V Daeichin1, J C Sluimer2, K van der Heiden1, I Skachkov1, K Kooiman1, A Janssen2, B Janssen3, J G Bosch1, N de Jong4, M J A P Daemen5, A F W van der Steen4. 1. Erasmus Medical Center, Thoraxcenter Biomedical Engineering, Rotterdam, Netherlands. 2. Department of Pathology, Maastricht University, CARIM, Maastricht, Netherlands. 3. Pharmacology & Toxicology, Maastricht University Medical Center, Maastricht, Netherlands. 4. Erasmus Medical Center, Thoraxcenter Biomedical Engineering, Rotterdam, Netherlands; Lab of Acoustical Wavefield Imaging, Delft University of Technology, Delft, the Netherlands. 5. Pathology, Amsterdam Medical Center, Amsterdam, Netherlands.
Abstract
AIM: The actual occurrence of spontaneous plaque rupture in mice has been a matter of debate. We report on an in vivo observation of the actual event of possible plaque disruption in a living ApoE(-/-) mouse. METHODS AND RESULTS: During live contrast-enhanced ultrasonography of a 50-week-old ApoE(-/-) male mouse, symptoms suggesting plaque disruption in the brachiocephalic artery were observed. Histological analysis confirmed the presence of advanced atherosclerotic lesions with dissections and intraplaque hemorrhage in the affected brachiocephalic trunk, pointing towards plaque rupture as the cause of the observed event. However, we did not detect a luminal thrombus or cap rupture, which is a key criterion for plaque rupture in human atherosclerosis. CONCLUSION: This study reports the real-time occurrence of a possible plaque rupture in a living ApoE(-/-) mouse.
AIM: The actual occurrence of spontaneous plaque rupture in mice has been a matter of debate. We report on an in vivo observation of the actual event of possible plaque disruption in a living ApoE(-/-) mouse. METHODS AND RESULTS: During live contrast-enhanced ultrasonography of a 50-week-old ApoE(-/-) male mouse, symptoms suggesting plaque disruption in the brachiocephalic artery were observed. Histological analysis confirmed the presence of advanced atherosclerotic lesions with dissections and intraplaque hemorrhage in the affected brachiocephalic trunk, pointing towards plaque rupture as the cause of the observed event. However, we did not detect a luminal thrombus or cap rupture, which is a key criterion for plaque rupture in humanatherosclerosis. CONCLUSION: This study reports the real-time occurrence of a possible plaque rupture in a living ApoE(-/-) mouse.
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