References of "Sakalihasan, Natzi"
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See detailProgression of Abdominal Aortic Aneurysm Towards Rupture: Refining Clinical Risk Assessment Using a Fully Coupled Fluid-Structure Interaction Method.
Xenos, Michalis; Labropoulos, Nicos; Rambhia, Suraj et al

in Annals of Biomedical Engineering (2014)

Rupture of abdominal aortic aneurysm (AAA) is associated with high mortality rates. Risk of rupture is multi-factorial involving AAA geometric configuration, vessel tortuosity, and the presence of ... [more ▼]

Rupture of abdominal aortic aneurysm (AAA) is associated with high mortality rates. Risk of rupture is multi-factorial involving AAA geometric configuration, vessel tortuosity, and the presence of intraluminal pathology. Fluid structure interaction (FSI) simulations were conducted in patient based computed tomography scans reconstructed geometries in order to monitor aneurysmal disease progression from normal aortas to non-ruptured and contained ruptured AAA (rAAA), and the AAA risk of rupture was assessed. Three groups of 8 subjects each were studied: 8 normal and 16 pathological (8 non-ruptured and 8 rAAA). The AAA anatomical structures segmented included the blood lumen, intraluminal thrombus (ILT), vessel wall, and embedded calcifications. The vessel wall was described with anisotropic material model that was matched to experimental measurements of AAA tissue specimens. A statistical model for estimating the local wall strength distribution was employed to generate a map of a rupture potential index (RPI), representing the ratio between the local stress and local strength distribution. The FSI simulations followed a clear trend of increasing wall stresses from normal to pathological cases. The maximal stresses were observed in the areas where the ILT was not present, indicating a potential protective effect of the ILT. Statistically significant differences were observed between the peak systolic stress and the peak stress at the mean arterial pressure between the three groups. For the ruptured aneurysms, where the geometry of intact aneurysm was reconstructed, results of the FSI simulations clearly depicted maximum wall stress at the a priori known location of rupture. The RPI mapping indicated several distinct regions of high RPI coinciding with the actual location of rupture. The FSI methodology demonstrates that the aneurysmal disease can be described by numerical simulations, as indicated by a clear trend of increasing aortic wall stresses in the studied groups, (normal aortas, AAAs and rAAAs). Ultimately, the results demonstrate that FSI wall stress mapping and RPI can be used as a tool for predicting the potential rupture of an AAA by predicting the actual rupture location, complementing current clinical practice by offering a predictive diagnostic tool for deciding whether to intervene surgically or spare the patient from an unnecessary risky operation. [less ▲]

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See detailSurgical treatment of bicuspid aortic valve disease: Knowledge gaps and research perspectives.
Della Corte, Alessandro; Body, Simon C.; Booher, Anna M. et al

in Journal of Thoracic and Cardiovascular Surgery (2014)

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See detail18F-FDG Uptake Assessed by PET/CT in Abdominal Aortic Aneurysms Is Associated with Cellular and Molecular Alterations Prefacing Wall Deterioration and Rupture.
Courtois, Audrey ULiege; Nusgens, Betty ULiege; Hustinx, Roland ULiege et al

in Journal of Nuclear Medicine (2013), 54

Rupture of abdominal aortic aneurysms (AAAs) leads to a significant morbidity and mortality in aging populations, and its prediction would be most beneficial to public health. Spots of positive uptake of ... [more ▼]

Rupture of abdominal aortic aneurysms (AAAs) leads to a significant morbidity and mortality in aging populations, and its prediction would be most beneficial to public health. Spots of positive uptake of 18F-FDG detected by PET are found in 12% of AAA patients (PET+), who are most often symptomatic and at high rupture risk. Comparing the 18F-FDG-positive site with a negative site from the same aneurysm and with samples collected from AAA patients with no 18F-FDG uptake should allow the discrimination of biologic alterations that would help in identifying markers predictive of rupture. METHODS: Biopsies of the AAA wall were obtained from patients with no 18F-FDG uptake (PET0, n = 10) and from PET+ patients (n = 8), both at the site of positive uptake and at a distant negative site of the aneurysmal wall. Samples were analyzed by immunohistochemistry, quantitative real-time polymerase chain reaction, and zymography. RESULTS: The sites of the aneurysmal wall with a positive 18F-FDG uptake were characterized by a strikingly increased number of adventitial inflammatory cells, highly proliferative, and by a drastic reduction of smooth muscle cells (SMCs) in the media as compared with their negative counterpart and with the PET0 wall. The expression of a series of genes involved in the maintenance and remodeling of the wall was significantly modified in the negative sites of PET+, compared with the PET0 wall, suggesting a systemic alteration of the aneurysmal wall. Furthermore, a striking increase of several matrix metalloproteinases (MMPs), notably the MMP1 and MMP13 collagenases, was observed in the positive sites, mainly in the adventitia. Moreover, PET+ patients were characterized by a higher circulating C-reactive protein. CONCLUSION: Positive 18F-FDG uptake in the aneurysmal wall is associated with an active inflammatory process characterized by a dense infiltrate of proliferating leukocytes in the adventitia and an increased circulating C-reactive protein. Moreover, a loss of SMC in the media and alterations of the expression of genes involved in the remodeling of adventitia and collagen degradation potentially participate in the weakening of the aneurysmal wall preceding rupture. [less ▲]

