Database : MEDLINE
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[PMID]: 29524462
[Au] Autor:Tigkiropoulos K; Sigala F; Tsilimigras DI; Moris D; Filis K; Melas N; Karamanos D; Kontogiannis C; Lazaridis I; Saratzis N
[Ad] Address:1(st) Department of Surgery, Aristotle University Thessaloniki, Papageorgiou General Hospital, Thessaloniki, Greece.
[Ti] Title:Endovascular Repair of Blunt Thoracic Aortic Trauma: Is Post-Implant Hypertension an Incidental Finding?
[So] Source:Ann Vasc Surg;, 2018 Mar 07.
[Is] ISSN:1615-5947
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Blunt thoracic aortic injury (BTAI) is the second most common cause of death in trauma patients. Nowadays, thoracic endovascular aortic repair (TEVAR) has become the treatment of choice due to lower rates of mortality, paraplegia and stroke. However, concerns have been raised whether graft implantation is related to the development of hypertension in the postoperative period. OBJECTIVES: To report short- and long-term outcomes of patients undergoing TEVAR for BTAIs at a tertiary hospital as well as investigate post-implant hypertension. MATERIALS & METHODS: Between January 2005 and January 2016, 23 patients with blunt thoracic aortic trauma underwent TEVAR. Median age was 44 years (range 18-73). Among them, 14 (60.9%) patients were diagnosed with aortic rupture, while 9 (39.1%) with pseudoaneurysm. Α single thoracic stent graft was deployed in 21 patients and the rest 2 patients received two stent grafts. RESULTS: Complete exclusion of the injury was feasible in all subjects (100% primary success). The left subclavian artery (SCA) was intentionally covered in 6 patients (26%). Intraoperative complications included one nonfatal stroke managed conservatively and one external iliac artery rupture, treated with iliofemoral bypass. One patient (4.3%) died on the first postoperative day in the intensive care unit (ICU) due to hemorrhagic shock. The overall 30-day mortality and morbidity were 4.3% and 8.7%, respectively. New-onset post-implantation arterial hypertension was observed in 8 (34.8%) previously non-hypertensive patients. Younger age (p=0.027) and SCA coverage (p=0.01) were identified as potential risk factors for the development of post-implant hypertension, whereas the presence of concomitant injuries (p=0.3) and intraoperative complications (p=0.1) were not. Following a median follow-up of 100 months (range, 18-120), six of them still remain on antihypertensive therapy, whereas the other 2 did not require permanent treatment. CONCLUSIONS: TEVAR is a safe approach in the treatment of BTAI associated with low short- and long-term morbidity and mortality rates. Lower age and SCA coverage may contribute to the development of post-implant hypertension. Further larger cohort studies are warranted in order to elucidate the underlying mechanisms of post-implant hypertension.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29523026
[Au] Autor:Hauge T; Kleven OC; Johnson E; Hofstad B; Johannessen HO
[Ad] Address:a Department of Surgery , Drammen Hospital , Drammen , Norway.
[Ti] Title:Outcome after stenting and débridement for spontaneous esophageal rupture.
[So] Source:Scand J Gastroenterol;:1-5, 2018 Mar 09.
[Is] ISSN:1502-7708
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Surgical repair has been the most common treatment of esophageal effort rupture (Boerhaave syndrome). Stent-induced sealing of the perforation has increasingly been used with promising results. We present our eight years´ experience with stent-based and organ-preserving treatment. MATERIALS AND METHODS: Medical records of 15 consecutive patients with Boerhaave syndrome from February 2007 to May 2015 were retrospectively registered in a database. Treatment was sealing of the perforation by stenting, chest tube drainage and débridement of the contaminated thorax. After median 25 months nine out of 10 patients responded to questions on fatigue and Ogilvie's dysphagia score. RESULTS: Fifteen patients, aged median 67.5 years (range 39-88), had a primary hospital stay of 20 days (range 1-80 days). Overall in-hospital mortality was 13%. Observation time was 44 months (range 0-87) and 10 patients were alive of August 2017. Ten patients (67%) needed surgical chest débridement. Five patients (33%) were restented for leakage, migration and for stent removal. Eleven patients (73%) had complications, which included pleural empyema (n = 4), fatal aortic bleeding, lung arterial bleeding, lung embolism, drain-induced lung laceration and respiratory failure. Dysphagia score was low (median 0.5) meaning that they were able to feed themselves. Total fatigue score (mean 14.6) was slightly increased (p = .05) compared with a reference population. CONCLUSIONS: The mortality rate after initial stenting of effort rupture seems to be comparable to standard surgical repair. Most patients required further intervention, either by restenting and/or surgical débridement. The functional result in these patients was satisfactory.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1080/00365521.2018.1448886

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[PMID]: 29505549
[Au] Autor:Yu H; Li Q; Chen C; Li T; Xiong JY; Qin Z; Luo M; Tan ZX; Liu T; Yu H; Yin XR; Yu H; Zhou RH
[Ad] Address:Department of Anesthesiology.
