Abstract #1748
THE ASSOCIATION BETWEEN PLAQUE SURFACE DISRUPTION AND FIBROUS CAP STATUS AT BASELINE AND VOLUME CHANGE OF INTRAPLAQUE HEMORRHAGE OVER TWO YEARS
Mohamed Kassem1,2, Tahnee Gorissen1, Mohamed AlBenwan1, Dianne van Dam-Nolen3, Madieke I Liem4, Rob J van der Geest5, Jeroen Hendrikse6, Werner H Werner Mess1,7, Paul J Nederkoorn4, Daniel Bos3,8, Patty Nelemans9, Robert Jan van Oostenbrugge1,10, and M Eline Kooi1,2
1CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, Netherlands, Maastricht, Netherlands, 2Department of Radiology and Nuclear Medicine, Maastricht University medical center (MUMC+), maastricht, Netherlands, 3Department of Radiology and Nuclear Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands, 4Department of Neurology, Amsterdam UMC, location AMC, Amsterdam, Amsterdam, Netherlands, 5Division of Image Processing, Department of Radiology, Leiden University Medical Center, Leiden, Netherlands, 6Radiology, University Medical Center Utrecht, Utrecht, Utrecht, Netherlands, 7Department of Clinical Neurophysiology, Maastricht University Medical Center+ (MUMC+), maastricht, Netherlands, 8Epidemiology, Erasmus MC, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands, 9Department of Epidemiology, Maastricht University, Maastricht, The Netherlands, maastricht, Netherlands, 10Department of Neurology, Maastricht University Medical Centre, maastricht, Netherlands
Synopsis
The factors that contribute to intraplaque hemorrhage (IPH) development within the carotid atherosclerotic plaque are incompletely understood. Previously, we demonstrated that IPH is associated with a thin/ruptured fibrous cap (TRFC) and disruption of the plaque surface on in a cross-sectional study. Baseline and 2 year’s follow-up carotid MR images of 110 patients from the Plaque at Risk (PARISK) study were analyzed. IPH volume change in TRFC at baseline was significant different (p=0.04) than thick fibrous cap group. Baseline IPH volumes are larger in patients with TRFC and disrupted plaque surface, but didn’t increase during the follow-up.
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