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      Biomechanical factors in atherosclerosis: mechanisms and clinical implications.

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          Abstract

          Blood vessels are exposed to multiple mechanical forces that are exerted on the vessel wall (radial, circumferential and longitudinal forces) or on the endothelial surface (shear stress). The stresses and strains experienced by arteries influence the initiation of atherosclerotic lesions, which develop at regions of arteries that are exposed to complex blood flow. In addition, plaque progression and eventually plaque rupture is influenced by a complex interaction between biological and mechanical factors-mechanical forces regulate the cellular and molecular composition of plaques and, conversely, the composition of plaques determines their ability to withstand mechanical load. A deeper understanding of these interactions is essential for designing new therapeutic strategies to prevent lesion development and promote plaque stabilization. Moreover, integrating clinical imaging techniques with finite element modelling techniques allows for detailed examination of local morphological and biomechanical characteristics of atherosclerotic lesions that may be of help in prediction of future events. In this ESC Position Paper on biomechanical factors in atherosclerosis, we summarize the current 'state of the art' on the interface between mechanical forces and atherosclerotic plaque biology and identify potential clinical applications and key questions for future research.

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          Author and article information

          Journal
          Eur Heart J
          European heart journal
          Oxford University Press (OUP)
          1522-9645
          0195-668X
          Nov 14 2014
          : 35
          : 43
          Affiliations
          [1 ] Department of Pathology and Immunology, University of Geneva, CMU, Rue Michel-Servet 1, CH-1211 Geneva, Switzerland brenda.kwakchanson@unige.ch paul.evans@sheffield.ac.uk.
          [2 ] Karolinska Institutet, Stockholm, Sweden.
          [3 ] University of Geneva, Geneva, Switzerland.
          [4 ] Bichat Hospital, Paris, France.
          [5 ] Academic Medical Center, Amsterdam, The Netherlands.
          [6 ] University of Pennsylvania, Philadelphia, PA, USA.
          [7 ] University Medical Center Urecht, Utrecht, The Netherlands.
          [8 ] KU Leuven, Leuven, Belgium.
          [9 ] Emory University, Atlanta, GA, USA.
          [10 ] Imperial College London, London, UK.
          [11 ] McGill University, Montreal, QC, Canada.
          [12 ] University of Oxford, Oxford, UK.
          [13 ] Ludwig-Maximilians-Universität (LMU), Munich, Germany.
          [14 ] CVPath Institute, Gaithersburg, MD, USA.
          [15 ] ErasmusMC, Rotterdam, The Netherlands.
          [16 ] Department of Cardiovascular Science, Medical School, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK brenda.kwakchanson@unige.ch paul.evans@sheffield.ac.uk.
          Article
          ehu353
          10.1093/eurheartj/ehu353
          4810806
          25230814
          eb2abc32-f9d7-483d-a826-361e65b24a43
          Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please email: journals.permissions@oup.com.
          History

          Atherosclerosis,Blood flow,Endothelial cell,Haemodynamics,Mechanotransduction,Plaque rupture

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