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See detailNew Insights Into Aortic Diseases A Report From the Third International Meeting on Aortic Diseases (IMAD3)
KUIVANIEMI, Helena; Sakalihasan, Natzi ULiege; LEDERLE, Franck et al

in Aorta (2013), 1

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See detailMultidimensional growth measurements of abdominal aortic aneurysms.
Martufi, Giampaolo; Auer, Martin; Roy, Joy et al

in Journal of Vascular Surgery (2013), 58(3), 748-55

BACKGROUND: Monitoring the expansion of abdominal aortic aneurysms (AAAs) is critical to avoid aneurysm rupture in surveillance programs, for instance. However, measuring the change of the maximum ... [more ▼]

BACKGROUND: Monitoring the expansion of abdominal aortic aneurysms (AAAs) is critical to avoid aneurysm rupture in surveillance programs, for instance. However, measuring the change of the maximum diameter over time can only provide limited information about AAA expansion. Specifically, regions of fast diameter growth may be missed, axial growth cannot be quantified, and shape changes of potential interest for decisions related to endovascular aneurysm repair cannot be captured. METHODS: This study used multiple centerline-based diameter measurements between the renal arteries and the aortic bifurcation to quantify AAA growth in 51 patients from computed tomography angiography (CTA) data. Criteria for inclusion were at least 1 year of patient follow-up and the availability of at least two sufficiently high-resolution CTA scans that allowed an accurate three-dimensional reconstruction. Consequently, 124 CTA scans were systematically analyzed by using A4clinics diagnostic software (VASCOPS GmbH, Graz, Austria), and aneurysm growth was monitored at 100 cross-sections perpendicular to the centerline. RESULTS: Monitoring diameter development over the entire aneurysm revealed the sites of the fastest diameter growth, quantified the axial growth, and showed the evolution of the neck morphology over time. Monitoring the development of an aneurysm's maximum diameter or its volume over time can assess the mean diameter growth (r = 0.69, r = 0.77) but not the maximum diameter growth (r = 0.43, r = 0.34). The diameter growth measured at the site of maximum expansion was ~16%/y, almost four times larger than the mean diameter expansion of 4.4%/y. The sites at which the maximum diameter growth was recorded did not coincide with the position of the maximum baseline diameter (rho = 0 .12; P = .31). The overall aneurysm sac length increased from 84 to 89 mm during the follow-up (P < .001), which relates to the median longitudinal growth of 3.5%/y. The neck length shortened, on average, by 6.2% per year and was accompanied by a slight increase in neck angulation. CONCLUSIONS: Neither maximum diameter nor volume measurements over time are able to measure the fastest diameter growth of the aneurysm sac. Consequently, expansion-related wall weakening might be inappropriately reflected by this type of surveillance data. In contrast, localized spots of fast diameter growth can be detected through multiple centerline-based diameter measurements over the entire aneurysm sac. This information might further reinforce the quality of aneurysm surveillance programs. [less ▲]

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See detailBiomechanical Rupture Risk Assessment in Patients with Abdominal Aortic Aneurysms: Introducing Rupture Risk Equivalent Diameter.
Roy, J; Swedenborg, J; Sakalihasan, Natzi ULiege et al

in Arteriosclerosis, Thrombosis and Vascular Biology (2012), 32(A103),

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See detailTraitement endovasculaire des dissections de l'aorte descendante (type B).
BRULS, Samuel ULiege; VAN DAMME, Hendrik ULiege; SakalihasanN, Natzi ULiege et al

in Revue Médicale de Liège (2012), 67(9), 468-74

Aortic dissection is one of the most serious aortic diseases by its potential for rupture, but also for other complications, such as cerebral or splanchnic ischemia, which may be fatal. If open surgery is ... [more ▼]

