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Clinical failure of arteriovenous neointimal hyperplasia (NIH) fistulae (AVF) is frequently due to juxta-anastomotic NIH (JANIH). Although the mouse AVF model recapitulates human AVF maturation, previous studies focused on the outflow vein distal to the anastomosis. We hypothesized that the juxta-anastomotic area (JAA) has increased NIH compared with the outflow vein. AVF was created in C57BL/6 mice without or with chronic kidney disease (CKD). Temporal and spatial changes of the JAA were examined using histology and immunofluorescence. Computational techniques were used to model the AVF. RNA-seq and bioinformatic analyses were performed to compare the JAA with the outflow vein. The jugular vein to carotid artery AVF model was created in Wistar rats. The neointima in the JAA shows increased volume compared with the outflow vein. Computational modeling shows an increased volume of disturbed flow at the JAA compared with the outflow vein. Endothelial cells are immediately lost from the wall contralateral to the fistula exit, followed by thrombus formation and JANIH. Gene Ontology (GO) enrichment analysis of the 1,862 differentially expressed genes (DEG) between the JANIH and the outflow vein identified 525 overexpressed genes. The rat jugular vein to carotid artery AVF showed changes similar to the mouse AVF. Disturbed flow through the JAA correlates with rapid endothelial cell loss, thrombus formation, and JANIH; late endothelialization of the JAA channel correlates with late AVF patency. Early thrombus formation in the JAA may influence the later development of JANIH. NEW & NOTEWORTHY: Disturbed flow and focal endothelial cell loss in the juxta-anastomotic area of the mouse AVF colocalizes with acute thrombus formation followed by late neointimal hyperplasia. Differential flow patterns between the juxta-anastomotic area and the outflow vein correlate with differential expression of genes regulating coagulation, proliferation, collagen metabolism, and the immune response. The rat jugular vein to carotid artery AVF model shows changes similar to the mouse AVF model. [ABSTRACT FROM AUTHOR]

Background: Ischemic stroke and disability caused by carotid artery stenosis have always been worldwide problems. At present, carotid endarterectomy (CEA) and transfemoral carotid artery stenting (TFCAS) have been commonly used to treat carotid artery stenosis. Recently, transcarotid artery revascularization (TCAR) seems to be another option. Methods: We searched PubMed and Embase to find literatures comparing TCAR with TFCAS and CEA. The primary outcomes were stroke, myocardial infarction (MI), transient ischemic attack (TIA), death, cranial nerve injure (CNI), and operative time. Secondary outcomes were stroke, death, MI in the elderly; cost; radiation; and entry site complication. Results: Initial search of the literature included 165 articles, of which 12 studies were chosen in the end. These studies demonstrated high technical success rate of TCAR. Patients who received TCAR had lower risks of death, stroke/death and less radiation exposure compared to TFCAS. In meta analysis, the risk of stroke was significantly lower in TCAR group than TFCAS (OR 0.63; 95%CI 0.47–0.85). And there was no significant difference in TIA and MI. TCAR was associated with shorter operative time, lower risk of CNI and less blood loss compared to CEA. In older patients, the effect of TCAR was significantly better than that of TFCAS. Conclusion: TCAR is associated with a lower risk of perioperative stroke compared to TFCAS. TCAR is also associated with shorter operative time, lower risk of CNI and less blood loss compared to CEA. TCAR may be a promising treatment option besides TFCAS and CEA. [ABSTRACT FROM AUTHOR]

We previously showed decellularized fish swim bladder can be used as vascular patch and tube graft in rats, mesenchymal stem cells (MSCs) have showed the capability to inhibit neointimal hyperplasia in different animal models. We hypothesized that decellularized fish swim bladder patch loaded with MSCs (bioinspired patch) can inhibit neointimal hyperplasia in a rat aortic patch angioplasty model. Rat MSCs were grown in vitro and flow cytometry was used to confirm their quality. 3.6 × 105 MSCs were mixed into 100 μl of sodium alginate (SA)/hyaluronic acid (HA) hydrogel, two layers of fish swim bladders (5 mm × 5 mm) were sutured together, bioinspired patch was created by injection of hydrogel with MSCs into the space between two layers of fish swim bladder patches. Decellularized rat thoracic aorta patch was used as control. Patches were harvested at days 1 and 14 after implantation. Samples were examined by histology, immunohistochemistry, and immunofluorescence. The decellularized rat thoracic aorta patch and the fish swim bladder patch had a similar healing process after implantation. The bioinspired patch had a similar structure like native aorta. Bioinspired patch showed a decreased neointimal thickness (p =.0053), fewer macrophages infiltration (p =.0090), and lower proliferation rate (p =.0291) compared to the double layers fish swim bladder patch group. Decellularized fish swim bladder patch loaded with MSCs can inhibit neointimal hyperplasia effectively. Although this is a preliminary animal study, it may have a potential application in large animals or clinical research. [ABSTRACT FROM AUTHOR]