In the absence of ischemic paraplegia or other injuries that require emergency surgery, endovascular treatment is a safe and efficient method for treating traumatic infrarenal aortic dissection.
The clearance of erythrocytes may be carried out by vascular cells in atherosclerotic conditions. • Phagocytosis by endothelial cells is more pronounced with aged and glycated erythrocytes.• Endothelial phagocytosis is enhanced with T2D erythrocytes.• Interactions between erythrocytes and endothelial cells occur in vivo, in atherothrombotic/diabetic conditions.
The Zenith stent-graft had the best resistance to dislodgment. An additional Palmaz stent placed at the proximal attachment site greatly improves endograft fixation regardless of the type of stent-graft. For complex aneurysm necks or for intraoperative type I endoleak management, an adjunctive Palmaz stent could be used.
Rationale:
Metabolic syndrome (MetS) is a cluster of interrelated risk factors for cardiovascular diseases and atherosclerosis. Circulating levels of large extracellular vesicles (lEVs), submicrometer-sized vesicles released from plasma membrane, from MetS patients were shown to induce endothelial dysfunction but their role in early stage of atherosclerosis and on vascular smooth muscle cells (SMC) remain to be fully elucidated.
Objective:
To determine the mechanisms by which lEVs lead to the progression of atherosclerosis in the setting of MetS.
Methods and Results:
Proteomic analysis revealed that the small GTPase, Rap1 was overexpressed in lEVs from MetS patients compared to those from non-MetS (nMetS) subjects. Rap1 was in GTP-associated active state in both types of lEVs and Rap1-lEVs levels correlated with increased cardiovascular risks including stenosis. MetS-lEVs, but not nMetS-lEVs, increased Rap1-dependent endothelial cell permeability. MetS-lEVs significantly promoted migration and proliferation of human aortic SMC and increased expression of pro-inflammatory molecules and activation of ERK5/p38 pathways. Neutralization of Rap1 by specific antibody or pharmacological inhibition of Rap1 with GGTi-298, completely prevented the effects of lEVs from MetS patients. HFD-fed ApoE
-/-
mice displayed an increased expression of Rap1 both in aortas and circulating lEVs. lEVs accumulated in plaque atherosclerotic lesions depending on the progression of atherosclerosis. lEVs from HFD-fed ApoE
-/-
mice, but not those from mice fed with a standard diet, enhanced SMC proliferation. Human atherosclerotic lesions were enriched in lEVs expressing Rap1.
Conclusions:
These data demonstrate that Rap1 carried by MetS-lEVs participates in the enhanced SMC proliferation, migration, pro-inflammatory profile and activation of ERK5/p38 pathways leading to vascular inflammation and remodeling, and atherosclerosis. These results highlight that Rap1 carried by MetS-lEVs may be a novel determinant of diagnostic value for cardiometabolic risk factors and suggest Rap1 as a promising therapeutic target against the development of atherosclerosis.
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