[Ti] Title:Effect of intralipid on myocardial injury during valve replacement surgery with concomitant radiofrequency ablation: A randomized controlled trial.
[So] Source:Medicine (Baltimore);97(1):e9603, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: This study aimed to evaluate the effect of intralipid postconditioning (ILPC) on myocardial damage in patients undergoing valve replacement surgery with concomitant radiofrequency ablation (RFA) for atrial fibrillation (AF). METHODS: Randomized patient and assessor-blind controlled trial conducted in adult patients undergoing valve replacement surgery with concomitant RFA. Sixty-nine patients were randomly assigned to ILPC group (n = 34) or control group (n = 35): ILPC group received an intravenous infusion of 20% intralipid (2 mL/kg) just 10 minutes before aortic cross-unclamping, and control group received an equivalent volume of normal saline. Serum cardiac troponin-T (cTnT) and creatine kinase-MB (CK-MB) was measured before surgery and at 4, 12, 24, 48, and 72 hours after surgery. The primary endpoints were the 72-hour area under the curve (AUC) for cTnT and CK-MB. RESULTS: The total 72-hour AUC of cTnT (P = .33) and CK-MB (P = .52) were comparable between 2 groups. The left ventricle ejection fraction at discharge (P = .011) was higher in the ILPC group than that in the control group, while the AF recurrence did not differ significantly between 2 groups. CONCLUSIONS: There was no observed beneficial effect of ILPC on myocardial injury documented by the cardiac biomarkers in patients undergoing valve replacement surgery with concomitant RFA, and the effect of intralipid against myocardial I/R injury is undetectable within the background of massive biomarker release following ablation owing to localized myocardial necrosis. Besides, there are no other published data about the cardioprotective role of intralipid in patients undergoing this procedure and benefits of this protection need further studies to validate.
[Mh] MeSH terms primary: Catheter Ablation/adverse effects
Fat Emulsions, Intravenous/therapeutic use
Heart Injuries/prevention & control
Phospholipids/therapeutic use
Soybean Oil/therapeutic use
[Mh] MeSH terms secundary: Adult
Atrial Fibrillation/surgery
Creatine Kinase, MB Form/blood
Emulsions/therapeutic use
Female
Heart Injuries/blood
Heart Injuries/etiology
Heart Valve Prosthesis Implantation
Humans
Male
Middle Aged
Prospective Studies
Troponin T/blood
[Pt] Publication type:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Name of substance:0 (Emulsions); 0 (Fat Emulsions, Intravenous); 0 (Phospholipids); 0 (Troponin T); 0 (soybean oil, phospholipid emulsion); 8001-22-7 (Soybean Oil); EC 2.7.3.2 (Creatine Kinase, MB Form)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009603

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[PMID]: 29425771
[Au] Autor:Rajasinghe HA; Miller LE; Krajcer Z
[Ad] Address:The Vascular Group of Naples, Naples, FL. Electronic address: HRajasinghe@tvgnaples.com.
[Ti] Title:Early Outcomes with Fast-Track EVAR in Teaching and Nonteaching Hospitals.
[So] Source:Ann Vasc Surg;, 2018 Feb 07.
