neointimal hyperplasia


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neointimal hyperplasia

An increase in the thickness of the lining of a blood vessel in response to injury or vascular reconstruction. It is an important cause of vein graft obstruction after coronary artery bypass surgery and in the premature closure of other vascular conduits, e.g., in dialysis access devices. It is characterized by the migration of smooth muscle cells into the graft, followed by the release of cytokines that damage the vessel wall and contribute to its degradation by inflammation.
See also: hyperplasia
References in periodicals archive ?
Kim et al., "The microRNA miR-132 targets Lrrfip1 to block vascular smooth muscle cell proliferation and neointimal hyperplasia," Atherosclerosis, vol.
Histological investigations have confirmed that venous neointimal hyperplasia is the predominant cause of stenotic lesions of AVF failure [4].
Combination of MMP-3 and MMP-9 knockout or knockdown reveals that MMP-3 mediated activation of MMP-9 is required and efficient in neointimal hyperplasia [123].
It was observed that both DES significantly decreased the neointimal hyperplasia, as well as the number of interventions at the end of one year, as compared to the BMS; however, sirolimus DES more efficiently decreased the angiographic neointima as compared to the Infinnium stent.
More than 50% of coronary artery bypass grafts (CABG) have failed by 10 years, and neointimal hyperplasia is a major factor in this process.
Effect of endothelial progenitor cells on neointimal hyperplasia and re-endothelialization of injured vessels
The main reason for early failure of small diameter grafts used in vascular surgery is thrombotic occlusion, whereas the main reason for late failure is neointimal hyperplasia (1-3).
Drug-eluting stents have been proposed as an alternative approach to decrease neointimal hyperplasia. Polymer coated stents can serve as a reservoir for local drug delivery.
Suppression of neointimal hyperplasia, the underlying cause of in-stent restenosis, by 17 beta-estradiol released from the stent surface, represents a novel approach for drug eluting stents and is the basis for the ETHOS I clinical study.
Paclitaxel, derived from the yew tree, inhibits microtubule formation in endothelial cells, disrupts mitosis and migration, and prevents neointimal hyperplasia.
Methods: Patients presenting neointimal hyperplasia documented by OCT reexamination after percutaneous coronary intervention were prospectively included from 2009 to 2011.
Interestingly it has been reported that andrographolide attenuates neointimal hyperplasia in a murine model of restenosis (21).