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Iron
Published in Yoshinobu Onuma, Patrick W.J.C. Serruys, Bioresorbable Scaffolds, 2017
Runlin Gao, Deyuan Zhang, Hong Qiu, Chao Wu, Ying Xia, Gui Zhang
Inflammatory reaction is one of the main causes of intimal hyperplasia. Inflammation score [8] for each individual strut was graded as 0–3: 0, no inflammatory cells surrounding the strut; 1, light, noncircumferential lymphohistiocytic infiltrate surrounding the strut; 2, localized, moderate to dense cellular aggregate surrounding the strut noncircumferentially; and 3, circumferential dense lymphohistiocytic cell infiltration of the strut. The average inflammation score for each cross-section was calculated by dividing the sum of inflammation scores by the total number of struts at the examined section [9]. The inflammatory reaction in the vessel wall of the stented segment was mild in both groups. The average inflammation score was approximately 1 at each time point with only a few infiltrating inflammatory cells surrounding the scaffold/stent struts; no thrombosis or tissue necrosis was observed. At each time point, inflammation scores did not differ statistically between groups. Although inflammation scores demonstrated no temporal variation within groups, inflammatory reaction tended to decrease over time.
Elements of Continuum Mechanics
Published in Clement Kleinstreuer, Biofluid Dynamics, 2016
Intimal hyperplasia is the rapid abnormal continued proliferation and overgrowth of smooth muscle cells in response to endothelial injury or dysfunction (Chervu and Moore, 1990). Endothelial injury or dysfunction often occurs at sites of bypass graft anastomoses, locations of balloon angioplasty, and stented vessels. At such locations, hemodynamic factors may be a primary or contributing source of endothelial dysfunction. Hyperplasia is often viewed as an accelerated form of atherosclerosis due to the similarities in the lesions. For example, Ross (1986) advanced the “response-to-injury” hypothesis to propose that intimal hyperplasia may be an early lesion on the pathway to atherosclerotic plaque. However, in similar sized plaques those developing due to hyperplasia tend to have a higher concentration of smooth muscle cells and a lower concentration of lipid accumulation than do atherosclerotic lesions which usually appear in low-shear regions (see Caro et al., 1971).
Mechanical Effects of Cardiovascular Drugs and Devices
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
One common example of a mechanically induced pathology is intimal hyperplasia, which occurs in the native circulation but also occurs much more rapidly following endovascular treatments such as percutaneous balloon angioplasty and stent placement. Intimal hyperplasia is usually initiated by an endothelial disruption, which occurs naturally during atherosclerotic plaque rupture or during a treatment of the blood vessel. During balloon angioplasty, the vessel wall is stretched, which results in an increase in smooth muscle cell proliferation. These cells migrate from the media to the intima, where they thicken the intimal layer and reduce the luminal opening of the blood vessel, restricting blood flow to downstream tissues.
Gelatin coating promotes in situ endothelialization of electrospun polycaprolactone vascular grafts
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Yuehao Xing, Yongquan Gu, Lianrui Guo, Jianming Guo, Zeqin Xu, Yonghao Xiao, Zhiping Fang, Cong Wang, Zeng-Guo Feng, Zhonggao Wang
Intimal hyperplasia is crucial to tissue engineering vascular graft for its long-term patency. The graft's intima thickness was defined as the distance between scaffold border to intima surface and measured using HE staining (Figure 7(A)). In 1 month, a single layer of ECs can be observed without intimal hyperplasia in both groups. While in 3 and 6 months, the intima thickness is much higher in the P-H group than the GP-H group. The intima thickness was stable in the GP-H group from 3 months to 6 months, while in the P-H group, the intima thickness significantly increased from 3 months to 6 months (Figure 7(B)). The results showed that there is no intimal hyperplasia in GP-H and P-H groups within 1 month. After 3 months, intimal hyperplasia was observed in both groups. Compared to P-H grafts, the intimal hyperplasia was milder in the GP-H grafts. Besides, intima thickness became more severe in the P-H grafts from 3 months to 6 months. While in the GP-H group, intima thickness was stable.
Agent-based modelling of the smooth muscle cells migration induced by mechanical vibration: a preliminary study
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2020
M. Reda, C. Noel, N. Settembre, J. Chambert, A. Lejeune, E. Jacquet
A sustained exposure to Hand-Arm transmitted-Vibration may cause various vascular pathologies such as the vibration-induced Raynaud’s Syndrome. This disorder is characterized at the tissue level by an arterial growth and remodelling potentially induced by an intimal hyperplasia phenomenon. The proliferation and migration of the Vascular Smooth Muscle Cells (VSMCs) are the keystone of this intimal hyperplasia phenomenon. Wall Shear Stress (WSS) alterations play a key role in inducing such mechanisms. Moreover, finger-transmitted-vibration is likely to be responsible for a WSS decrease (Noel and Settembre 2017). So, the aim of our work is to develop an Agent-Based Model (ABM) of the WSS-modulated arterial growth induced by finger-transmitted vibration. This study is intended for the agent-based migration model.
A review on the treatment of intimal hyperplasia with perivascular medical devices: role of mechanical factors and drug release kinetics
Published in Expert Review of Medical Devices, 2023
Ankur J. Raval, Jigisha K. Parikh, Meghal A. Desai
Targeted local controlled drug delivery involves delivery at a constant and predetermined rate, thereby improving pharmacological efficacy, minimizing frequent dosing, reducing potential side effects, and ensuring patient safety [42]. These systems are prominent in treating diseases requiring long-term drug delivery and involve patient compliance. A sustained drug delivery system with desired release kinetics could be designed using different concepts of controlled drug delivery to treat intimal hyperplasia. In broader terms, intimal hyperplasia can be treated via two different routes, viz. intravascular and perivascular.