Aortic dissection is one of the most serious aortic diseases by its potential for rupture, but also for other complications, such as cerebral or splanchnic ischemia, which may be fatal. If open surgery is the rule for lesions of the ascending aorta (type A), type B (not concerning the ascending aorta) is first a matter of medical treatment except when complications are present. In this case the placement of a stentgraft is a valuable alternative to open surgery. We report a patient presenting with a type B aortic dissection, characterized by rapid expansion and complicated by peri-aortic leakage, who was successfully treated by thoracic aortic stentgraft placement. This was done in a hybrid operating room associating the characteristics of a classical operating room for cardio-vascular surgery with those of an interventional radiology suite. [less ▲]

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See detailOn the potential increase of the oxidative stress status in patients with abdominal aortic aneurysm.
PINCEMAIL, Joël ULiege; Defraigne, Jean-Olivier ULiege; Cheramy-Bien, J. P. et al

in Redox Report: Communications in Free Radical Research (2012), 17(4), 139-44

BACKGROUND: Abdominal aortic aneurysm (AAA) is a major cause of preventable deaths in older patients. Oxidative stress has been suggested to play a key role in the pathogenesis of AAA. However, only few ... [more ▼]

BACKGROUND: Abdominal aortic aneurysm (AAA) is a major cause of preventable deaths in older patients. Oxidative stress has been suggested to play a key role in the pathogenesis of AAA. However, only few studies have been conducted to evaluate the blood oxidative stress status of AAA patients. METHODS AND RESULTS: Twenty seven AAA patients (mean age of 70 years) divided into two groups according to AAA size (</= 50 or > 50 mm) were compared with an age-matched group of 18 healthy subjects. Antioxidants (vitamins C and E, beta-carotene, glutathione, thiols, and ubiquinone), trace elements (selenium, copper, zinc, and copper/zinc ratio) and markers of oxidative damage to lipids (lipid peroxides, antibodies against oxidized patients, and isoprostanes) were measured in each subject. The comparison of the three groups by ordinal logistic regression showed a significant decrease of the plasma levels of vitamin C (P = 0.011), alpha-tocopherol (P = 0.016) but not when corrected for cholesterol values, beta-carotene (P = 0.0096), ubiquinone (P = 0.014), zinc (P = 0.0035), and of selenium (P = 0.0038), as AAA size increased. By contrast, specific markers of lipid peroxidation such as the Cu/Zn ratio (P = 0.046) and to a lesser extent isoprostanes (P = 0.052) increased. CONCLUSION: The present study emphasizes the potential role of the oxidative stress in AAA disease and suggests that an antioxidant therapy could be of interest to delay AAA progression. [less ▲]

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See detailApolipoprotein(a) genetic sequence variants associated with systemic atherosclerosis and coronary atherosclerotic burden but not with venous thromboembolism.
Helgadottir, Anna; Gretarsdottir, Solveig; Thorleifsson, Gudmar et al

in Journal of the American College of Cardiology (2012), 60(8), 722-9

OBJECTIVES: The purpose of this study is investigate the effects of variants in the apolipoprotein(a) gene (LPA) on vascular diseases with different atherosclerotic and thrombotic components. BACKGROUND ... [more ▼]

OBJECTIVES: The purpose of this study is investigate the effects of variants in the apolipoprotein(a) gene (LPA) on vascular diseases with different atherosclerotic and thrombotic components. BACKGROUND: It is unclear whether the LPA variants rs10455872 and rs3798220, which correlate with lipoprotein(a) levels and coronary artery disease (CAD), confer susceptibility predominantly via atherosclerosis or thrombosis. METHODS: The 2 LPA variants were combined and examined as LPA scores for the association with ischemic stroke (and TOAST [Trial of Org 10172 in Acute Stroke Treatment] subtypes) (effective sample size [n(e)] = 9,396); peripheral arterial disease (n(e) = 5,215); abdominal aortic aneurysm (n(e) = 4,572); venous thromboembolism (n(e) = 4,607); intracranial aneurysm (n(e) = 1,328); CAD (n(e) = 12,716), carotid intima-media thickness (n = 3,714), and angiographic CAD severity (n = 5,588). RESULTS: LPA score was associated with ischemic stroke subtype large artery atherosclerosis (odds ratio [OR]: 1.27; p = 6.7 x 10(-4)), peripheral artery disease (OR: 1.47; p = 2.9 x 10(-14)), and abdominal aortic aneurysm (OR: 1.23; p = 6.0 x 10(-5)), but not with the ischemic stroke subtypes cardioembolism (OR: 1.03; p = 0.69) or small vessel disease (OR: 1.06; p = 0.52). Although the LPA variants were not associated with carotid intima-media thickness, they were associated with the number of obstructed coronary vessels (p = 4.8 x 10(-12)). Furthermore, CAD cases carrying LPA risk variants had increased susceptibility to atherosclerotic manifestations outside of the coronary tree (OR: 1.26; p = 0.0010) and had earlier onset of CAD (-1.58 years/allele; p = 8.2 x 10(-8)) than CAD cases not carrying the risk variants. There was no association of LPA score with venous thromboembolism (OR: 0.97; p = 0.63) or intracranial aneurysm (OR: 0.85; p = 0.15). CONCLUSIONS: LPA sequence variants were associated with atherosclerotic burden, but not with primarily thrombotic phenotypes. [less ▲]

