| 1. |
- Lachat, Mario, et al.
(författare)
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Periscope Endograft Technique to Revascularize the Left Subclavian Artery During Thoracic Endovascular Aortic Repair
- 2013
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Ingår i: Journal of Endovascular Therapy. - 1526-6028 .- 1545-1550. ; 20:6, s. 728-734
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To present early and midterm results of the periscope endograft (PG) technique to maintain left subclavian artery (LSA) blood flow in thoracic endovascular aortic repairs (TEVAR) involving zone 3. Methods: From April 2010 to January 2013, 14 consecutive high-risk patients (11 men; mean age 70 8 years, range 56-87) underwent TEVAR with the PG technique for 10 thoracic aortic aneurysms (TAA), 2 traumatic aortic ruptures, and 2 aortic dissections without a suitable landing zone (>2 cm distal to the LSA). Five procedures were performed emergently for rupture (3 TAAs and the 2 trauma cases). Two patients had a periscope deployed in an aberrant right subclavian artery. The periscope endografts were sized 1 to 2 mm larger than the branch artery at the intended landing zone. The caudal end was extended distal to the intended distal landing site of the thoracic stent-graft, which was usually deployed after the PG. Both the PG and thoracic stent-grafts were generally molded using the kissing balloon technique. Outcomes analyzed were immediate technical success, perioperative mortality and morbidity, aneurysm diameter change, and periscope endograft patency. Results: Immediate technical success was 100%, with all procedures completed as planned. Perioperatively, one periscope occluded and one of the ruptured TAA patients died. One percutaneous access site hematoma required only conservative management. At a mean follow-up of 26 +/- 9 months (range 9-37), there was no additional PG occlusion. The Kaplan-Meier estimate of PG patency was 93% at 2 years. Conclusion: The periscope endograft is a simple technique to maintain perfusion to the LSA in cases where the aortic stent-graft crosses its ostium. The PG technique can be performed transfemorally and even percutaneously, and it can be applied to all supraaortic branches. Early and midterm results are encouraging, but more experience and long-term results are mandatory before this technique can be widely recommended.
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| 2. |
- Oppi, Sara, et al.
(författare)
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Macrophage NCOR1 protects from atherosclerosis by repressing a pro-atherogenic PPAR gamma signature
- 2020
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Ingår i: European Heart Journal. - : OXFORD UNIV PRESS. - 0195-668X .- 1522-9645. ; 41:9, s. 995-1005
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Tidskriftsartikel (refereegranskat)abstract
- Aims Nuclear receptors and their cofactors regulate key pathophysiological processes in atherosclerosis development. The transcriptional activity of these nuclear receptors is controlled by the nuclear receptor corepressors (NCOR), scaffolding proteins that form the basis of large corepressor complexes. Studies with primary macrophages demonstrated that the deletion of Ncor1 increases the expression of atherosclerotic molecules. However, the role of nuclear receptor corepressors in atherogenesis is unknown. Methods and results We generated myeloid cell-specific Ncor1 knockout mice and crossbred them with low-density lipoprotein receptor and results (Ldlr) knockouts to study the role of macrophage NCOR1 in atherosclerosis. We demonstrate that myeloid cellspecific deletion of nuclear receptor corepressor 1 (NCOR1) aggravates atherosclerosis development in mice. Macrophage Ncorl-deficiency leads to increased foam cell formation, enhanced expression of pro-inflammatory cytokines, and atherosclerotic lesions characterized by larger necrotic cores and thinner fibrous caps. The immunometabolic effects of NCOR1 are mediated via suppression of peroxisome proliferator-activated receptor gamma (PPAR gamma) target genes in mouse and human macrophages, which lead to an enhanced expression of the CD36 scavenger receptor and subsequent increase in oxidized low-density lipoprotein uptake in the absence of NCOR1. Interestingly, in human atherosclerotic plaques, the expression of NCOR1 is reduced whereas the PPAR gamma signature is increased, and this signature is more pronounced in ruptured compared with non-ruptured carotid plaques. Conclusions Our findings show that macrophage NCOR1 blocks the pro-atherogenic functions of PPAR gamma in atherosclerosis and suggest that stabilizing the NCOR1-PPAR gamma binding could be a promising strategy to block the pro-atherogenic functions of plaque macrophages and lesion progression in atherosclerotic patients.
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| 3. |
- Sörelius, Karl, et al.
(författare)
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Endovascular treatment of mycotic aortic aneurysms: a European multicenter study.
- 2014
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Ingår i: Circulation. - : Lippincott Williams & Wilkins. - 1524-4539 .- 0009-7322. ; 130:24, s. 2136-42
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Tidskriftsartikel (refereegranskat)abstract
- Mycotic aortic aneurysm (MAA) is a rare and life-threatening disease. The aim of this European multicenter collaboration was to study the durability of endovascular aortic repair (EVAR) of MAA, by assessing late infection-related complications and long-term survival.
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