Endovascular Repair of Ascending Aortic Pseudoaneurysm Using Transfemoral Frame-Coiling Under Total Cerebral Protection.

Ascending aortic pseudoaneurysms are associated with prior cardiac surgery and have a high chance of rupture. Open surgery is challenging given its likely reoperative nature. Various endovascular therapies have been described but are sometimes complicated by stroke. We present a patient with a prior coronary artery bypass grafting who was referred for an incidental 3-cm saccular ascending aortic pseudoaneurysm who was successfully treated with frame coiling under total cerebral embolic protection using the SENTINEL device. We propose that endovascular obliteration of ascending aortic pseudoaneurysms is a viable option in patients unfit for open repair and advocate for total cerebral embolic protection as an important adjunct.

Galectin-1 regulates tissue exit of specific dendritic cell populations.

During inflammation, dendritic cells emigrate from inflamed tissue across the lymphatic endothelium into the lymphatic vasculature and travel to regional lymph nodes to initiate immune responses. However, the processes that regulate dendritic cell tissue egress and migration across the lymphatic endothelium are not well defined. The mammalian lectin galectin-1 is highly expressed by vascular endothelial cells in inflamed tissue and has been shown to regulate immune cell tissue entry into inflamed tissue. Here, we show that galectin-1 is also highly expressed by human lymphatic endothelial cells, and deposition of galectin-1 in extracellular matrix selectively regulates migration of specific human dendritic cell subsets. The presence of galectin-1 inhibits migration of immunogenic dendritic cells through the extracellular matrix and across lymphatic endothelial cells, but it has no effect on migration of tolerogenic dendritic cells. The major galectin-1 counter-receptor on both dendritic cell populations is the cell surface mucin CD43; differential core 2 O-glycosylation of CD43 between immunogenic dendritic cells and tolerogenic dendritic cells appears to contribute to the differential effect of galectin-1 on migration. Binding of galectin-1 to immunogenic dendritic cells reduces phosphorylation and activity of the protein-tyrosine kinase Pyk2, an effect that may also contribute to reduced migration of this subset. In a murine lymphedema model, galectin-1(-/-) animals had increased numbers of migratory dendritic cells in draining lymph nodes, specifically dendritic cells with an immunogenic phenotype. These findings define a novel role for galectin-1 in inhibiting tissue emigration of immunogenic, but not tolerogenic, dendritic cells, providing an additional mechanism by which galectin-1 can dampen immune responses.

Unique Presentation of an Inflammatory Abdominal Aortic Aneurysm With Rhabdomyolysis.

OBJECTIVE: This study reports the case of a 72 year old male who presented with rhabdomyolysis and a symptomatic juxtarenal inflammatory abdominal aortic aneurysm (IAAA). He underwent open repair of his IAAA with a polytetrafluoroethylene graft using the transperitoneal approach. RESULTS: The patient's aneurysm had significant inflammation with a thick rind of friable tissue overlying the native aorta. He had no history of autoimmune disease to serve as a potential trigger of his symptomatic IAAA. Prior to his presentation, however, he did experience three months of myalgia, with a concomitant creatine kinase elevation to 20,000 U/L and gross haematuria. CONCLUSION: It is proposed that rhabdomyolysis and its accompanying inflammatory state may serve as a trigger for IAAA.

Distal landing zone optimization before endovascular repair of aortic dissection.

