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Markers of inflammation collocate with increased wall stress in human coronary arterial plaque

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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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Correspondence to Raymond Peter Vito.

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Hallow, K.M., Taylor, W.R., Rachev, A. et al. Markers of inflammation collocate with increased wall stress in human coronary arterial plaque. Biomech Model Mechanobiol 8, 473–486 (2009). https://doi.org/10.1007/s10237-009-0151-8

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  • DOI: https://doi.org/10.1007/s10237-009-0151-8

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