[Is] ISSN:1615-5947
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: The influence of hospital teaching status on fast-track endovascular aneurysm repair (EVAR) outcomes is unknown. This study explored the feasibility, safety, and effectiveness of a fast-track EVAR protocol at teaching and nonteaching hospitals. METHODS: Patients underwent a fast-track EVAR protocol composed of bilateral percutaneous access using a 14F stent graft, avoidance of general anesthesia and intensive care admission, and next-day discharge. Patients were followed up for 1 month post-treatment. Participating hospitals were categorized by teaching status (teaching versus nonteaching) and compared for perioperative and 30-day outcomes. RESULTS: Between October 2014 and May 2016, 250 patients were enrolled at 31 centers in the United States. The study included 186 patients treated among 21 teaching hospitals and 64 patients treated among 10 nonteaching hospitals. Fast-track EVAR protocol completion was higher at teaching hospitals (91% vs. 73%, P = 0.01). Intensive care admission was avoided in 99% of patients at teaching hospitals versus 84% at nonteaching hospitals (P < 0.001). The ability to complete all other fast-track EVAR elements was proportionally higher at teaching hospitals, but differences were not statistically different. In-hospital outcomes by teaching status were comparable overall. Median time to discharge was 25 and 26 hr, respectively. There were no reports of type III endoleak, abdominal aortic aneurysm rupture, or secondary intervention. Comparing teaching versus nonteaching hospitals, there were no differences in major adverse events (1% vs. 0%), type I endoleak (0% vs. 2%), limb occlusion (1% vs. 0%), all-cause mortality (1% vs. 0%), and 30-day readmissions (1% vs. 3%). CONCLUSIONS: A fast-track EVAR protocol can be implemented with high success in well-selected patients at teaching and nonteaching hospitals. Health care resource utilization, perioperative data, and 30-day outcomes were excellent overall, with higher frequency of intensive care admission at nonteaching hospitals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 16552 MEDLINE  
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[PMID]: 29238189
[Au] Autor:Zhang CY; Sun XY; Ouyang JM; Gui BS
[Ad] Address:Institute of Biomineralization and Lithiasis Research, Jinan University, Guangzhou.
[Ti] Title:Diethyl citrate and sodium citrate reduce the cytotoxic effects of nanosized hydroxyapatite crystals on mouse vascular smooth muscle cells.
[So] Source:Int J Nanomedicine;12:8511-8525, 2017.
[Is] ISSN:1178-2013
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Objective: This study aimed to investigate the damage mechanism of nanosized hydroxyapatite (nano-HAp) on mouse aortic smooth muscle cells (MOVASs) and the injury-inhibiting effects of diethyl citrate (Et Cit) and sodium citrate (Na Cit) to develop new drugs that can simultaneously induce anticoagulation and inhibit vascular calcification. Methods: The change in cell viability was evaluated using a cell proliferation assay kit, and the amount of lactate dehydrogenase (LDH) released was measured using an LDH kit. Intracellular reactive oxygen species (ROS) and mitochondrial damage were detected by DCFH-DA staining and JC-1 staining. Cell apoptosis and necrosis were detected by Annexin V staining. Intracellular calcium concentration and lysosomal integrity were measured using Fluo-4/AM and acridine orange, respectively. Results: Nano-HAp decreased cell viability and damaged the cell membrane, resulting in the release of a large amount of LDH. Nano-HAp entered the cells and damaged the mitochondria, and then induced cell apoptosis by producing a large amount of ROS. In addition, nano-HAp increased the intracellular Ca concentration, leading to lysosomal rupture and cell necrosis. On addition of the anticoagulant Et Cit or Na Cit, cell viability and mitochondrial membrane potential increased, whereas the amount of LDH released, ROS, and apoptosis rate decreased. Et Cit and Na Cit could also chelate with Ca to inhibit the intracellular Ca elevations induced by nano-HAp, prevent lysosomal rupture, and reduce cell necrosis. High concentrations of Et Cit and Na Cit exhibited strong inhibitory effects. The inhibitory capacity of Na Cit was stronger than that of Et Cit at similar concentrations. Conclusion: Both Et Cit and Na Cit significantly reduced the cytotoxicity of nano-HAp on MOVASs and inhibited the apoptosis and necrosis induced by nano-HAp crystals. The chelating function of citrate resulted in both anticoagulation and binding to HAp. Et Cit and Na Cit may play a role as anticoagulants in reducing injury to the vascular wall caused by nano-HAp.
