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323 results on '"Stangl, V."'

2. Patient-reported functional and symptomatic outcomes in patients with mild cognitive disorder undergoing transcatheter aortic valve implantation - A secondary analysis of a randomized controlled trial

Author

Thevathasan, T, primary, Hornig, C, additional, Leistner, D M, additional, Suendermann, S, additional, Unbehaun, A, additional, Sherif, M, additional, Haghikia, A, additional, Stangl, K, additional, Falk, V, additional, Landmesser, U, additional, Dreger, H, additional, Stangl, V, additional, and Brand, A, additional

Published
2023
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3. Macrophage uptake switches on OCT contrast of superparamagnetic nanoparticles for imaging of atherosclerotic plaques

Author

Ariza de Schellenberger A, Poller WC, Stangl V, Landmesser U, and Schellenberger E

Subjects
Atherosclerotic plaques, macrophages, ferumoxytol, superparamagnetic iron oxide particles, Optical coherence tomography, Magnetic resonance imaging, Medicine (General), R5-920
Abstract

Angela Ariza de Schellenberger,1,* Wolfram C Poller,2,* Verena Stangl,2 Ulf Landmesser,3 Eyk Schellenberger1 1Department of Radiology, Charité-Universitätsmedizin Berlin, Germany; 2Department of Interventional Cardiology, Charité-Universitätsmedizin Berlin, Germany; 3Department of Cardiology, Charité- Universitätsmedizin Berlin, Berlin Institute of Health (BIH) and Deutsches Zentrum für Herz-Kreislaufforschung (DZHK), Berlin, Germany *These authors contributed equally to this work Background: Optical coherence tomography (OCT) is an intravascular, high-resolution imaging technique that is used to characterize atherosclerotic plaques. However, the identification of macrophages as important markers of inflammation and plaque vulnerability remains difficult. Here, we investigate whether the uptake of very small iron oxide particles (VSOP) in macrophages, that cluster in phagolysosomes and allow high-quality magnetic resonance imaging (MRI) of atherosclerotic plaques, and uptake of ferumoxytol nanoparticles enhance detection of macrophages by OCT.Materials and methods: RAW 264.7 macrophage cells were incubated with VSOP (1 and 2 mM Fe) that have been clinically tested and ferumoxytol (8.9 mM Fe) that is approved for iron deficiency treatment and currently investigated as an MRI contrast agent. The light scattering of control macrophages, nanoparticle-labeled macrophages (2,000,000 in 500 µL) and nanoparticle suspensions was measured in synchronous wavelength scan mode using a fluorescence spectrophotometer. For OCT analyses, pellets of 8,000,000 non-labeled, VSOP-labeled and ferumoxytol-labeled RAW 264.7 macrophages were imaged and analyzed on an OPTIS™ OCT imaging system.Results: Incubation with 1 and 2 mM VSOP resulted in uptake of 7.1±1.5 and 12±1.5 pg Fe per cell, which increased the backscattering of the macrophages in spectrophotometry 2.5- and 3.6-fold, whereas incubation with 8.9 mM Fe ferumoxytol resulted in uptake of 6.6±2 pg Fe per cell, which increased the backscattering 1.5-fold at 700 nm. In contrast, backscattering of non-clustered nanoparticles in suspension was negligible. Accordingly, OCT imaging could visualize significantly increased backscattering and signal attenuation of nanoparticle-labeled macrophages in comparison with controls.Conclusion: We conclude that VSOP and, to a lesser extent, ferumoxytol increase light scattering and attenuation when taken up by macrophages and can serve as a multimodal imaging probe for MRI and OCT to improve macrophage detection in atherosclerotic plaques by OCT in the future. Keywords: intravascular, inflammation, vulnerability, multimodal imaging, optical coherence tomography, magnetic resonance imaging

Published
2018

4. Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.

