Atherosclerotic Calcifications Have a Local Effect on the Peel Behavior of Human Aortic Media

Author:

Donahue Carly L.1ORCID,Badal Ruturaj M.2,Younger Thomas S.1,Guan Weihua3,Tolkacheva Elena G.4,Barocas Victor H.1

Affiliation:

1. Department of Biomedical Engineering, University of Minnesota , Nils Hasselmo Hall, Room 7-115, 321 Church St SE, Minneapolis, MN 55455

2. Department of Mechanical Engineering, University of Minnesota , Minneapolis, MN 55455

3. Division of Biostatistics, School of Public Health, University of Minnesota , Minneapolis, MN 55455

4. Department of Biomedical Engineering, University of Minnesota , Nils Hasselmo Hall, Room 7-115, 321 Church St SE, Minneapolis, MN 55455; Institute for Engineering in Medicine, University of Minnesota, Minneapolis, MN 55455

Abstract

Abstract Aortic dissections, characterized by the propagation of a tear through the layers of the vessel wall, are critical, life-threatening events. Aortic calcifications are a common comorbidity in both acute and chronic dissections, yet their impact on dissection mechanics remains unclear. Using micro-computed tomography (CT) imaging, peel testing, and finite element modeling, this study examines the interplay between atherosclerotic calcifications and dissection mechanics. Samples cut from cadaveric human thoracic aortas were micro-CT imaged and subsequently peel-tested to map peel tension curves to the location of aortic calcifications. Empirical mode decomposition separated peel tension curves into high and low-frequency components, with high-frequency effects corresponding to interlamellar bonding mechanics and low-frequency effects to peel tension fluctuations. Finally, we used an idealized finite element model to examine how stiff calcifications affect aortic failure mechanics. Results showed that atherosclerosis influences dissection behavior on multiple length scales. Experimentally, atherosclerotic samples exhibited higher peel tensions and greater variance in the axial direction. The variation was driven by increased amplitudes of low-frequency tension fluctuations in diseased samples, indicating that more catastrophic propagations occur near calcifications. The simulations corroborated this finding, suggesting that the low-frequency changes resulted from the presence of a stiff calcification in the vessel wall. There were also modifications to the high-frequency peel mechanics, a response likely attributable to alterations in the microstructure and interlamellar bonding within the media. Considered collectively, these findings demonstrate that dissection mechanics are modified in aortic media nearby and adjacent to aortic calcifications.

Funder

American Heart Association

National Institutes of Health

National Science Foundation

Publisher

ASME International

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