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See detailIncreased oxidative stress status is associated with abdominal aortic aneurysm
PINCEMAIL, Joël ULiege; Defraigne, Jean-Olivier ULiege; Albert, Adelin ULiege et al

in University of Ferrara (Ed.) Second Internaional conference on environmental stressors in biology and medicine (2011, October)

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See detailBM-573 INHIBITS THE EARLY ATHEROSCLEROTIC LESIONS IN APO-E DEFICIENT MICE BY BLOCKING TP RECEPTORS AND THROMBOXANE SYNTHASE
Cherdon, Céline ULiege; Rolin, Stéphanie; Hanson, Julien ULiege et al

in Congress of the International Society of Thrombosis and Hemostasis- 57th Annual SSC Meeting (2011, July)

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently ... [more ▼]

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently received a lot of attention. This study aimed to investigate the effect of a dual thromboxane synthase inhibitor and thromboxane receptor antagonist (BM-573) and ASA on lesion formation in apolipoprotein E-deficient mice. The combination of ASA and BM-573 was also studied. Plasma measurements demonstrated that the treatments did not affect body weight or plasma cholesterol levels. BM-573, but not ASA, significantly decreased atherogenic lesions as demonstrated by macroscopic analysis. Both treatments alone inhibited TXB(2) synthesis but only BM-573 and the combination therapy were able to decrease firstly, plasma levels of soluble intracellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) and secondly, the expression of these proteins in the aortic root of Apo E. These results were confirmed in endothelial cell cultures derived from human saphenous vein endothelial cells (HSVECs). In these cells, BM-573 also prevented the increased mRNA expression of ICAM-1 and VCAM-1 induced by U-46619 and 8-iso-PGF(2(). Our results show that a molecule combining receptor antagonism and thromboxane synthase inhibition is more efficient in delaying atherosclerosis in Apo E(-/-) mice than sole inhibition of TXA(2) formation. [less ▲]

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See detailBM-573 inhibits the development of early atherosclerotic lesions in Apo E deficient mice by blocking TP receptors and thromboxane synthase.
Cherdon, Céline ULiege; Rolin, Stephanie; Hanson, Julien ULiege et al

in Prostaglandins and Other Lipid Mediators (2011)

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently ... [more ▼]

Atherosclerosis is the principal cause of mortality in industrialized countries. Its development is influenced by several mediators of which thromboxane A(2) (TXA(2)) and 8-iso-PGF(2() have recently received a lot of attention. This study aimed to investigate the effect of a dual thromboxane synthase inhibitor and thromboxane receptor antagonist (BM-573) and ASA on lesion formation in apolipoprotein E-deficient mice. The combination of ASA and BM-573 was also studied. Plasma measurements demonstrated that the treatments did not affect body weight or plasma cholesterol levels. BM-573, but not ASA, significantly decreased atherogenic lesions as demonstrated by macroscopic analysis. Both treatments alone inhibited TXB(2) synthesis but only BM-573 and the combination therapy were able to decrease firstly, plasma levels of soluble intracellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) and secondly, the expression of these proteins in the aortic root of Apo E. These results were confirmed in endothelial cell cultures derived from human saphenous vein endothelial cells (HSVECs). In these cells, BM-573 also prevented the increased mRNA expression of ICAM-1 and VCAM-1 induced by U-46619 and 8-iso-PGF(2(). Our results show that a molecule combining receptor antagonism and thromboxane synthase inhibition is more efficient in delaying atherosclerosis in Apo E(-/-) mice than sole inhibition of TXA(2) formation. [less ▲]

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See detailAneurysm : epidemiology, aetiology and pathology.
Sakalihasan, Natzi ULiege; KUIVANIEMI, HELENA; Nusgens, Betty ULiege et al

