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Sökning: WFRF:(Melki Vilyam)

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1.
  • Ebeling Barbier, Charlotte, et al. (författare)
  • Percutaneous Closure in Transfemoral Aortic Valve Implantation : A Single-Centre Experience
  • 2015
  • Ingår i: Cardiovascular and Interventional Radiology. - : Springer Science and Business Media LLC. - 0174-1551 .- 1432-086X. ; 38:6, s. 1438-1443
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: To report the experience of a percutaneous closure device used for transfemoral transcatheter aortic valve implantation (TAVI) in an unselected patient and operator population.MATERIALS AND METHODS: Eighty-two consecutive patients (32 women, 50 men) who underwent transfemoral TAVI between September 2009 and February 2014 at our hospital were retrospectively reviewed for percutaneous closure device (PCD) failure, vascular complications, and bleeding. The diameter and calcification of the common femoral artery (CFA) and the thickness of the subcutaneous fat layer in the groin were assessed on computed tomography images.RESULTS: The incidences of PCD failure and minor and major vascular complications were 19.5 % (n = 16/82), 19.5 % (n = 16/82), and 7 % (n = 6/82) respectively. 8.5 % (n = 7/82) had a minor perioperative bleeding, 6 % (n = 5/82) had a major bleeding, and none had any life-threatening bleeding. When PCD failed, haemostasis was obtained with fascia suturing, covered stent placement, or with surgical cutdown. Thirty-day mortality and 1-year all-cause mortality were 8.5 % (n = 7/82) and 19.5 % (n = 16/82), respectively. In a multiple regression analysis, the CFA diameter and the presence of severe calcification were independently related to PCD failure (correlation coefficient = -0.24, p = 0.027 and correlation coefficient = 0.23, p = 0.036, respectively).CONCLUSION: PCD failure was related to a small CFA diameter and to a severely calcified CFA. Failure could largely be managed with minimally invasive techniques such as covered stents or fascia suturing.
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3.
  • Melki, Vilyam, et al. (författare)
  • Effect of Glyceryl Trinitrate on Staphylococcus aureus Growth and Leukocyte Activation during Simulated Extracorporeal Circulation
  • 2014
  • Ingår i: The thoracic and cardiovascular surgeon. - : Georg Thieme Verlag KG. - 0171-6425 .- 1439-1902. ; 62:5, s. 402-408
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Previously, nitric oxide has been shown to possess antimicrobial effects. In this study, we aim to test the effect of glyceryl trinitrate (GTN) on Staphylococcus aureus growth during simulated extracorporeal circulation (SECC) and also to examine the effect of S. aureus, alone and in combination with GTN, on activation markers of the innate immune system during SECC. Methods In an in vitro system of SECC, we measured GTN-induced changes in markers of leukocyte activation in whole blood caused by S. aureus infestation, as well as the effect of GTN on S. aureus growth. Results GTN had no effect on S. aureus growth after 240 minutes SECC. Staphylococcus aureus reduced the expression of granulocyte Fc gamma-receptor CD32 but stimulated the expression of monocyte CD32. Staphylococcus aureus stimulated expression of some leukocyte adhesion key proteins, activation marker CD66b, lipopolysaccharide-receptor CD14, and C3b-receptor CD35. Staphylococcus aureus and GTN addition induced significant increases in monocyte CD63 (lysosomal granule protein) levels. Conclusion GTN does not affect S. aureus growth during SECC and has no effect on SECC-induced leukocyte activation.
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4.
  • Melki, Vilyam, 1972-, et al. (författare)
  • Effect of simulated extracorporeal circulation and glyceryl-tri-nitrate on leukocyte activation.
  • 2014
  • Ingår i: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1401-7431 .- 1651-2006. ; 48:1, s. 59-64
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives. During extracorporeal circulation (ECC), a mechanical pump and an oxygenator replace the functions of the heart and lungs. The aim of this study is to test the effect of the nitric oxide donor glyceryl-tri-nitrate on activation markers of the innate immune system during simulated ECC. Design. Whole blood concentrations of selected leukocyte adhesion molecules, complement system components and myeloperoxidase (MPO) were measured in an in vitro system of simulated ECC. Results. Simulated ECC stimulated the expression of monocyte LPS-receptor CD14 and C3b-receptor CD35. Glyceryl-tri-nitrate significantly reduced the expression of leukocyte Fcγ receptor CD32 over time, compared to control. Simulated ECC increased the concentrations of MPO, terminal complement complex, and complement component C3a. Addition of glyceryl-tri-nitrate did not significantly affect these changes. Conclusions. Simulated ECC induces the increased expression of some leukocyte markers. Glyceryl-tri-nitrate addition significantly reduces the expression of some leukocyte activation markers.
