Babaniamansour Parto, Mohammadi Maryam, Babaniamansour Sepideh, Aliniagerdroudbari Ehsan
Department of Biomedical Engineering, University of Kentucky, Lexington, Kentucky, USA.
Department of Biomedical Engineering, University of Isfahan, Isfahan.
J Med Signals Sens. 2020 Nov 11;10(4):267-273. doi: 10.4103/jmss.JMSS_48_19. eCollection 2020 Oct-Dec.
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.
In this article, the coronary artery was modeled by ANSYS. First, fibrous cap thickness was increased from 40 μm to 250 μm 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.
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.
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.
内膜、中膜和外膜是动脉的三层结构。它们具有不同的结构和力学性能。动脉内膜层的损伤会引发炎症反应,这通常是动脉粥样硬化斑块形成的原因。动脉粥样硬化斑块主要由平滑肌细胞和钙组成。然而,斑块的几何形状和力学性能会随时间变化。血流是斑块生物力学应力的来源。动脉粥样硬化斑块破裂前所能承受的最大应力取决于纤维帽厚度、脂质核心、钙化及动脉狭窄程度。当动脉粥样硬化斑块破裂时,血液会与凝血因子接触。这就是为什么斑块破裂是主要致死原因之一。
在本文中,冠状动脉由ANSYS软件进行建模。首先,在保持其他参数不变的情况下,将纤维帽厚度从40μm增加到250μm。然后,在保持其他参数不变的情况下,将脂质池百分比从10%增加到90%。此外,为了研究钙对斑块易损性的影响,分别以团聚钙和微钙形式对钙进行建模。
结果表明,随着帽厚度增加,动脉粥样硬化斑块应力呈指数下降。较大的脂质池会导致斑块更易破裂。此外,分析表明,与非钙化斑块相比,钙化斑块中的最大斑块应力通常会增加。
斑块应力取决于钙是在管腔附近团聚还是远离管腔。然而,在这两种情况下,钙化斑块中更多钙的沉积都会降低最大斑块应力。