[Mh] MeSH terms primary: Citrates/pharmacology
Durapatite/adverse effects
Muscle, Smooth, Vascular/cytology
Nanoparticles/adverse effects
[Mh] MeSH terms secundary: Animals
Anticoagulants/pharmacology
Apoptosis/drug effects
Calcinosis/prevention & control
Calcium/metabolism
Cell Survival/drug effects
Cells, Cultured
Durapatite/chemistry
Membrane Potential, Mitochondrial/drug effects
Mice
Mitochondria/drug effects
Mitochondria/metabolism
Muscle, Smooth, Vascular/drug effects
Muscle, Smooth, Vascular/metabolism
Nanoparticles/chemistry
Reactive Oxygen Species/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anticoagulants); 0 (Citrates); 0 (Reactive Oxygen Species); 0 (diethyl citrate); 1Q73Q2JULR (sodium citrate); 91D9GV0Z28 (Durapatite); SY7Q814VUP (Calcium)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:171215
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S145386

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[PMID]: 29519942
[Au] Autor:Huang X; Yue Z; Wu J; Chen J; Wang S; Wu J; Ren L; Zhang A; Deng P; Wang K; Wu C; Ding X; Ye P; Xia J
[Ad] Address:From the Department of Cardiovascular Surgery, Union Hospital (X.H., Z.Y., J.C., J.W., P.D., K.W., C.W., X.D., J.X.), Department of Cardiovascular Medicine, Central Hospital of Wuhan (A.Z., P.Y.), Department of Cardiovascular Surgery, Central Hospital of Wuhan (J.X.), Key Laboratory for Molecular Di
[Ti] Title:MicroRNA-21 Knockout Exacerbates Angiotensin II-Induced Thoracic Aortic Aneurysm and Dissection in Mice With Abnormal Transforming Growth Factor-ß-SMAD3 Signaling.
[So] Source:Arterioscler Thromb Vasc Biol;, 2018 Mar 08.
[Is] ISSN:1524-4636
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Thoracic aortic aneurysm and dissection (TAAD) are severe vascular conditions. Dysfunctional transforming growth factor-ß (TGF-ß) signaling in vascular smooth muscle cells and elevated angiotensin II (AngII) levels are implicated in the development of TAAD. In this study, we investigated whether these 2 factors lead to TAAD in a mouse model and explored the possibility of using microRNA-21 ( ) for the treatment of TAAD. APPROACH AND RESULTS: TAAD was developed in heterozygous (S3 ) mice infused with AngII. We found that p-ERK- and p-JNK-associated was higher in TAAD lesions. We hypothesize that downregulation of mitigate TAAD formation. However, (S3 21 ) mice exhibited conspicuous TAAD formation after AngII infusion. The vascular wall was dilated, and aortic rupture occurred within 23 days during AngII infusion. We then examined canonical and noncanonical TGF-ß signaling and found that knockout in S3 mice increased SMAD7 and suppressed canonical TGF-ß signaling. Vascular smooth muscle cells lacking TGF-ß signals tended to switch from a contractile to a synthetic phenotype. The silencing of with lentivirus prevented AngII-induced TAAD formation in S3 21 mice. CONCLUSIONS: Our study demonstrated that knockout exacerbated AngII-induced TAAD formation in mice, which was associated with TGF-ß signaling dysfunction. Therapeutic strategies targeting TAAD should consider unexpected side effects associated with alterations in TGF-ß signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 29519940
[Au] Autor:Kusters PJH; Seijkens TTP; Beckers L; Lievens D; Winkels H; de Waard V; Duijvestijn A; Lindquist Liljeqvist M; Roy J; Daugherty A; Newby A; Gerdes N; Lutgens E
[Ad] Address:From the Department of Medical Biochemistry, Academic Medical Center, University of Amsterdam, The Netherlands (P.J.H.K., T.T.P.S., L.B., D.L., H.W., V.d.W., E.L.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians University, Munich, Germany (T.T.P.S., D.L., H.W., N.G., E.L.); Depa
[Ti] Title:CD40L Deficiency Protects Against Aneurysm Formation.
[So] Source:Arterioscler Thromb Vasc Biol;, 2018 Mar 08.
