Endovascular extension grafts, coil embolization, and conversion to open surgery each may be used to effectively repair endoleak. Selection of the treatment method used is determined by the anatomic characteristics of the endoleak and the patient's ability to tolerate conventional repair. Conversion to open repair was uniformly successful. Deployment of an extension cuff was successful when complete closure of the endoleak was achieved. Embolic coils were effective for retrograde endoleaks and provided stabilization of AAA size in selected patients with attachment site endoleaks in limited follow-up.

While promising, this midterm experience with commercially available devices highlights the shortcomings of current stent-graft technology. Three significant advancements are required to fulfill the potential of this important treatment method: a stent graft with a durable proximal and distal fixation device, enhanced engineering to accommodate high thoracic aortic fatigue forces, and a mechanism to adapt to aortic arch and visceral segment branches to enable treatment of lesions that extend to or include these vessels.

Background-Synthetic vascular grafts cannot be used in small vessels because of graft failure caused by thrombosis and neointima formation. Rapid endothelialization may overcome this limitation. We hypothesized that a magnetic graft would be able to capture and retain endothelial cells labeled with paramagnetic particles. Methods and Results-Porcine blood derived endothelial cells were allowed to endocytose superparamagnetic iron oxide microspheres. Cell survival was assessed by trypan blue exclusion and demonstrated a dose-dependent cell survival of 75% to 95%. A flexible magnetic sheet was annealed to the external surface of a knitted Dacron graft. Labeled cells (10 6 /mL) were placed within the graft for 5 minutes. Confocal and electron microscopy confirmed uniform cell capture at the magnetized surface. The effect of shear forces on the adherent cells was evaluated in a flow chamber. The cells remained attached at rates up to 300 mL/min, with cell loss commencing at 400 mL/min. Prototype magnetic grafts were implanted in porcine carotid arteries. Labeled cells were placed within the graft for 10 minutes at the time of implantation. The grafts were evaluated after one day and uniform cell coverage was noted on the magnetized surface. In comparison, relatively few labeled cells were seen attached to a nonmagnetized surface. Key Words: coronary disease Ⅲ endothelium Ⅲ grafting Ⅲ surgery Ⅲ magnet T he major limitation of prosthetic vascular grafts is their tendency to occlude after various periods of time. This occlusion rate is higher for smaller-diameter grafts and precludes their use in a significant number of medical applications, most notably in coronary artery bypass grafting. Numerous studies have shown that failure is secondary to graft occlusion, either because of thrombogenicity of the synthetic material or because of encroachment of tissue (intimal hyperplasia) into the lumen of the graft at anastomotic sites. 1 A potential way to limit graft failure would be to provide rapid, uniform, and complete coverage with a functional endothelial layer. In a pioneering study, Stump et al have shown that a Dacron patch suspended in the flow, without contact with the vessel wall, was covered with endothelial colonies within 7 days of implantation. 2 Early efforts at graft endothelialization with the use of mature endothelial cells, 3-8 although promising, were limited by difficulties related to obtaining cells in significant numbers. The recent description of circulating endothelial progenitor cells 9 has provided a new source for cellular seeding of grafts. We have previously shown that blood-derived endothelial outgrowth cells (EOCs) are effective in preventing restenosis and can restore vascular function in animal models of arterial injury. 10 Previous work used prolonged vascular occlusion to enable cell adhesion to the vessel wall, an approach that cannot be used in clinical settings. We hypothesized that local cell capture and retention could be accomplished by using magnetic forces. EOCs were rendered magn...

In response to vascular injury, vascular smooth muscle cells (VSMCs) may switch from a contractile to a proliferative phenotype thereby contributing to neointima formation. Previous studies showed that the long noncoding RNA (lncRNA) is critical for paraspeckle formation and tumorigenesis by promoting cell proliferation and migration. However, the role of in VSMC phenotypic modulation is unknown. Herein we showed that expression was induced in VSMCs during phenotypic switching in vivo and in vitro. Silencing in VSMCs resulted in enhanced expression of SM-specific genes while attenuating VSMC proliferation and migration. Conversely, overexpression of in VSMCs had opposite effects. These in vitro findings were further supported by in vivo studies in which knockout mice exhibited significantly decreased neointima formation following vascular injury, due to attenuated VSMC proliferation. Mechanistic studies demonstrated that sequesters the key chromatin modifier WDR5 (WD Repeat Domain 5) from SM-specific gene loci, thereby initiating an epigenetic "off" state, resulting in down-regulation of SM-specific gene expression. Taken together, we demonstrated an unexpected role of the lncRNA in regulating phenotypic switching by repressing SM-contractile gene expression through an epigenetic regulatory mechanism. Our data suggest that is a therapeutic target for treating occlusive vascular diseases.

No abstract

Iatrogenic aortic injuries after spinal surgery have been described, but are rare. We describe a case of a 77-year-old woman who underwent surgical correction of a debilitating spinal deformity at an outside institution. Postoperative thoracic spine radiographs and computed tomography scans revealed a misplaced pedicle screw at T5, which was impinging on the descending thoracic aortic wall. The patient was brought to the operating room, where a thoracic stent graft was deployed under fluoroscopic guidance as the malpositioned screw was manually retracted. The patient had an uneventful postoperative course, and was discharged within 24 hours. This case represents a rare but potentially morbid vascular complication of spinal instrumentation surgery that was successfully treated without the need for thoracotomy.

Cystic adventitial disease (CAD) is a rare condition in which cyst is found within a vessel, typically producing symptoms of vascular compromise. Most commonly located in the popliteal artery near the knee, it has been reported in arteries and veins throughout the body. Its pathogenesis has been poorly understood and various surgical approaches have been recommended. We extrapolated some recent information about a similar condition, intraneural ganglion cyst affecting the deep fibular (peroneal) nerve, to the prototype, CAD of the popliteal artery. In intraneural ganglion cysts affecting the deep fibular nerve we have shown that an articular (neural) branch is the conduit between the superior tibiofibular joint and the main parent nerve for which epineurial dissection of joint fluid can occur. We hypothesized that the same principles would apply to CAD and that an articular (vascular) branch would be the conduit from the knee joint leading to dissection to the main parent vessel. We reviewed five patients with CAD of the popliteal artery in whom MRIs were available: two treated by the primary author well familiar with the proposed articular theory, and three treated by others at our institution, less familiar with it. We then reviewed the literature critically to assess for additional evidence to support our articular (synovial) theory and an anatomic explanation. In the two cases treated by the primary author a joint connection was identified on high resolution MRI prospectively and intraoperatively through the middle genicular artery (MGA); postoperatively in these cases there was no recurrence. In the other three cases, a joint connection was not identified on imaging or at operation. Reinterpretation of these cases revealed a joint connection through the MGA in the one patient who had preoperative imaging and subclinical persistence/recurrence in the two patients who underwent postoperative MRIs done for other reasons. Our review of the literature and imaging studies revealed unrecognized joint connections in CAD to the knee and other joints as well as evidence that the MGA is the conduit in cases of CAD of the popliteal artery. We believe that adventitial cysts originate in neighboring joints and dissect within articular (vascular) branches. In our opinion, the unifying articular theory and the principles introduced for intraneural ganglion cysts apply equally to common and rare sites of adventitial cysts.

MR.A preferential p110␣/␥ PI3K inhibitor attenuates experimental inflammation by suppressing the production of proinflammatory mediators in a NF-Bdependent manner.