Author

Hardy, SA, Liesinger, L, Patrick, R, Poettler, M, Rech, L, Gindlhuber, J, Mabotuwana, NS, Ashour, D, Stangl, V, Bigland, M, Murtha, LA, Starkey, MR, Scherr, D, Hansbro, PM, Hoefler, G, Campos Ramos, G, Cochain, C, Harvey, RP, Birner-Gruenberger, R, Boyle, AJ, Rainer, PP, Hardy, SA, Liesinger, L, Patrick, R, Poettler, M, Rech, L, Gindlhuber, J, Mabotuwana, NS, Ashour, D, Stangl, V, Bigland, M, Murtha, LA, Starkey, MR, Scherr, D, Hansbro, PM, Hoefler, G, Campos Ramos, G, Cochain, C, Harvey, RP, Birner-Gruenberger, R, Boyle, AJ, and Rainer, PP

Abstract

Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk.

Published
2023

5. G(q)-mediated arrhythmogenic signaling promotes atrial fibrillation

Author

Hohendanner, F., Prabhu, A., Wilck, N., Stangl, V., Pieske, B., Stangl, K., and Althoff, T.F.

Subjects
Cardiovascular and Metabolic Diseases
Abstract

BACKGROUND: Atrial fibrillation (AF) is promoted by various stimuli like angiotensin II, endothelin-1, epinephrine/norepinephrine, vagal activation, or mechanical stress, all of which activate receptors coupled to G-proteins of the Ga(q)/Ga(11)-family (G(q)). Besides pro-fibrotic and pro-inflammatory effects, G(q)-mediated signaling induces inositol trisphosphate receptor (IP(3)R)-mediated intracellular Ca(2+) mobilization related to delayed after-depolarisations and AF. However, direct evidence of arrhythmogenic G(q)-mediated signaling is absent. METHODS AND RESULTS: To define the role of G(q) in AF, transgenic mice with tamoxifen-inducible, cardiomyocyte-specific Ga(q)/Ga(11)-deficiency (G(q)-KO) were created and exposed to intracardiac electrophysiological studies. Baseline electrophysiological properties, including heart rate, sinus node recovery time, and atrial as well as AV nodal effective refractory periods, were comparable in G(q)-KO and control mice. However, inducibility and mean duration of AF episodes were significantly reduced in G(q)-KO mice-both before and after vagal stimulation. To explore underlying mechanisms, left atrial cardiomyocytes were isolated from G(q)-KO and control mice and electrically stimulated to study Ca(2+)-mobilization during excitation-contraction coupling using confocal microscopy. Spontaneous arrhythmogenic Ca(2+) waves and sarcoplasmic reticulum content-corrected Ca(2+) sparks were less frequent in G(q)-KO mice. Interestingly, nuclear but not cytosolic Ca(2+) transient amplitudes were significantly decreased in G(q)-KO mice. CONCLUSION: G(q)-signaling promotes arrhythmogenic atrial Ca(2+)-release and AF in mice. Targeting this pathway, ideally using G(q)-selective, biased receptor ligands, may be a promising approach for the treatment and prevention of AF. Importantly, the atrial-specific expression of the G(q)-effector IP(3)R confers atrial selectivity mitigating the risk of life-threatening ventricular pro-arrhythmic effects.

Published
2023

9. Contrast-enhanced MR imaging of atherosclerosis using citrate-coated superparamagnetic iron oxide nanoparticles: calcifying microvesicles as imaging target for plaque characterization