[Is] ISSN:1524-4636
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The mechanisms underlying formation of arterial aneurysms remain incompletely understood. Because inflammation is a common feature during the progressive degeneration of the aortic wall, we studied the role of the costimulatory molecule CD40L, a major driver of inflammation, in aneurysm formation. APPROACH AND RESULTS: Transcriptomics data obtained from human abdominal aortic aneurysms and normal aortas revealed increased abundance of both CD40L and CD40 in media of thrombus-free and thrombus-covered human abdominal aortic aneurysms samples. To further unravel the role of CD40L in aneurysm formation, apolipoprotein E-deficient ( ) and mice were infused with angiotensin II for 7 and 28 days. Only a minority of mice (33% and 17%) developed (dissecting) aneurysms compared with 75% and 67% of littermates after 7 and 28 days of infusion, respectively. Total vessel area of the aorta at the suprarenal level was 52% smaller in angiotensin II-infused mice compared with that in angiotensin II-infused mice. Chimeric mice repopulated with bone marrow afforded a similar protection against dissecting aneurysm formation. Moreover, lack of CD40L protected mice from fatal aneurysm rupture. T helper cell and macrophage accumulation in aneurysmal tissue was reduced in mice with a concomitant decrease in expression of proinflammatory chemo- and cytokines. In addition, aneurysms of mice displayed reduced abundance of matrix metalloproteinase-13 and an increase in tissue inhibitor of metalloproteinase-3 while activity of matrix metalloproteinase-2 and matrix metalloproteinase-9 was diminished. CONCLUSIONS: Deficiency of (hematopoietic) CD40L protects against dissecting aneurysm formation and reduces the incidence of fatal rupture. This is associated with a decreased accumulation and activation of inflammatory cells and a dampened protease activity in the arterial wall.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 29519688
[Au] Autor:Coscas R; Dupont S; Mussot S; Louedec L; Etienne H; Morvan M; Chiocchia G; Massy Z; Jacob MP; Michel JB
[Ad] Address:UMR 1148, Inserm Paris 7, Denis Diderot University, Xavier Bichat Hospital, Paris, France; UMR 1173, Inserm Paris 11, Faculty of Health Sciences Simone Veil, Versailles Saint-Quentin-en-Yvelines University, Paris-Saclay University, Montigny-le-Bretonneux, France; Department of Vascular Surgery, Ambr
[Ti] Title:Exploring antibody-dependent adaptive immunity against aortic extracellular matrix components in experimental aortic aneurysms.
[So] Source:J Vasc Surg;, 2018 Mar 05.
[Is] ISSN:1097-6809
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Recent evidence suggests that adaptive immunity develops during abdominal aortic aneurysm evolution. Uncertainties remain about the antigens implicated and their role in inducing rupture. Because antigens from the extracellular matrix (ECM) have been suspected, the aim of this experimental study was to characterize the role of adaptive immunity directed against antigens from the aortic ECM. METHODS: In a first step, an experimental model of abdominal aortic aneurysm rupture based on adaptive immunity against the ECM was developed and characterized. Forty 4-week-old male Lewis rats were divided into two groups. In the ECM group (n = 20), rats were presensitized against the guinea pig aortic ECM before implantation of a decellularized aortic xenograft (DAX). In the control group (n = 20), rats were not presensitized before DAX implantation. In each group, half the rats were sacrificed at day 3 to analyze early mechanisms involved after DAX implantation. In a second step, we aimed to assess which ECM component was most efficient in inducing rupture. For this purpose, the nonfibrillar and fibrillar ECM components were sequentially extracted from the guinea pig aortic wall. Forty Lewis rats were then divided into four groups. Each group was presensitized against one ECM component (structural glycoproteins and proteoglycans, collagen, elastin alone, and elastin-associated glycoproteins) before DAX implantation. Apart from those that experienced rupture, rats were sacrificed at day 21. Xenografts were harvested for histologic, immunofluorescence, and conditioned medium analyses. RESULTS: In total, early aortic rupture occurred in 80% of the ECM group vs 0% of the control group (P < .001). In the ECM group, major circumferential immunoglobulin deposits were observed in combination with the C3 complement fraction, without cell infiltration. Conditioned medium analysis revealed that matrix metalloproteinase 9 and myeloperoxidase levels and elastase activities were significantly increased in this group. Immunofluorescence analysis demonstrated that myeloperoxidase co-localized with tissue-free DNA and histone H4, highlighting local neutrophil activation and formation of neutrophil extracellular traps. Following differential presensitization, it appeared that rats presensitized against structural glycoproteins and proteoglycans were significantly more susceptible to rupture after DAX implantation. CONCLUSIONS: Stimulating adaptive immunity against the aortic ECM, especially structural glycoproteins and proteoglycans, triggers rupture after DAX implantation. Further studies are needed to assess the precise proteins involved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 29465630
[Au] Autor:Liungman K; Mani K; Wanhainen A; Bosaeus L; Lachat M
[Ti] Title:Safety and Functionality of a Guidewire Fixator: Clinical Investigation of a New Endovascular Tool.
