The Relation between Atherosclerosis Plaque Composition and Plaque Rupture

Parto Babaniamansour, Maryam Mohammadi, Sepideh Babaniamansour, Ehsan Aliniagerdroudbari

DOI: 10.4103/jmss.JMSS_48_19

Abstract


Background: Intima, media, and adventitia are three layers of arteries. They have different structures and different mechanical properties. Damage to intima layer of arteries leads to an inflammatory response, which is usually the reason for atherosclerosis plaque formation. Atherosclerosis plaques mainly consist of smooth muscle cells and calcium. However, plaque geometry and mechanical properties change during time. Blood flow is the source of biomechanical stress to the plaques. Maximum stress that atherosclerosis plaque can burden before its rupture depends on fibrous cap thickness, lipid core, calcification, and artery stenosis. When atherosclerotic plaque ruptures, the blood would be in contact with coagulation factors. That is why plaque rupture is one of the main causes of fatality. Methods: In this article, the coronary artery was modeled by ANSYS. First, fibrous cap thickness was increased from 40 Micro m to 250 Micro m by keeping other parameters constant. Then, the lipid pool percentage was incremented from 10% to 90% by keeping other parameters unchanged. Furthermore, for investigating the influence of calcium in plaque vulnerability, calcium was modeled in both agglomerated and microcalcium form. Results: It is proved that atherosclerosis plaque stress decreases exponentially as cap thickness increases. Larger lipid pool leads to more vulnerable plaques. In addition, the analysis showed maximum plaque stress usually increases in calcified plaque as compared with noncalcified plaque. Conclusions: The plaque stress is dependent on whether calcium is agglomerated near the lumen or far from it. However, in both cases, the deposition of more calcium in calcified plaque reduces maximum plaque stress.

Keywords


Atherosclerosis plaque, biomechanical stress, calcification, fibrous cap thickness, lipid core

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References


Alves-Lopes R, Touyz RM, Montezano AC. Cell Biology of Vessels. In Touyz R., Delles C. (eds) Textbook of Vascular Medicine. Springer, Cham; 2019. p. 23-30.

Saxton A, Manna B. Anatomy, Thorax, Heart Right Coronary Arteries. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019.

Moroni F, Ammirati E, Norata GD, Magnoni M, Camici PG. The role of monocytes and macrophages in human atherosclerosis, plaque neoangiogenesis, and atherothrombosis. Mediators Inflamm 2019;2019:7434376.

Mercer J, Guzik TJ, Atherosclerosis. In: Touyz RM, Delles C, editors. Textbook of Vascular Medicine. Cham: Springer International Publishing; 2019. p. 215-28.

Da Luz PL, Libby P, Laurindo FR, Chagas AC. Chapter 33-Endothelium in Atherosclerosis: Plaque Formation and Its Complications. In Endothelium and Cardiovascular Diseases: Vascular biology and clinical syndromes, Da Luz PL, Libby P, Laurindo FR, Chagas AC (eds.). Elsevier, London, UK; 2018. p. 493-512.

Peña E, Cilla M, Latorre ÁT, Martínez MA, Gómez A, Pettigrew RI.et al. Chapter 16-Emergent biomechanical factors predicting vulnerable coronary atherosclerotic plaque rupture. In Biomechanics of Coronary Atherosclerotic Plaque Peña E, Cilla M, Latorre ÁT, Martínez MA, Gómez A, Pettigrew RI. et al. (eds.). Elsevier, London, UK; 2020. p. 367-87.

Stefanadis C, Antoniou CK, Tsiachris D, Pietri P. Coronary atherosclerotic vulnerable plaque: Current Perspectives. J Am Heart Assoc 2017;6:e005543.

Fishbein MC. The vulnerable and unstable atherosclerotic plaque. Cardiovasc Pathol 2010;19:6-11.

Ohayon J, Finet G, Le Floc'h S, Cloutier G, Gharib AM, Heroux J, et al. Biomechanics of atherosclerotic coronary plaque: Site, stability and in vivo elasticity modeling. Ann Biomed Eng 2014;42:269-79.

Rezvani-Sharif A, Tafazzoli-Shadpour M, Kazemi-Saleh D, Sotoudeh-Anvari M. Stress analysis of fracture of atherosclerotic plaques: Crack propagation modeling. Med Biol Eng Comput 2017;55:1389-400.

Li ZY, Howarth S, Trivedi RA, U-King-Im JM, Graves MJ, Brown A, et al. Stress analysis of carotid plaque rupture based on in vivo high resolution MRI. J Biomech 2006:39:2611-22.

Teng Z, Sadat U, Ji G, Zhu C, Young VE, Graves MJ, et al. Lumen irregularity dominates the relationship between mechanical stress condition, fibrous-cap thickness, and lumen curvature in carotid atherosclerotic plaque. J Biomech Eng 2011;133:034501.

Tang D, Yang C, Zheng J, Woodard PK, Saffitz JE, Petruccelli JD, et al. Local maximal stress hypothesis and computational plaque vulnerability index for atherosclerotic plaque assessment. Ann Biomed Eng 2005;33:1789-801.

Libby P, Pasterkamp G. Requiem for the 'vulnerable plaque'. Eur Heart J 2015;36:2984-7.

Cilla M, Peña E, Martínez MA. 3D computational parametric analysis of eccentric atheroma plaque: Influence of axial and circumferential residual stresses. Biomech Model Mechanobiol 2012;11:1001-13.

Thondapu V, Bourantas CV, Foin N, Jang IK, Serruys PW, Barlis P. Biomechanical stress in coronary atherosclerosis: Emerging insights from computational modelling. Eur Heart J 2017;38:81-92.

Akyildiz AC, Speelman L, Nieuwstadt HA, van Brummelen H, Virmani R, van der Lugt A, et al. The effects of plaque morphology and material properties on peak cap stress in human coronary arteries. Comput Methods Biomech Biomed Engin 2016;19:771-9.

Liang X, Xenos M, Alemu Y, Rambhia SH, Lavi I, Kornowski R, et al. Biomechanical factors in coronary vulnerable plaque risk of rupture: Intravascular ultrasound-based patient-specific fluid-structure interaction studies. Coron Artery Dis 2013;24:75-87.

Huang H, Virmani R, Younis H, Burke AP, Kamm RD, Lee RT. The impact of calcification on the biomechanical stability of atherosclerotic plaques. Circulation 2001;103:1051-6.

Stolarski, T, Nakasone Y, Yoshimoto S. Engineering Analysis with ANSYS Software. 2nd ed. Butterworth-Heinemann, Oxford, UK; 2018.

Baldewsing RA, de Korte CL, Schaar JA, Mastik F, van der Steen AF. Finite element modeling and intravascular ultrasound elastography of vulnerable plaques: Parameter variation. Ultrasonics 2004;42:723-9.


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