Author

Wagner S, Schnorr J, Ludwig A, Stangl V, Ebert M, Hamm B, and Taupitz M

Subjects
Medicine (General), R5-920
Abstract

Susanne Wagner,1 Jörg Schnorr,1 Antje Ludwig,2 Verena Stangl,2 Monika Ebert,1 Bernd Hamm,1 Matthias Taupitz11Department of Radiology, Section of Experimental Radiology, Charité – Universitätsmedizin Berlin, Campus Charité Mitte, and Campus Benjamin Franklin, Berlin, Germany; 2Department of Cardiology, Section of Experimental Cardiology, Charité – Universitätsmedizin Berlin, Campus Charité Mitte, Berlin, GermanyObjective: To evaluate the suitability of citrate-coated very small superparamagnetic iron oxide particles (VSOP) as a contrast agent for identifying inflammation in atherosclerotic lesions using magnetic resonance imaging (MRI).Methods and results: VSOP, which have already been evaluated as a blood pool contrast agent for MR angiography in human clinical trials, were investigated in Watanabe heritable hyperlipidemic rabbits to determine to what extent their accumulation in atherosclerotic lesions is a function of macrophage density and other characteristics of progressive atherosclerotic plaques. In advanced atherosclerotic lesions, a significant MRI signal loss was found within 1 hour after intravenous administration of VSOP at the intended clinical dose of 0.05 mmol Fe/kg. Histological examinations confirmed correlations between the loss of MRI signal in the vessel wall and the presence of Prussian blue-stained iron colocalized with macrophages in the plaque cap, but surprisingly also with calcifying microvesicles at the intimomedial interface. Critical electrolyte magnesium chloride concentration in combination with Alcian blue stain indicates that highly sulfated glycosaminoglycans are a major constituent of these calcifying microvesicles, which may serve as the key molecules for binding VSOP due to their highly complexing properties.Conclusion: Calcifying microvesicles and macrophages are the targets for intravenously injected VSOP in atherosclerotic plaques, suggesting that VSOP-enhanced MRI may render clinically relevant information on the composition and inflammatory activity of progressive atherosclerotic lesions at risk of destabilization.Keywords: atherosclerosis, inflammation, magnetic resonance imaging, iron oxide nanoparticles, glycosaminoglycans, calcifying microvesicles

Published
2013

13. Extracellular Matrix Protein 1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction

Author

Hardy, S, Patrick, R, Liesinger, L, Pöttler, M, Rech, L, Gindlhuber, J, Mabotuwana, N, Ashour, D, Stangl, V, Bigland, M, Murtha, L, Starkey, M, Scherr, D, Hansbro, P, Höfler, G, Ramos, G, and Cochain, C

Subjects
Cardiovascular System & Hematology, 1102 Cardiorespiratory Medicine and Haematology, 1117 Public Health and Health Services
Abstract

Background Fibrosis is a hallmark of heart disease, particularly following myocardial infarction (MI) and in heart failure. We previously identified a key role for extracellular matrix protein (ECM1) in wound healing post-MI but the cellular origin and mechanism of ECM1 remained elusive. Here, we investigate the spatiotemporal cellular origin of ECM1 in healthy and diseased human and mouse hearts, and ECM1 dependent human cardiac fibroblast (HuCFb) signalling mechanisms. Methods ECM1 specific analysis of existing single-cell/-nuclei RNA sequencing data was conducted. ECM1 expression was assessed in non-failing (NF), ischaemic (ICM) and dilated (DCM) failing human heart tissue via immunoblotting (n=8), immunohistochemistry (ICM; n=8, NF; n=4) and mRNA in-situ hybridisation (n=3). HuCFbs were treated with recombinant ECM1 and assessed via phosphoproteomics (n=6), wound healing assay (n=4), MTT assay (n=8), qPCR (n=6). Results ECM1 originates from fibroblasts, macrophages/monocytes (MΦ/Mo), and pericytes/vascular cells in uninjured human and mouse hearts. In mouse hearts post-MI, ECM1 originates predominantly from M1MΦ/Mo at day-3, and myofibroblasts and M2MΦ’s at day-7, and expression correlated with cell-cell communication, collagen organisation, inflammation, adhesion, and migration. Fittingly, ECM1 expression was upregulated in human ICM (p=0.048) and DCM (p=0.027), localised interstitially to fibrotic, inflammatory, and peri-vascular areas. In vitro, ECM1 inhibited HuCFb migration (p=0.044) and CCL2 mRNA expression, and stimulated inflammatory (IL-6, IL-1β), fibrotic (TGF-β1, Col1a2), and non-canonical Wnt5a mRNA expression (p

