Journal Article10.1007/S10237-009-0151-8
Markers of inflammation collocate with increased wall stress in human coronary arterial plaque.
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TL;DR: A monotonic spatial relationship between mechanical stress and activated NF-κB that was consistent in all stages of plaque progression was found, and progression-dependent relationships between stress and both macrophage presence and MMP-1 expression were identified.
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Abstract: In this study, we hypothesized that spatial relationships exist between the local mechanical environment and inflammatory marker expression in atherosclerotic plaques, and that these relationships are plaque-progression dependent. Histologic cross-sections were collected at regular intervals along the length of diseased human coronary arteries and classified as early, intermediate, advanced, or mature based on their morphological features. For each cross-section, the spatial distribution of stress was determined using a 2D heterogeneous finite element model, and the corresponding distribution of selected inflammatory markers (macrophages, matrix metalloproteinase-1 [MMP-1], and nuclear factor-kappa B [NF-κB]) were determined immunohistochemically. We found a monotonic spatial relationship between mechanical stress and activated NF-κB that was consistent in all stages of plaque progression. We also identified progression-dependent relationships between stress and both macrophage presence and MMP-1 expression. These findings add to our understanding of the role of mechanical stress in stimulating the inflammatory response, and help explain how mechanical factors may regulate complex biological changes in remodeling.
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Citations
Role of biomechanical forces in the natural history of coronary atherosclerosis
Adam J. Brown,Zhongzhao Teng,Paul C. Evans,Jonathan H. Gillard,Habib Samady,Martin R. Bennett +5 more
TL;DR: Experimental and clinical data highlight that biomechanical forces, including wall shear stress (WSS) and plaque structural stress (PSS), have an important role in the natural history of coronary atherosclerosis.
Mapping elasticity moduli of atherosclerotic plaque in situ via atomic force microscopy
TL;DR: Force mapping experiments using atomic force microscopy were conducted in apolipoprotein E-deficient mouse, which represents the most widely used experimental model for studying mechanisms underlying the development of atherosclerotic lesions, to determine elasticity (Young's) moduli that were related to the underlying histological plaque structure.
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Mouse models of plaque rupture.
TL;DR: Although no mouse model examined completely simulates the entire process of plaque rupture, the brachiocephalic artery in ApoE-deficient mice fed a high-fat diet, with or without angiotensin II infusion, is a practically feasible model for plaque rupture.
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Exploring the relationship between biomechanical stresses and coronary atherosclerosis.
James N. Cameron,Ojas H. Mehta,Michael Michail,Jasmine Chan,Stephen J. Nicholls,Martin R. Bennett,Adam J. Brown +6 more
TL;DR: The calculation of coronary biomechanical stresses from first principles and computational methods are presented, including endothelial shear stress (ESS), plaque structural stress (PSS) and axial plaque stress (APS), and the future potential for refining treatment options and predicting future ischaemic events is explored.
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Beneficial changes of serum calcification markers and contralateral carotid plaques echogenicity after combined carotid artery stenting plus intensive lipid-lowering therapy in patients with bilateral carotid stenosis.
Nikolaos P E Kadoglou,Thomas Gerasimidis,Alkistis Kapelouzou,Anestis Moumtzouoglou,Efthimios D. Avgerinos,John D. Kakisis,Panayotis E. Karayannacos,Christos D. Liapis +7 more
TL;DR: Ipsilateral CAS plus intensive lipid-lowering therapy was associated with enhanced contralateral carotid plaque stability and attenuated inflammatory burden and calcification inhibitors to a greater extent than atorvastatin therapy alone in patients with bilateralcarotid stenosis.
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