Spinal Cord Ischemia Rescue after Hybrid Total Arch Repair with Frozen Elephant Trunk: A Case Report.

Frozen elephant trunk repair is a technique described to simplify total arch repair for Stanford type A aortic dissection. Spinal cord ischemia is a devastating complication after frozen elephant trunk repair. In this report, we describe a case of spinal cord ischemia resulting in paralysis after frozen elephant trunk repair. Our spinal cord ischemia protocol was implemented and rescued patients from paraplegia. We report a dedicated spinal cord ischemia protocol that can rescue patients from paraplegia after hybrid arch repair with frozen elephant trunk.

Case report of retrograde in situ fenestration of the thoracic stent graft with reentry device in a patient with aortobronchial fistula.

RATIONALE: In situ fenestration may be necessary to preserve branch arteries during thoracic endovascular aortic repair (TEVAR) when there is an inadequate landing zone. PATIENT CONCERNS: We report the case of a 74-year-old man presenting with recurrent hemoptysis. DIAGNOSES: Based on computed tomography (CT) angiogram and bronchoscopy, diagnosis was aorto-bronchial fistula. INTERVENTIONS: We performed retrograde in situ fenestration with reentry catheter (Pioneer Plus, Volcano Corporation, San Diego, CA) to preserve the left subclavian artery following TEVAR for aorto-bronchial fistula. OUTCOMES: Following this procedure, the patient had a patent left subclavian artery and no evidence of endoleak. The patient had no further episodes of hemoptysis. LESSONS: The retrograde in situ fenestration with reentry catheter strategy is an option for patients when carotid-subclavian bypass is deemed unsafe.

Osteoclastogenesis in Abdominal Aortic Aneurysms: A New Therapeutic Target.

Abdominal aortic aneurysms (AAA) are a major cause of death. Currently, the mainstay of treatment for AAA is surgical repair and there are no FDA approved medical therapies for AAA. Much research is in progress to discover new medical therapies for AAA. The pathophysiology of AAA is understood to be a complex interplay of inflammatory and proteolytic processes that degenerate the aneurysm wall. Arterial calcification, which is observed in AAA but to a lesser extent than in arterial occlusive disease, occurs in a highly regulated manner in a similar process as mineral deposition in bone. Osteoblasts-like cells are responsible for mineral deposition in atherosclerotic plaques. Recently, osteoclast-like cells - the catabolic counterpart to osteoblasts - were discovered in atherosclerotic plaques. Additionally, osteoclast-like cells are present in the wall of AAA but not in healthy aortas. Osteoclast-like cells secrete matrix metalloproteinases (MMP) - proteases implicated in arterial aneurysm wall degeneration - and may contribute to the degredation of the aneurysm wall. Inhibiting osteoclast-like cells may prevent aneurysm progression by reducing tissue levels of MMPs. In this review, we discuss the pathophysiology of AAA formation and the current role of medical therapy in treatment of AAA. Furthermore, we highlight the emerging hypothesis that osteoclasts play a key role in the development of AAA and discuss therapies to inhibit osteoclastogenesis in AAA.

Alternative conduit for infrageniculate bypass in patients with critical limb ischemia.

BACKGROUND: Autologous great saphenous vein (GSV) has always been considered the gold standard conduit for infrainguinal revascularization. When GSV is inadequate or unavailable, alternative conduits have been used. In this study, we compared modern outcomes of different conduit types used in lower extremity bypass (LEB) for patients with critical limb ischemia (CLI). METHODS: The Vascular Study Group of New England database (2003-2014) was queried for patients who underwent infrageniculate bypass originating from the femoral arteries. Conduit types were categorized as single-segment GSV, alternative autologous conduit (AAC), and nonautologous conduit (NAC). Primary outcomes were 1-year freedom from major adverse limb event (MALE), MALE-free survival, and primary graft patency. Multivariable Cox regression was used to adjust for demographics and comorbidities. RESULTS: LEB was performed in 2148 patients, of which 1125 were to below-knee popliteal (BK-Pop) and 1023 to infrapopliteal artery (IPA) targets. The baseline characteristics differed among the conduit groups: Patients in the GSV group were younger and had fewer comorbidities than in the AAC groups. Patients undergoing BK-Pop bypass with NAC had higher rates of postoperative myocardial infarction (7.1%) and postoperative (5.8%) and 1-year death (40.8%) than in those with GSV (3.1%, 2%, and 31.7%, respectively) and AAC (0%, 0%, and 25%, respectively). In multivariable analysis, conduit type did not make a difference in 1-year MALE, MALE-free survival, or primary graft patency for BK-Pop bypasses. For IPA bypasses, NAC use was associated with higher rates of postoperative (6.4%) and in-hospital death (4.5%) compared with GSV (2.5% and 1.4%, respectively) and AAC (2.9% and 1.9%, respectively). In adjusted analysis, NAC was associated with higher risk of MALE (hazard ratio [HR], 1.50; 95% confidence interval [CI], 1.03-2.20; P = .036) and primary patency loss (HR, 1.3; 95% CI, 0.91-1.89), and lower MALE-free survival (HR, 1.47; 95% CI, 1.03-2.09; P = .035) compared with GSV. There was no difference between the NAC and AAC groups. CONCLUSIONS: Conduit type does not affect outcomes in BK-Pop bypass. In the absence of single-segment GSV, the use of AAC for IPA bypass does not appear to confer any additional benefit of MALE, MALE-free survival, or graft patency compared with prosthetic grafts at 1-year follow-up.

Plasma expanders stabilize human microvessels in microfluidic scaffolds.

Plasma expanders such as dextran and hydroxyethyl starch (HES) are important components of solutions designed to maintain vascular volume in the clinical setting and to preserve organs ex vivo before transplantation. Here, we show that these polymers also exert stabilizing effects on engineered microvessels in microfluidic type I collagen and fibrin scaffolds. Standard growth media, which did not contain dextran or HES, led to severe leakage, vascular collapse, and catastrophic failure of perfusion. Remarkably, vessels that were provided with 3% dextran or 5% HES had few focal leaks, maintained adhesion to the scaffold, and were typically viable and patent for at least 2 weeks. We found that the junctional marker VE-cadherin localized to a wide band in the presence of plasma expanders, but only at concentrations that also stabilized vessels. In conjunction with a previous computational model (Wong et al., Biomaterials 2010;31:4706-4714), our results suggest that plasma expanders stabilize microvessels via physical mechanisms that enhance VE-cadherin localization at junctions and thereby limit vascular leakiness.

Effect of mechanical factors on the function of engineered human blood microvessels in microfluidic collagen gels.

This work examines how mechanical signals affect the barrier function and stability of engineered human microvessels in microfluidic type I collagen gels. Constructs that were exposed to chronic low flow displayed high permeabilities to bovine serum albumin and 10 kDa dextran, numerous focal leaks, low size selectivity, and short lifespan of less than one week. Higher flows promoted barrier function and increased longevity; at the highest flows, the barrier function rivaled that observed in vivo, and all vessels survived to day 14. By studying the physiology of microvessels of different geometries, we established that shear stress and transmural pressure were the dominant mechanical signals that regulated barrier function and vascular stability, respectively. In microvessels that were exposed to high flow, elevation of intracellular cyclic AMP further increased the selectivity of the barrier and strongly suppressed cell proliferation. Computational models that incorporated stress dependence successfully predicted vascular phenotype. Our results indicate that the mechanical microenvironment plays a major role in the functionality and stability of engineered human microvessels in microfluidic collagen gels.