Published
2022

16. Extracellular Matrix Protein 1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction

Author

Hardy, S., primary, Patrick, R., additional, Liesinger, L., additional, Pöttler, M., additional, Rech, L., additional, Gindlhuber, J., additional, Mabotuwana, N., additional, Ashour, D., additional, Stangl, V., additional, Bigland, M., additional, Murtha, L., additional, Starkey, M., additional, Scherr, D., additional, Hansbro, P., additional, Höfler, G., additional, Ramos, G., additional, Cochain, C., additional, Harvey, R., additional, Birner-Gruenberger, R., additional, Boyle, A., additional, and Rainer, P., additional

Published
2022
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27. Randomized clinical trial comparing a rivaroxaban-based with an antiplatelet-based strategy for cerebral embolization after TAVR (EARTH TAVR)-a magnetic resonance imaging substudy of the GALILEO trial

Author

Froehlich, G.M, primary, Falk, V, additional, Endres, M, additional, Stangl, V, additional, Woehrle, J, additional, Steinbeck, L, additional, Erbay, A, additional, Rudolph, T, additional, Geisler, T, additional, Leistner, D, additional, Nolte, C, additional, Hausler, G, additional, Fiebach, J, additional, Dangas, G, additional, and Landmesser, U, additional

Published
2020
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36. P727Metabolic and functional differences between male and female endothelial cells from umbilical cords (HUVEC) of twin pairs

Author

Lorenz, M, primary, Blaschke, B, additional, Benn, A, additional, Hammer, E, additional, Witt, E, additional, Kirwan, J, additional, Fritsche-Guenther, R, additional, Gloaguen, Y, additional, Kramer, F, additional, Kappert, K, additional, Brunner, P, additional, Dreger, H, additional, Stangl, K, additional, Knaus, P, additional, and Stangl, V, additional

Published
2019
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39. Right heart function in impaired left ventricular diastolic function: 2D speckle tracking echocardiography-based and Doppler tissue imaging-based analysis of right atrial and ventricular function

Author

Brand, A., Bathe, M., Oertelt-Prigione, S., Seeland, U., Rucke, M., Regitz-Zagrosek, V., Stangl, K., Knebel, F., Stangl, V., Dreger, H., Brand, A., Bathe, M., Oertelt-Prigione, S., Seeland, U., Rucke, M., Regitz-Zagrosek, V., Stangl, K., Knebel, F., Stangl, V., and Dreger, H.

Abstract

Item does not contain fulltext, AIM: The aim of our study was to describe right atrial (RA) and right ventricular (RV) function, assessed by Doppler tissue imaging and 2D speckle tracking echocardiography (2DSTE), in women with signs of early impaired left ventricular diastolic function (DD). METHODS AND RESULTS: In a cross-sectional trial, standard parameters of diastolic and right heart function were investigated in 438 women of the Berlin Female Risk Evaluation (BEFRI) study. In a subset of women, average peak systolic RA strain (RAS), as well as the average peak systolic RV strain of the free wall (RVS free wall) and of all RV segments (average RV strain; RVS Avg), was analyzed using 2DSTE. Compared to women with normal diastolic function (DD0), RAS, RVS free wall and RVS Avg were significantly reduced in DD (43.1% +/- 11.9%, -26.7% +/- 5.6%, and -23.3% +/- 3.5% in DD0; vs 35.1% +/- 10.4%, -23.9% +/- 5.5%, and -20.6% +/- 3.8% in DD; P < .01). Peak RV myocardial velocity (RV-IVV) and acceleration during isovolumetric contraction (RV-IVA) were markedly higher in DD (15.0 +/- 3.9 cm/s and 3.1 +/- 1.0 m/s(2) in DD vs 11.9 +/- 3.2 cm/s and 2.8 +/- 0.8 m/s(2) in DD0; P < .05). RAS and RV-IVV were significantly associated with DD after adjustment to age, BMI, and left atrial strain in multivariate regression analysis. CONCLUSION: Systolic right heart function is significantly altered in DD. DTI as well as 2DSTE constitute sensitive echocardiographic tools that enable the diagnosis of impaired right heart mechanics in early-staged DD.