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5.
  • Melki, Vilyam, 1972-, et al. (författare)
  • Enhanced growth of Staphylococcus aureus after nitric oxide supplementation during simulated extracorporeal circulation
  • 2010
  • Ingår i: The thoracic and cardiovascular surgeon. - : Georg Thieme Verlag KG. - 0171-6425 .- 1439-1902. ; 58:2, s. 81-85
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Several factors contribute to postoperative bacterial infections in cardiac surgery. Long operation times and the use of extracorporeal circulation increase the risk of infection. Nitric oxide has been shown to possess a broad spectrum antimicrobial effect. Methods: In this study, we investigated the effect of nitric oxide on S. aureus growth in whole blood during simulated extracorporeal circulation. Results: S. aureus growth increased 6.2-fold after 180 min SECC in the presence of nitric oxide. Leukocyte counts remained unchanged without any differences between the groups. We observed a steady increase in markers of oxidative stress and activity of the innate immune system. Myeloperoxidase levels increased 8-fold, and C3a and terminal complement complex by 2-fold after 180 min. Conclusion: S. aureus growth is not due to the effect of nitric oxide on the innate immune system but from its effect on the bacteria itself. It has been shown that nitric oxide stimulates the expression of inducible lactate dehydrogenase, specific to S. aureus, which improves its resistance to oxidative stress, and may give S. aureus a survival advantage resulting in increased growth.
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6.
  • Melki, Vilyam, 1972- (författare)
  • Nitric oxide : An ally in extracorporeal circulation?
  • 2016
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Many complications associated with heart surgery are due to the negative effects of extracorporeal circulation (ECC). Some of these complications may be attributed to ECC-induced activation of inflammation and coagulation pathways. The inflammatory reaction may be caused by the interaction of blood components with air and the artificial surfaces of the ECC, from substances produced due to ischaemia-reperfusion injury of the heart and lungs, and from increased release of endotoxin from ischemic intestines. Staphylococcus aureus (S. aureus) infections are the leading cause of respiratory, skin and soft tissue, and bloodstream infections. Nitric oxide (NO) is a gaseous signaling molecule involved in many physiological and pathological processes. The role of NO in infection and inflammation is complex. NO may contribute to morbidity by acting as a vasodilator, myocardial depressant, and cytotoxic mediator. On the other hand, NO may have a salutary role through microvascular, cytoprotective, immunoregulatory, and antimicrobial properties. A simulated extracorporeal circulation (SECC) model is a closed circuit, including a roller pump, an oxygenator, a venous reservoir and polyvinyl chloride (PVC) tubing, where human blood is circulated. The SECC model allows studies of the blood and its components, without any influence from other organ systems. The aim of this work was to investigate NO effects during SECC and in S. aureus infection.Study I. Human blood was circulated through SECC during 3 hours, and leukocyte granule release was studied. Results indicated that NO addition during SECC is pro-inflammatory by stimulating leukocyte activation and granule release, and has no effect on oxygen free radical production and interleukin release.Study II. Investigating the effect of NO on S. aureus growth in whole blood during 180 min SECC, results showed a 6.2 fold growth in the presence of NO. Results indicated that by stimulating the expression of inducible lactate dehydrogenase, specific to S. aureus, NO may improve S. aureus resistance to oxidative stress, giving the pathogen a survival advantage.Study III. In an in vitro system of SECC, we measured glyceryl trinitrate (GTN) induced changes in leukocyte activation in whole blood caused by S. aureus infestation, as well as the effect of GTN on S. aureus growth. Results indicated that GTN does not affect S. aureus growth during SECC and has no effect on SECC-induced leukocyte activation.Study IV. Whole blood concentrations of selected leukocyte adhesion molecules, complement system components and myeloperoxidase  were measured in an in vitro system of SECC. Results indicated that SECC induces the increased expression of some leukocyte markers and that GTN addition significantly reduces the expression of some leukocyte activation markers.
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