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The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
The term ‘intimal hyperplasia’ is used to describe the intimal thickening associated with arteriosclerosis, in which smooth muscle cells, collagen, and elastic deposition are present in the intima (see Figure 7.3). This is also a feature of ageing and should not be confused with atherosclerosis. There are a variety of confusing terms used synonymously to describe this intimal thickening, such as neointima, fibromuscular hyperplasia, adaptive intimal thickening, hypertrophy, and fibroplasia. It is a ubiquitous response of the vessel wall to any injury and is responsible for angioplasty-related stenosis and experimental endothelial damage with instruments; it also occurs in hypertension. ‘Arteriosclerosis obliterans’ is a term applied to the occlusive arterial disease in the small- and medium-sized arteries of the lower extremities.
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.
Optical coherence tomography assessment for cardiac allograft vasculopathy after heart transplantation
Published in Hiram G. Bezerra, Guilherme F. Attizzani, Marco A. Costa, OCT Made Easy, 2017
Sameer J. Khandhar, Guilherme Oliveira
IVUS has been utilized after transplantation to study CAV since the 1990s, and therefore there are several large prospective studies to provide insight into disease progression and prognosis. These IVUS-based studies have clearly shown a worse prognosis once there is intimal thickness of greater than 500 microns, which is not surprising since this represents a severe form of CAV. However, the impact of early intimal hyperplasia not detectable by the resolution of IVUS is not known, and further OCT studies are required to answer this.
Mechanistic exploration of Yiqi Liangxue Shengji prescription on restenosis after balloon injury by integrating metabolomics with network pharmacology
Published in Pharmaceutical Biology, 2023
Tianshi Mao, Long Xie, Yanqiong Guo, Xiang Ji, Jie Wan, Xiaoyun Cui, Qian Fan, Wei Liu, Shuai Wang, Wenbo Han, Qian Lin, Wenhao Jia
All rats were weighed weekly. In terms of body weight, there were no significant differences observed between the groups. Subsequently, ultrasound was performed to detect the intimal condition and verify the successful construction of the intimal hyperplasia model (Figure 2). Intimal hyperplasia developed in the abdominal aorta 28 days after balloon injury. IMT was significantly increased in the model group (0.23 ± 0.02 mm) compared with the sham group (0.10 ± 0.01 mm, p < 0.01), while prominent decreases in the IMT were observed in the YQLXSJ group (0.20 ± 0.01 mm) and positive group (0.19 ± 0.01 mm) in comparison with the model group (p < 0.01). Regarding vascular function, the diastolic and systolic functions of the abdominal aorta in the model group (PSV 562.64 ± 58.24 mm/s, EDV 32.28 ± 7.92 mm/s, RI 0.94 ± 0.01) were notably worse than those in the sham group (PSV 386.61 ± 42.60 mm/s, EDV 80.28 ± 7.15 mm/s, RI 0.79 ± 0.02, p < 0.01). Both YQLXSJ (PSV 414.28 ± 13.65 mm/s, EDV 48.01 ± 4.11 mm/s, RI 0.88 ± 0.01) and atorvastatin (PSV 433.71 ± 29.68 mm/s, EDV 49.40 ± 43.99 mm/s, RI 0.88 ± 0.01) improved vasomotor function and reduced vascular resistance (p < 0.01).
Nuclear receptor subfamily 1 group D member 1 suppresses the proliferation, migration of adventitial fibroblasts, and vascular intimal hyperplasia via mammalian target of rapamycin complex 1/β-catenin pathway
Published in Clinical and Experimental Hypertension, 2023
Ke Peng, Mingliang Wang, Jun Wang, Qiang Wang, De Li, Xiongshan Sun, Yongjian Yang, Dachun Yang
Intimal hyperplasia is a crucial process for ISR (5). Adventitia, an important part of the vascular wall, serves as an active participant in the vascular diseases (30). Recent research showed that AFs, the main component of vascular adventitia, were involved in intimal hyperplasia and vascular remodeling (30,31). Nevertheless, the underlying mechanisms are largely unknown. Our current study demonstrates that NR1D1 suppresses the proliferation and migration of AFs. NR1D1-mediated regulation of AFs depends on the downregulation of β-catenin and mTORC1. Inhibition of β-catenin by NR1D1 relies on the decreased activity of mTORC1. Importantly, NR1D1 also suppresses the early-stage proliferation of AFs within adventitia and subsequent intimal hyperplasia. Therefore, our data highlight a crucial role of NR1D1 in the treatment of intimal hyperplasia-associated vascular diseases.
Pathophysiology and management of saphenous vein graft disease
Published in Expert Review of Cardiovascular Therapy, 2023
Elizabeth C. Ghandakly, Aaron E. Tipton, Faisal G. Bakaeen
Intermediate and late SVG failure are due to intimal hyperplasia and atherosclerosis, respectively (Figure1). Intimal hyperplasia is an adaptive pathology of the vein conduit in response to the arterial circulation which occurs during the first year. Both increased pressure and circumferential stress induce vascular smooth muscle cell proliferation and ultimately result in stenosis [25]. This process is initially beneficial in allowing the graft to provide laminar flow to the coronary, but leads to stenosis when it progresses unabated. Late SVG failure caused by atherosclerotic changes can start to occur around 1 year and begin with foam cell infiltration. In postmortem analysis of SVG failure, fibrointimal thickening and necrotic core lesions were seen 2 to 5 years after CABG [26]. These lesions expand resulting in plaque rupture and, ultimately, thrombosis of the graft [27]. The time course for these atherosclerotic changes are significantly accelerated when compared with native coronaries, with a 2% loss of SVG per year between the second- and seventh-year post-CABG and a 5% loss per year between the seventh and twelfth years [28].