China
Africa
Explore chapters and articles related to this topic
Complications of hemodialysis access
Published in Sachinder Singh Hans, Mark F. Conrad, Vascular and Endovascular Complications, 2021
Mia Miller, Prakash Jayanthi, William Oppat
Treatment for symptomatic venous hypertension secondary to central venous stenosis includes endovascular angioplasty and stenting versus open surgical management. Endovascular approach harvests concern that angioplasty may not be as effective in vessels with increased elasticity and recoil. Angioplasty has even been shown to accelerate restenosis, with recurrent lesions showing a more aggressive neointimal hyperplasia.66 Therefore, close follow-up for non- or mildly symptomatic CVS is recommended, with judicious use of PTA as needed. However, when requiring treatment, PTA is the first-line approach recommended by KDOQI, with stenting reserved for angioplasty failure.67 The caveat with angioplasty alone is an excellent early technical result but a poor long-term primary patency with patency outcomes of 50% at 6 months and 25% at 12 months. There are significant variabilities, however, in the reporting of the nature and severity of lesion, outcomes, patient populations, instruments, and techniques used. Secondary patency can be significantly better with repeated angioplasty, even without use of stent.66
Results of PREVENT III: A Multicenter, Randomized Trial of Edifoligide for the Prevention of Vein Graft Failure in Lower Extremity Bypass Surgery
Published in Juan Carlos Jimenez, Samuel Eric Wilson, 50 Landmark Papers Every Vascular and Endovascular Surgeon Should Know, 2020
Juan Carlos Jimenez, Samuel Eric Wilson
Bypass grafts offer a unique opportunity for targeted drug or biologic interventions. The tissue is readily accessible for local delivery of agents prior to the initiation of the post-implantation response. Most vein grafts have minimal pre-existing pathology and thus treatment strategy can focus on modulation of the downstream healing process to reduce stenosis and occlusion. However, the mechanisms underlying vein graft disease are complex, involving inflammation, thrombosis, cell migration, proliferation, and matrix metabolism.3–6 Surgical handling of the vein results in significant, yet highly variable, degrees of endothelial loss, cellular and biochemical injury. The prototypical mid-term vein graft lesion demonstrates profound intimal thickening comprised of both cells (actin (+) vascular smooth muscle cells [VSMC] and/or myofibroblasts) and matrix, with variable degrees of adventitial fibrosis. Animal studies have demonstrated a brisk early proliferative response in the vein graft wall following arterialization. This process resembles neointimal hyperplasia following arterial injury (e.g., angioplasty) but is longer in duration. Moreover, a certain degree of wall thickening is required for biomechanical stabilization of the venous graft within the arterial hemodynamic environment.
Optical coherence tomography for late stent failure
Published in Hiram G. Bezerra, Guilherme F. Attizzani, Marco A. Costa, OCT Made Easy, 2017
Tej Sheth, Anthony Fung, Catalin Toma
A radically different etiology for ST is the process of neoatherosclerosis evolving to plaque rupture or erosion and acute thrombus formation.2,19,25 Unlike the previous scenarios, the stent struts are well covered with tissue in this case, and the thrombus originates from the exposed necrotic lipid core or from endothelial erosion. Neoatherosclerosis is a continuum of the spectrum of neointimal hyperplasia, where in addition to smooth muscle proliferation, lipid deposition, calcification, and intraplaque angiogenesis can occur, similar to a native coronary atherosclerotic plaque. By OCT, neoatherosclerosis typically has heterogeneous signal intensity with diffuse edges and high attenuation suggestive of lipid pools or sharply defined areas of signal attenuation suggestive of calcium deposition.26 Plaque rupture is sometimes seen as a fissure in the neointimal fibrous cap with communication to the lipid pool.27 Plaque rupture can occur spontaneously or as a consequence of stent fracture. ST due to neoatherosclerosis tends to occur late following stent implant,28 unlike the prior scenarios of stent malapposition that are seen earlier.
