemorrhage, and a thin and/or ruptured fibrous cap was assessed on multisequence magnetic resonance imaging. We found significantly lower Ktrans in the symptomatic carotid plaque compared with the asymptomatic side (0.057±0.002 min−1 versus 0.062±0.002 min−1; P=0.033). There was an increased number of slices with intraplaque hemorrhage (0.9±1.6 versus 0.3±0.8, P=0.002) and lipid-rich necrotic core (1.4±1.9 versus 0.8±1.4, P=0.016) and a higher prevalence of plaques with a thin and/or ruptured fibrous cap (32% versus 17%, P=0.023) at the symptomatic side. Conclusions: Ktrans was significantly lower in symptomatic carotid plaques, indicative for a decrease of plaque microvasculature in symptomatic plaques. This could be related to a larger amount of necrotic tissue in symptomatic plaques. Clinical Trial Registration: URL: http://www.clinicaltrials.gov.uk. Unique identifier: NCT01208025.

Original languageEnglish
Article numbere011832
Number of pages7
JournalJournal of the American Heart Association
Volume8
Issue number8
DOIs
Publication statusPublished - 16 Apr 2019

Funding

This research was performed within the framework of CTMM, the Center for Translational Molecular Medicine (www.ctmm. nl), project PARISk (grant 01C-202), and supported by the Dutch Heart Foundation. This project received funding from the European Union (EU) Horizon 2020 Research and Innovation Programme under the Marie Skłodowska-Curie grant agreement No 722609. Wildberger and Kooi are supported by Stichting de Weijerhorst.

Keywords

  • angiogenesis
  • atherosclerosis
  • ischemic stroke
  • magnetic resonance imaging

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