Effects of mechanical properties and atherosclerotic artery size on biomechanical plaque disruption - mouse vs. human.
Mouse models of atherosclerosis are extensively being used to study the mechanisms of atherosclerotic plaque development and the results are frequently extrapolated to humans. However, major differences have been described between murine and human atherosclerotic lesions and the determination of similarities and differences between these species has been largely addressed recently. This study takes over and extends previous studies performed by our group and related to the biomechanical characterization of both mouse and human atherosclerotic lesions. Its main objective was to determine the distribution and amplitude of mechanical stresses including peak cap stress (PCS) in aortic vessels from atherosclerotic apoE(-/-) mice, in order to evaluate whether such biomechanical data would be in accordance with the previously suggested lack of plaque rupture in this model. Successful finite element analysis was performed from the zero-stress configuration of aortic arch sections and mainly indicated (1) the modest role of atherosclerotic lesions in the observed increase in residual parietal stresses in apoE(-/-) mouse vessels and (2) the low amplitude of murine PCS as compared to humans. Overall, the results from the present study support the hypothesis that murine biomechanical properties and artery size confer less propensity to rupture for mouse lesions in comparison with those of humans.
INSERM, UMR_S 1039, Radiopharmaceutiques Biocliniques, Faculté de Médecine de Grenoble, Grenoble, France.
Laurent M
LM
Riou
INSERM, UMR_S 1039, Radiopharmaceutiques Biocliniques, Faculté de Médecine de Grenoble, Grenoble, France.
Alexis
A
Broisat
INSERM, UMR_S 1039, Radiopharmaceutiques Biocliniques, Faculté de Médecine de Grenoble, Grenoble, France.
Catherine
C
Ghezzi
Department of Hemodynamics and Interventional Cardiology, Hospices Civils de Lyon and Claude Bernard University Lyon1, INSERM Unit 886, Lyon, France.
Gérard
G
Finet
Department of Hemodynamics and Interventional Cardiology, Hospices Civils de Lyon and Claude Bernard University Lyon1, INSERM Unit 886, Lyon, France.
Gilles
G
Rioufol
Laboratory of Integrative Cardiovascular Imaging Science, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Ahmed M
AM
Gharib
Laboratory of Integrative Cardiovascular Imaging Science, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. Electronic address: rpettig@mail.nih.gov.
Roderic I
RI
Pettigrew
Laboratory TIMC-IMAG/DyCTiM, UJF, CNRS UMR 5525, In(3)S, Grenoble, France; Polytech Annecy-Chambéry, University of Savoie, Le Bourget du Lac, France. Electronic address: jacques.ohayon@imag.fr.
Jacques
J
Ohayon
D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics; D001158:Arteries / Q000473:pathology; D050197:Atherosclerosis / Q000473:pathology / Q000503:physiopathology*; D001696:Biomechanical Phenomena / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D020342:Finite Element Analysis; D006801:Humans; D051379:Mice; D008955:Models, Cardiovascular; D058426:Neointima / Q000473:pathology / Q000503:physiopathology; D058226:Plaque, Atherosclerotic / Q000473:pathology / Q000503:physiopathology*; D012422:Rupture, Spontaneous; D013045:Species Specificity; D013314:Stress, Mechanical
D001057:Apolipoproteins E
Artery size; Human; Mechanical properties; Mouse; Plaque disruption