BACKGROUND: The general goals of endovascular management in chronic distal thoracic aortic dissection are optimizing the true lumen, maintaining branch patency, and promoting false lumen (FL) thrombosis. Distal seal can be challenging in chronic distal thoracic aortic dissection due to the well-established secondary fenestrations and fibrotic septum. We describe our approach of distal landing zone optimization (DLZO) to enable full-diameter contact of the distal endoprosthesis. MATERIALS AND METHODS: Our experience includes 19 procedures in 16 patients (12 male, age 68 ± 8 years) between May 2014 and November 2017. A history of previous ascending repair for type A dissection was present in 8 patients. Treatment indication was enlarging aneurysm in all subjects, and 4 patients had associated chronic visceral or distal ischemia. Point septal fenestrations were expanded by serial balloon dilation and/or wire-pull approaches. Balloon molding was used to ensure complete endograft apposition and FL collapse. RESULTS: One death occurred due to aortic perforation during wire-pull fenestration in a patient with heavily calcified and angulated aorta. The remaining procedures were accomplished safely and successfully. Balloon fenestration was used in 16 procedures, alone or in combination with a limited wire pull component. Adjunct procedures for distal seal included surgeon-modified fenestrated stent graft (3), iliac branch device (3), parallel superior mesenteric artery stent-graft (1), renal artery or superior mesenteric artery stent-graft (4), iliac stent (3), and plug obliteration of FL (5). Reintervention was required in 3 patients due to delayed loss of seal after the initial procedure (3, 8, and 12 months). Two were managed by repeat DLZO and distal extension. The third had distal extension via a surgeon-modified fenestrated stent-graft component. Follow-up imaging was available in 14 patients (16.0 ± 12.5 months, range: 1-33), with stable or regressed sac diameter with complete or near-complete thrombosis of the FL in all patients. CONCLUSIONS: DLZO enabled creation of a distal seal zone in all patients. Residual retrograde filling of the FL is a marker of procedure failure, especially when seal segment length or feasible endoprosthesis oversizing are marginal. Insufficient landing segment can be circumvented with the use of a fenestrated or branched device to accomplish seal in the visceral aorta or iliac bifurcation. Adjunct FL ablation is also a valuable technique to promote FL thrombosis.

Endovascular management of an acute type B aortic dissection in a patient with fibromuscular dysplasia.

We report the case of a 44-year-old woman who developed an acute type B aortic dissection caused by an entry tear from an aneurysmal left common iliac artery that extended retrograde to the proximal descending thoracic aorta. She experienced refractory chest pain despite optimal medical management, thereby indicating repair. Endovascular aortic repair was subsequently performed. Intraoperatively, fibromuscular dysplasia was diagnosed by the characteristic appearance of her renal arteries. The patient tolerated the procedure and had resolution of her chest pain. In summary, we present a highly unusual case of type B aortic dissection resulting from a retrograde common iliac artery tear in a patient with fibromuscular dysplasia.

Assessing the roles of galectins in regulating dendritic cell migration through extracellular matrix and across lymphatic endothelial cells.

Leukocyte migration from the bloodstream into tissues, and from tissues to lymph nodes, depends on expression of specific adhesion and signaling molecules by vascular endothelial cells and lymphatic endothelial cells. Tissue damage and microbial infection induce vascular endothelial cells to up-regulate expression of adhesion molecules to facilitate entry of several leukocyte populations from blood into tissues. Many of these cells then leave inflamed tissue and migrate to regional lymph nodes. A critical population that emigrates from inflamed tissue is dendritic cells. Dendritic cells in tissue have to migrate through extracellular matrix and across a layer of lymphatic endothelial cells to enter the lymphatic vasculature. Little is known about the adhesion molecules expressed by lymphatic endothelial cells or the processes required for the critical step of dendritic cell exit from tissues, specifically migration through the extracellular matrix and basal-to-apical migration across the lymphatic endothelial cell layer into lymphatic vasculature.Members of the galectin family of carbohydrate binding proteins are expressed in both vascular and lymphatic endothelial cells. Dynamic changes in galectin expression during inflammation are known to regulate leukocyte tissue entry during inflammation. However, the roles of galectin family members expressed by lymphatic endothelial cells in leukocyte tissue exit remain to be explored.Here, we describe an in vitro transmigration assay that mimics dendritic cell tissue exit in the presence and absence of galectin protein. Fluorescently labeled human dendritic cell migration through extracellular matrix and across human lymphatic endothelial cells is examined in the presence and absence of recombinant human galectin protein.