Published
2018

41. Immunoproteasome subunit β5i/LMP7-deficiency in atherosclerosis

Author

Hewing, B., Ludwig, A., Dan, C., Poetzsch, M., Hannemann, C., Petry, A., Lauer, D., Görlach, A., Kaschina, E., Müller, D.N., Baumann, G., Stangl, V., Stangl, K., and Wilck, N.

Subjects
Cardiovascular and Metabolic Diseases
Abstract

Management of protein homeostasis by the ubiquitin-proteasome system is critical for atherosclerosis development. Recent studies showed controversial results on the role of immunoproteasome (IP) subunit {beta}5i/LMP7 in maintenance of protein homeostasis under cytokine induced oxidative stress. The present study aimed to investigate the effect of {beta}5i/LMP7-deficiency on the initiation and progression of atherosclerosis as a chronic inflammatory, immune cell driven disease. LDLR(-/-)LMP7(-/-) and LDLR(-/-) mice were fed a Western-type diet for either 6 or 24 weeks to induce early and advanced stage atherosclerosis, respectively. Lesion burden was similar between genotypes in both stages. Macrophage content and abundance of polyubiquitin conjugates in aortic root plaques were unaltered by {beta}5i/LMP7-deficiency. In vitro experiments using bone marrow-derived macrophages (BMDM) showed that {beta}5i/LMP7-deficiency did not influence macrophage polarization or accumulation of polyubiquitinated proteins and cell survival upon hydrogen peroxide and interferon-γ treatment. Analyses of proteasome core particle composition by Western blot revealed incorporation of standard proteasome subunits in {beta}5i/LMP7-deficient BMDM and spleen. Chymotrypsin-, trypsin- and caspase-like activities assessed by using short fluorogenic peptides in BMDM whole cell lysates were similar in both genotypes. Taken together, deficiency of IP subunit {beta}5i/LMP7 does not disturb protein homeostasis and does not aggravate atherogenesis in LDLR(-/-) mice.

Published
2017

42. P1488Treatment of severe tricuspid regurgitation in patients with advanced heart failure with caval vein implantation of the edwards sapien XT valve (TRICAVAL): a controlled prospective randomized trial

Author

Laule, M, primary, Mattig, I, additional, Hewing, B, additional, Schoebel, C, additional, Knebel, F, additional, Lauten, A, additional, Lembcke, A, additional, Thoenes, M, additional, Baumann, G, additional, Stangl, V, additional, Landmesser, U, additional, Stangl, K, additional, and Dreger, H, additional

Published
2018
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43. Gender in cardiovascular diseases: impact on clinical manifestations, management, and outcomes

Author

EUGenMed, Cardiovascular Clinical Study Group (), Regitz-Zagrosek, V., Oertelt-Prigione, S., Prescott, E., Franconi, F., Gerdts, E., Foryst-Ludwig, A., Maas, A.H., Kautzky-Willer, A., Knappe-Wegner, D., Kintscher, U., Ladwig, K.-H., Schenck-Gustafsson, K., and Stangl, V.

Subjects
Male, medicine.medical_specialty, Pathology, Drug-Related Side Effects and Adverse Reactions, Heart Diseases, Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], MEDLINE, Disease, 030204 cardiovascular system & hematology, Affect (psychology), 03 medical and health sciences, Sex Factors, 0302 clinical medicine, Epidemiology, medicine, Humans, 030212 general & internal medicine, business.industry, Cardiovascular Agents, Human development (humanity), Sexual hormones, Treatment Outcome, Hypertension, Needs assessment, Female, Cardiology and Cardiovascular Medicine, Vascular function, business, Needs Assessment, Clinical psychology
Abstract