Book published by SPRINGER (2011)

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See detailAnalysis of positional candidate genes in the AAA1 susceptibility locus for abdominal aortic aneurysms on chromosome 19.
Lillvis, J. H.; Kyo, Y.; Tromp, G. et al

in BMC Medical Genetics (2011), 12(1), 14

ABSTRACT: BACKGROUND: Abdominal aortic aneurysm (AAA) is a complex disorder with multiple genetic risk factors. Using affected relative pair linkage analysis, we previously identified an AAA ... [more ▼]

ABSTRACT: BACKGROUND: Abdominal aortic aneurysm (AAA) is a complex disorder with multiple genetic risk factors. Using affected relative pair linkage analysis, we previously identified an AAA susceptibility locus on chromosome 19q13. This locus has been designated as the AAA1 susceptibility locus in the Online Mendelian Inheritance in Man (OMIM) database. METHODS: Nine candidate genes were selected from the AAA1 locus based on their function, as well as mRNA expression levels in the aorta. A sample of 394 cases and 419 controls was genotyped for 41 SNPs located in or around the selected nine candidate genes using the Illumina GoldenGate platform. Single marker and haplotype analyses were performed. Three genes (CEBPG, PEPD and CD22) were selected for DNA sequencing based on the association study results, and exonic regions were analyzed. Immunohistochemical staining of aortic tissue sections from AAA and control individuals was carried out for the CD22 and PEPD proteins with specific antibodies. RESULTS: Several SNPs were nominally associated with AAA (p < 0.05). The SNPs with most significant p-values were located near the CCAAT enhancer binding protein (CEBPG), peptidase D (PEPD), and CD22. Haplotype analysis found a nominally associated 5-SNP haplotype in the CEBPG/PEPD locus, as well as a nominally associated 2-SNP haplotype in the CD22 locus. DNA sequencing of the coding regions revealed no variation in CEBPG. Seven sequence variants were identified in PEPD, including three not present in the NCBI SNP (dbSNP) database. Sequencing of all 14 exons of CD22 identified 20 sequence variants, five of which were in the coding region and six were in the 3'-untranslated region. Five variants were not present in dbSNP. Immunohistochemical staining for CD22 revealed protein expression in lymphocytes present in the aneurysmal aortic wall only and no detectable expression in control aorta. PEPD protein was expressed in fibroblasts and myofibroblasts in the media-adventitia border in both aneurysmal and non-aneurysmal tissue samples. CONCLUSIONS: Association testing of the functional positional candidate genes on the AAA1 locus on chromosome 19q13 demonstrated nominal association in three genes. PEPD and CD22 were considered the most promising candidate genes for altering AAA risk, based on gene function, association evidence, gene expression, and protein expression. [less ▲]

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See detailNovel aspects of the pathogenesis of aneurysms of the abdominal aorta in humans.
Michel, Jérôme ULiege; Martin-Ventura, J. L.; Egido, J. et al

in Cardiovascular Research (2011)

Aneurysm of the abdominal aorta (AAA) is a particular, specifically localized form of atherothrombosis, providing a unique human model of this disease. The pathogenesis of AAA is characterized by a ... [more ▼]

Aneurysm of the abdominal aorta (AAA) is a particular, specifically localized form of atherothrombosis, providing a unique human model of this disease. The pathogenesis of AAA is characterized by a breakdown of the extracellular matrix due to an excessive proteolytic activity, leading to potential arterial wall rupture. The roles of matrix metalloproteinases and plasmin generation in progression of AAA have been demonstrated both in animal models and in clinical studies. In the present review, we highlight recent studies addressing the role of the haemoglobin-rich, intraluminal thrombus and the adventitial response in the development of human AAA. The intraluminal thrombus exerts its pathogenic effect through platelet activation, fibrin formation, binding of plasminogen and its activators, and trapping of erythrocytes and neutrophils, leading to oxidative and proteolytic injury of the arterial wall. These events occur mainly at the intraluminal thrombus-circulating blood interface, and pathological mediators are conveyed outwards, where they promote matrix degradation of the arterial wall. In response, neo-angiogenesis, phagocytosis by mononuclear cells, and a shift from innate to adaptive immunity in the adventitia are observed. Abdominal aortic aneurysm thus represents an accessible spatiotemporal model of human atherothrombotic progression towards clinical events, the study of which should allow further understanding of its pathogenesis and the translation of pathogenic biological activities into diagnostic and therapeutic applications. [less ▲]

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