Ketogenic diet inhibits neointimal hyperplasia by suppressing oxidative stress and inflammation
Published in Clinical and Experimental Hypertension, 2023
Xuefei Xu, Limin Xie, Lili Chai, Xiaoming Wang, Jinhu Dong, Jipei Wang, Pengwei Yang
Neointimal hyperplasia is the primary mechanism underlying atherosclerosis and restenosis after percutaneous coronary intervention (1). The process is complex, involving multiple cell types and vascular wall components, and among them, vascular smooth muscle cells (VSMCs) typically play the most important roles (2,3). In response to vascular injury, inflammatory stimuli or growth factors, VSMCs switch from a quiescent contractile phenotype to an active synthetic phenotype. Synthetic VSMCs migrate and proliferate, and their accumulation directly contributes to neointima formation, and thereafter narrowing of vessels (4). The narrowing of vessels influences oxygen supply, thus resulting in the ischemia of organs including myocardium and brain (5,6). Although many researchers have devoted large amount of effort to the prevention and therapy of neointimal hyperplasia, few clinical strategies with satisfactory safety and efficacy have been developed. Therefore, it is urgent to explore new strategy for the treatment of neointimal hyperplasia.
Delivery of rivaroxaban and chitosan rapamycin microparticle with dual antithrombosis and antiproliferation functions inhibits venous neointimal hyperplasia
Published in Drug Delivery, 2022
Peng Sun, Haoliang Wu, Hao He, Liwei Zhang, Yuanfeng Liu, Cong Zhang, Chunyang Lou, Jingan Li, Hualong Bai
Neointimal hyperplasia is still the leading cause of graft failure after vascular interventions (Goel et al., 2012), it is a complex process including acute platelet deposition, inflammatory cell accumulation, and smooth muscle cell proliferation (Hristov and Weber, 2008; Lee and Roy-Chaudhury, 2009; Muto et al., 2007). Heparin, rapamycin or paclitaxel coated stents or balloons have been widely used in clinic; although these instruments contributed to a better patency rate, but none of these grafts showed a long term success in clinic (Kandzari et al., 2017; Cochrane Vascular Group, 2016; Tepe et al., 2017). Current protocols are mainly focusing on one step in the process of neointimal hyperplasia, like anti-thrombosis or anti-proliferation, this maybe the cause of the unsatisfactory result of the drug coated balloon and stent (Mehta et al., 2011). So, new methods are needed to decrease neointimal hyperplasia, especially in basic research. We recently showed a three-layered hydrogel patch with hierarchical releasing of PLGA nanoparticle drugs decrease neointimal hyperplasia in a rat inferior vena cava (IVC) venoplasty model, this hierarchical releasing system can significantly and effectively inhibit venous neointimal hyperplasia (Wei et al., 2022). But that drug delivery system is complex, so a simpler drug delivery system is needed.
Clinical considerations after endovascular therapy of peripheral artery disease
Published in Expert Review of Cardiovascular Therapy, 2021
Stefanos Giannopoulos, Ehrin J. Armstrong
Nonetheless U/S can also be used for direct visualization of the target arteries, measurement of blood flow at the target vessel and approximation of potential arterial stenosis. After experts’ consensus hemodynamically significant stenosis would be any arterial narrowing greater than 70% of the target lumen diameter, corresponding to a peak systolic velocity greater than 300 cm/s and peak systolic velocity ratio over 3.0 [103]. Due to the lower costs, the lack of radiation, the noninvasive nature of the procedure and accessibility to U/S devices have made this imaging modality the first choice for follow up after EVT for PAD, although the level of evidence has been low [98,104,105]. Additionally, as restenosis after EVT is mostly attributed to neointimal hyperplasia, which diffusely affects the target vessel, often a diagnostic angiogram is necessary before a decision for re-intervention can be made [105]. Thus, specific duplex ultrasound diagnostic criteria are needed depending on lesion location, lesion characteristics (e.g. length, chronic total occlusion, calcification) and EVT devices utilized [81,106].