In the vast majority of cardiovascular diseases (CVDs), there are well-described differences between women and men in epidemiology, pathophysiology, clinical manifestations, effects of therapy, and outcomes.1–3 These differences arise on one hand from biological differences among women and men, which are called sex differences. They are due to differences in gene expression from the sex chromosomes and subsequent differences in sexual hormones leading to differences in gene expression and function in the CV system, e.g. in vascular function and NO signalling, in myocardial remodelling under stress, or metabolism of drugs by sex-specific cytochrome expression. Sex differences are frequently reproducible in animal models. In contrast, gender differences are unique to the human. They arise from sociocultural processes, such as different behaviours of women and men; exposure to specific influences of the environment; different forms of nutrition, lifestyle, or stress; or attitudes towards treatments and prevention. These are equally important for CVDs. Both sex and gender (S&G) influence human development ( Figure 1 ). Since it is almost impossible to distinguish properly between effects of S&G in the medical field, the EUGenMed writing group decided to discuss both of them together and to use the term S&G for all medical relevant differences between women and men in the present review. Figure 1 Interaction between sex and gender during lifetime: societal conditions (upper) as well as biological facts (lower) affect germ cells, the newborn, the adult, and the development of disease in women and men. In its current research framework programme ‘Horizon 2020’, the EU calls for the inclusion of the gender dimension into biomedical research since ‘it helps improve the scientific quality …

Published
2016

44. HIT Poster session 2P479Strain concordance in a real-world setting: experience in our laboratory after equipment upgradeP4803D echocardiography is a fast-learning and reliable method for the measurements of left atrial volumesP481Echocardiographic parameters associated with long-term appropriate antiarrhythmic therapies in cardiac resynchronization therapy defibrillator patientsP482Noninvasively measured global wasted myocardial work allows for quantitative assessment of typical left ventricular mechanical dyssynchrony pattern in patients with left bundle branch blockP483The impact of adherence to physical exercise on the improvement of cardiovascular remodeling and metabolic status in healthy untrained postmenopausal womenP484The impact of the latest chamber quantification recommendations on the prediction of left atrial appendage thrombus presenceP485The cardiac-enriched miRNAs plasma levels (miR-1, miR-133a, miR-499) reflect the impaired left ventricular systolic function and correlate with cardiac necrosis markers in early phase of NSTE-ACSP486Acute regional myocardial deformation changes in patients with severe aortic stenosis and preserved ejection fraction after isolated aortic valve replacementP487Left ventricular rotational deformation in asymptomatic patients with chronic aortic regurgitation and normal left ventricular ejection fraction P488The appropriate use of transthoracic echocardiography for the exclusion of infective endocarditisP489In patients with hypertrophic cardiomyopathy, left ventricular mass and shape by three-dimensional echocardiography are related with dynamic obstruction and functional capacityP490Mitral leaflet sizing in hypertrophic cardiomyopathy: impact of method and timingP491Echocardiographic predictors of atrial fibrillation in obese womenP492Echocardiographic risk factors for 30 day mortality after the hybrid procedure for hypoplastic left heart syndromeP493Left ventricular mass is an independent predictor of coronary flow reserve: insights from a single centre stress echo cohortP494Transesophageal echocardigoraphy uner conscious sedation for guiding cryoballoon pulmonary vein isolation in paroxysmal atrial fibrillation - the safety and feasibility studyP495Transesophageal echocardigoraphy under conscious sedation for guiding cryoballoon pulmonary vein isolation in paroxysmal atrial fibrillation - the safety and feasibility studyP496Three-dimensional trans-esophageal echocardiography assessment of the immediate morphological changes of the mitral annulus after percutaneous mitral edge-to-edge repairP497Clinical value of global and regional longitudinal strain in prediction of myocardial ischemia in asymptomatic diabetes type 2 patientsP499Comparison of prognostic operative risk impact on the global longitudinal strain right ventricle (GLS RV) and tricuspid annular plane systolic excursion (TAPSE) values in patients with ischemic cardioP498Right heart function in early diastolic dysfunction: 2D speckle-tracking echocardiography-based assessment of right atrial and right ventricular functionP500 Comparison of 2D, 3D transesophageal echocardiography and computed tomography during the assessment of left atrial appendage closure