[So] Source:Innovations (Phila);13(1):51-53, 2018 Jan/Feb.
[Is] ISSN:1559-0879
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: A new endovascular tool, the Liungman Guidewire Fixator, has been developed to simplify endovascular treatment in complex aortic aneurysms. The device has been extensively tested in bench models and animal trials. To verify the safety and functionality demonstrated in the porcine model, the device was tested in ten patients undergoing endovascular aortic repair (EVAR) or fenestrated endovascular aortic repair (f-EVAR) treatment for abdominal aortic aneurysm. METHODS: The Liungman Guidewire Fixator consists of a braided stent-like, cylindrical structure with conical ends and a central channel for a 0.035″ guidewire. When in use, it is slid along the guidewire and positioned in the target artery, where the Liungman Guidewire Fixator interacts with the arterial wall by anchoring the guidewire to the wall through a radial force. The Liungman Guidewire Fixator allows for uninterrupted blood flow passed the point of fixation. In this study, the Liungman Guidewire Fixator was tested in ten patients undergoing EVAR or f-EVAR treatment for abdominal aortic aneurysm. The device was deployed and retrieved crossover into the hypogastric artery, and the occurrence of thrombotic occlusion, arterial dissection, and vascular rupture or trauma was studied using angiography, as well as device ability to withstand guidewire tension. RESULTS: There were no instances of occlusion, dissection, or vascular trauma detected using angiography. In all cases, deployment and retrieval were successful, and the devices could withstand an applied tension of 3 N. In one instance, retrieval was challenging because of significant tortuosity, which was resolved by a coaxial catheterization. CONCLUSIONS: Deployment was uneventful in all ten patients. Retrieval according to the intended instruction for use was performed in nine of the patients. In one patient, a coaxial catheterization was necessary. All devices withstood a retention force of 3 N.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1097/IMI.0000000000000468

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[PMID]: 29515038
[Au] Autor:Cikach FS; Koch CD; Mead TJ; Galatioto J; Willard BB; Emerton KB; Eagleton MJ; Blackstone EH; Ramirez F; Roselli EE; Apte SS
[Ad] Address:Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio, USA.
[Ti] Title:Massive aggrecan and versican accumulation in thoracic aortic aneurysm and dissection.
[So] Source:JCI Insight;3(5), 2018 Mar 08.
[Is] ISSN:2379-3708
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Proteoglycan accumulation is a hallmark of medial degeneration in thoracic aortic aneurysm and dissection (TAAD). Here, we defined the aortic proteoglycanome using mass spectrometry, and based on the findings, investigated the large aggregating proteoglycans aggrecan and versican in human ascending TAAD and a mouse model of severe Marfan syndrome. The aortic proteoglycanome comprises 20 proteoglycans including aggrecan and versican. Antibodies against these proteoglycans intensely stained medial degeneration lesions in TAAD, contrasting with modest intralamellar staining in controls. Aggrecan, but not versican, was increased in longitudinal analysis of Fbn1mgR/mgR aortas. TAAD and Fbn1mgR/mgR aortas had increased aggrecan and versican mRNAs, and reduced expression of a key proteoglycanase gene, ADAMTS5, was seen in TAAD. Fbn1mgR/mgR mice with ascending aortic dissection and/or rupture had dramatically increased aggrecan staining compared with mice without these complications. Thus, aggrecan and versican accumulation in ascending TAAD occurs via increased synthesis and/or reduced proteolytic turnover, and correlates with aortic dissection/rupture in Fbn1mgR/mgR mice. Tissue swelling imposed by aggrecan and versican is proposed to be profoundly deleterious to aortic wall mechanics and smooth muscle cell homeostasis, predisposing to type-A dissections. These proteoglycans provide potential biomarkers for refined risk stratification and timing of elective aortic aneurysm repair.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher


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