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  1. Free, publicly-accessible full text available October 1, 2023
  2. Background The mechanical rupture of an atheroma cap may initiate a thrombus formation, followed by an acute coronary event and death. Several morphology and tissue composition factors have been identified to play a role on the mechanical stability of an atheroma, including cap thickness, lipid core stiffness, remodeling index, and blood pressure. More recently, the presence of microcalcifications (μCalcs) in the atheroma cap has been demonstrated, but their combined effect with other vulnerability factors has not been fully investigated. Materials and methods We performed numerical simulations on 3D idealized lesions and a microCT-derived human coronary atheroma, to quantitatively analyze the atheroma cap rupture. From the predicted cap stresses, we defined a biomechanics-based vulnerability index (VI) to classify the impact of each risk factor on plaque stability, and developed a predictive model based on their synergistic effect. Results Plaques with low remodeling index and soft lipid cores exhibit higher VI and can shift the location of maximal wall stresses. The VI exponentially rises as the cap becomes thinner, while the presence of a μCalc causes an additional 2.5-fold increase in vulnerability for a spherical inclusion. The human coronary atheroma model had a stable phenotype, but it was transformed into a vulnerablemore »plaque after introducing a single spherical μCalc in its cap. Overall, cap thickness and μCalcs are the two most influential factors of mechanical rupture risk. Conclusions Our findings provide supporting evidence that high risk lesions are non-obstructive plaques with softer (lipid-rich) cores and a thin cap with μCalcs. However, stable plaques may still rupture in the presence of μCalcs.« less
    Free, publicly-accessible full text available October 6, 2023
  3. Abstract Purpose . Laboratory models of human arterial tissues are advantageous to examine the mechanical response of blood vessels in a simplified and controllable manner. In the present study, we investigated three silicone-based materials for replicating the mechanical properties of human arteries documented in the literature. Methods . We performed uniaxial tensile tests up to rupture on Sylgard184, Sylgard170 and DowsilEE-3200 under different curing conditions and obtained their True (Cauchy) stress-strain behavior and Poisson’s ratios by means of digital image correlation (DIC). For each formulation, we derived the constitutive parameters of the 3-term Ogden model and designed numerical simulations of tubular models under a radial pressure of 250 mmHg. Results . Each material exhibits evident non-linear hyperelasticity and dependence on the curing condition. Sylgard184 is the stiffest formulation, with the highest shear moduli and ultimate stresses at relative low strains ( μ 184  = 0.52–0.88 MPa, σ 184  = 15.90–16.54 MPa, ε 184  = 0.72–0.96). Conversely, Sylgard170 and DowsilEE-3200 present significantly lower shear moduli and ultimate stresses that are closer to data reported for arterial tissues ( μ 170  = 0.33–0.7 MPa σ 170  = 2.61–3.67 MPa, ε 170  = 0.69–0.81; μ dow = 0.02–0.09 MPa σ dow = 0.83–2.05 MPa, ε dow = 0.91–1.05). Undermore »radial pressure, all formulations except DowsilEE-3200 at 1:1 curing ratio undergo circumferential stresses that remain in the elastic region with values ranging from 0.1 to 0.18 MPa. Conclusion . Sylgard170 and DowsilEE-3200 appear to better reproduce the rupture behavior of vascular tissues within their typical ultimate stress and strain range. Numerical models demonstrate that all three materials achieve circumferential stresses similar to human common carotid arteries (Sommer et al 2010), making these formulations suited for cylindrical laboratory models under physiological and supraphysiological loading.« less
    Free, publicly-accessible full text available August 2, 2023
  4. Atherosclerosis and vascular disease of larger arteries are often associated with hypoxia within the layers of the vascular wall. In this review, we begin with a brief overview of the molecular changes in vascular cells associated with hypoxia and then emphasize the transport mechanisms that bring oxygen to cells within the vascular wall. We focus on fluid mechanical factors that control oxygen transport from lumenal blood flow to the intima and inner media layers of the artery, and solid mechanical factors that influence oxygen transport to the adventitia and outer media via the wall's microvascular system—the vasa vasorum (VV). Many cardiovascular risk factors are associated with VV compression that reduces VV perfusion and oxygenation. Dysfunctional VV neovascularization in response to hypoxia contributes to plaque inflammation and growth. Disturbed blood flow in vascular bifurcations and curvatures leads to reduced oxygen transport from blood to the inner layers of the wall and contributes to the development of atherosclerotic plaques in these regions. Recent studies have shown that hypoxia-inducible factor-1α (HIF-1α), a critical transcription factor associated with hypoxia, is also activated in disturbed flow by a mechanism that is independent of hypoxia. A final section of the review emphasizes hypoxia in vascular stentingmore »that is used to enlarge vessels occluded by plaques. Stenting can compress the VV leading to hypoxia and associated intimal hyperplasia. To enhance oxygen transport during stenting, new stent designs with helical centrelines have been developed to increase blood phase oxygen transport rates and reduce intimal hyperplasia. Further study of the mechanisms controlling hypoxia in the artery wall may contribute to the development of therapeutic strategies for vascular diseases.« less
  5. Vascular stenting is a common intervention for the treatment for atherosclerotic plaques. However, stenting still has a significant rate of restenosis caused by intimal hyperplasia formation. In this study, we evaluate whether stent overexpansion leads to Vasa Vasorum (VV) compression, which may contribute to vascular wall hypoxia and restenosis. An idealized multilayered fibroatheroma model including Vasa Vasorum was expanded by three coronary stent designs up to a 1.3:1 stent/artery luminal diameter ratio (exp1.1, exp1.2, exp1.3) using a finite element analysis approach. Following Poiseuille’s law for elliptical sections, the fold increase in flow resistance was calculated based on VV compression in the Intima (Int), Media (Med) and Adventitia (Adv). The VV beneath the plaque experiences the smallest degree of compression, while the opposite wall regions are highly affected by stent overexpansion. The highest compressions for Adv, Med and Int at exp1.1 are 60.7, 65.9, 72.3%, at exp1.2 are 62.1, 67.3, 73.5% and at expp1.3 are 63.2, 68.7, 74.8%. The consequent fold increase in resistance to flow for Adv, Med and Int at exp1.1 is 3.3, 4.4, 6.6, at exp1.2 is 3.5, 4.7, 7.2 and at exp1.3 is 3.8, 5.1, 7.9. Stent overexpansion induces significant VV compression, especially in the Intima andmore »Media layers, in agreement with previously observed Media necrosis and loss in elasticity after stenting. The observed steep increase in flow resistance suggests the blood flow and associated oxygen delivery would drop up to five times in the Media and almost eight in the Intima, which may lead to intimal hyperplasia and restenosis« less