Endovascular therapy with PTA or PTS for central venous stenosis is safe, with low rates of technical failure. Multiple additional interventions are the rule with both treatments. Although neither offers truly durable outcomes, PTS does not improve on the patency rates more than PTA and does not add to the longevity of ipsilateral hemodialysis access sites.

A. The mouse aortocaval fistula recapitulates human arteriovenous fistula maturation. Am J Physiol Heart Circ Physiol 305: H1718 -H1725, 2013. First published October 4, 2013 doi:10.1152/ajpheart.00590.2013.-Several models of arteriovenous fistula (AVF) have excellent patency and help in understanding the mechanisms of venous adaptation to the arterial environment. However, these models fail to exhibit either maturation failure or fail to develop stenoses, both of which are critical modes of AVF failure in human patients. We used high-resolution Doppler ultrasound to serially follow mice with AVFs created by direct 25-gauge needle puncture. By day 21, 75% of AVFs dilate, thicken, and increase flow, i.e., mature, and 25% fail due to immediate thrombosis or maturation failure. Mature AVF thicken due to increased amounts of smooth muscle cells. By day 42, 67% of mature AVFs remain patent, but 33% of AVFs fail due to perianastomotic thickening. These results show that the mouse aortocaval model has an easily detectable maturation phase in the first 21 days followed by a potential failure phase in the subsequent 21 days. This model is the first animal model of AVF to show a course that recapitulates aspects of human AVF maturation. aortocaval fistula; arteriovenous fistula; maturation; mouse; model THE ARTERIOVENOUS FISTULA (AVF) is the most common access chosen for hemodialysis as the first-line therapy before renal replacement. Despite the superiority of AVF access compared with its alternatives, AVFs are still far from perfect. AVFs fail to "mature," e.g., dilate, thicken, and increase flow, before the beginning of dialysis in ϳ20 -50% of cases, with the majority of AVFs requiring some additional therapeutic intervention to mature successfully (9,14,20,21). In addition, 1-yr primary AVF patency rates are typically only 60 -65%, with many mature AVFs subsequently failing secondarily due to neointimal hyperplasia, generally perianastomotic (2,4,7,19,21,22). The poor patency of AVFs clearly reflects our imperfect understanding of the biology of venous remodeling to the arterial environment.The AVF has been studied using several models, including the surgical anastomosis model as well as the puncture model (1, 5, 6, 8, 10 -12, 15-17). All of these models have strengths and weakness, including technical difficulty due to surgery as well as the use of animals larger than mice (1,5,8,12,15,16). A common feature of all these models is that they are good models of surgical access, with good patency; unfortunately, they fail to exhibit a percentage of animals that either fail to mature or fail to develop stenoses in long-term followup, both of which are both important aspects of understanding modes of failure of human AVF.Recent advances in ultrasound technology have allowed increasingly accurate analysis of blood flow within small vessels, such as in a mouse, as well as allowing the ability to serially examine the same mouse over time. We used this technology to observe the time course of venous remodeling in the mouse ao...

Introduction Several clinical trials are currently evaluating stem cell therapy for patients with critical limb ischemia that have no other surgical or endovascular options for revascularization. However, these trials are conducted with different protocols, including use of different stem cell populations and different injection protocols, providing little means to compare trials and guide therapy. Accordingly, we developed a murine model of severe ischemia to allow methodical testing of relevant clinical parameters. Methods High femoral artery ligation and total excision of the superficial femoral artery (SFA) was performed on C57BL/6 mice. MNC were isolated from the bone marrow of donor mice, characterized using FACS, and injected (5×105−2×106) into the semimembranosus (proximal) or gastrocnemius (distal) muscle. Vascular and functional outcomes were measured using invasive Doppler, laser Doppler perfusion imaging, and the Tarlov and ischemia scores. Histological analysis included quantification of muscle fiber area and number as well as capillary density. Results Blood flow and functional outcomes were improved in MNC-treated mice as compared to controls over 28 days (Flow: P < .0001; Tarlov: P = .0004; ischemia score: P = .0002). MNC-treated mice also showed greater gastrocnemius fiber area (P = .0053) and increased capillary density (P = .0004). Dose-response analysis showed increased angiogenesis and gastrocnemius fiber area but no changes in macroscopic vascular flow or functional scores. Mice injected proximally to the ischemic area had overall similar functional outcomes to mice injected more distally, but increased muscle flow, capillary density, and gastrocnemius fiber area (P < .05). Conclusions High femoral ligation with complete excision of the SFA is a reliable model of severe hind limb ischemia in C57BL/6 mice that shows a response to MNC-treatment for both functional and vascular outcomes. A dose response to MNC injection appears to be present, at least microscopically, suggesting that an optimal cell number for stem cell therapy exists and that preclinical testing needs to be performed to optimally guide human trials. Injection of MNC proximal to the site of ischemia may provide some different outcomes compared to distal injection and warrants additional study.

Neointimal hyperplasia (NIH) in bypass conduits such as veins and prosthetic grafts is an important clinical entity that limits the long-term success of vascular interventions. Although the development of NIH in the conduits shares many of the same features of NIH that develops in native arteries after injury, vascular grafts are exposed to unique circumstances that predispose them to NIH, including surgical trauma related to vein handling, hemodynamic changes creating areas of low flow, and differences in biocompatibility between the conduit and the host environment. Multiple different approaches, including novel surgical techniques and targeted gene therapies, have been developed to target and prevent the causes of NIH. Recently, the PREVENT trials, the first molecular biology trials in vascular surgery aimed at preventing NIH, have failed to produce improved clinical outcomes, highlighting the incomplete knowledge of the pathways leading to NIH in vascular grafts. In this review, we aim to summarize the pathophysiologic pathways that underlie the formation of NIH in both vein and synthetic grafts and discuss current and potential mechanical and molecular approaches under investigation that may limit NIH in vascular grafts.

Catheter directed thrombolysis without universal prophylactic IVC filter placement is safe and effective in treating acute DVT. Pulmonary embolization did not occur during CDT. Selective rather than routine IVC filter placement is a safe and appropriate approach.

Veins are exposed to the arterial environment during two common surgical procedures, creation of vein grafts and arteriovenous fistulae (AVF). In both cases veins adapt to the arterial environment that is characterized by different hemodynamic conditions and increased oxygen tension compared to the venous environment. Successful venous adaptation to the arterial environment is critical for long term success of the vein graft or AVF, and in both cases is generally characterized by venous dilation and wall thickening. However, AVF are exposed to a high flow, high shear stress, low pressure arterial environment, and adapt mainly via outward dilation with less intimal thickening. Vein grafts are exposed to a moderate flow, moderate shear stress, high pressure arterial environment, and adapt mainly via increased wall thickening with less outward dilation. We review the data that describe these differences, as well as the underlying molecular mechanisms that mediate these processes. Despite extensive research, there are few differences in the molecular pathways that regulate cell proliferation and migration or matrix synthesis, secretion, or degradation currently identified between vein graft adaptation and AVF maturation that account for the different types of venous adaptation to arterial environments.

CAS for radiation arteritis has poor long-term anatomic outcome and can present with late asymptomatic occlusions. These findings suggest that these patients require closer postoperative surveillance and raise the question of whether CAS is appropriate for carotid occlusive lesions caused by radiation arteritis.

MetS is prevalent among patients undergoing carotid revascularization. MetS patients are at a greater risk for perioperative morbidity as well as stroke, MI, and MAE during follow-up when compared to patients without MetS. Long-term stroke prevention is poor in the presence of MetS. MetS should be considered a significant risk factor for patients undergoing carotid revascularization.