Author

Cueva Recalde, JF., primary, Velcea, A., primary, Aguiar Rosa, S., primary, Surkova, E., primary, Bucciarelli, V., primary, Kupczynska, K., primary, Miskowiec, D., primary, Reskovic Luksic, V., primary, Verseckaite, R., primary, Jillott, N., primary, Muraru, D., primary, Borizanova, A., primary, Caroli, S., primary, Guerreiro, S., primary, Mahmoud, HM., primary, Peovska Mitevska, I., primary, Babukov, R., primary, Brecht, A., primary, Garcia-Sanchez, MJ., primary, Gayan Ordas, J., additional, Lacambra Blasco, I., additional, Mihaila, S., additional, Andronic, AA., additional, Marcu, S., additional, Vinereanu, D., additional, Galrinho, A., additional, Branco, L., additional, Timoteo, A., additional, Cunha, P., additional, Lousinha, A., additional, Valente, B., additional, Pereira Silva, T., additional, Oliveira, M., additional, Cruz Ferreira, R., additional, Aalen, J., additional, Samset, E., additional, Bidviene, J., additional, Aruta, P., additional, Romeo, G., additional, Sambugaro, F., additional, Badano, LP., additional, Muraru, D., additional, Bianco, F., additional, Di Blasio, A., additional, Izzicupo, P., additional, Ghinassi, B., additional, Napolitano, G., additional, Di Baldassarre, A., additional, Gallina, S., additional, Michalski, B., additional, Miskowiec, D., additional, Kasprzak, JD., additional, Lipiec, P., additional, Kupczynska, K., additional, Simiera, M., additional, Wejner-Mik, P., additional, Wierzbowska-Drabik, K., additional, Ojrzanowski, M., additional, Pasalic, M., additional, Separovic Hanzevacki, J., additional, Mizariene, V., additional, Montvilaite, A., additional, Unikaite, R., additional, Bieseviciene, M., additional, Jurkevicius, R., additional, Wilson, S., additional, Marotta, C., additional, Calore, C., additional, Surkova, E., additional, Palermo, C., additional, Iliceto, S., additional, Kinova, E., additional, Kundurzhiev, T., additional, Goudev, A., additional, Bellsham-Revell, HR., additional, Bell, AJ., additional, Miller, OI., additional, Simpson, JM., additional, Raposo, L., additional, Andrade, MJ., additional, Horta, E., additional, Reis, C., additional, Almeida, M., additional, Mendes, M., additional, Qawoq, HD., additional, Zycinski, P., additional, Wcislo, T., additional, Abdel Raouf, O., additional, Kheir, A., additional, Halawa, S., additional, Al-Ghamdi, M., additional, Ghabashi, A., additional, Srbinovska, E., additional, Antova, E., additional, Bosevski, M., additional, Bazilev, VV., additional, Bartosh, FL., additional, Bathe, M., additional, Oertelt-Prigione, S., additional, Seeland, U., additional, Regitz-Zagrosek, V., additional, Baumann, G., additional, Stangl, K., additional, Stangl, V., additional, Knebel, F., additional, Dreger, H., additional, Barreiro-Perez, M., additional, Arribas-Jimenez, A., additional, Martin-Garcia, A., additional, Diaz-Pelaez, E., additional, Rama-Merchan, JC., additional, Cruz-Gonzalez, I., additional, and Sanchez, PL., additional

Published
2016
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45. Gender in cardiovascular diseases: impact on clinical manifestations, management, and outcomes

Author

Regitz-Zagrosek, V., Oertelt, S., Prescott, E., Franconi, F., Gerdts, E., Foryst-Ludwig, A., Maas, A.H.E.M., Kautzky-Willer, A., Knappe-Wegner, D., Kintscher, U., Ladwig, K.H., Schenck-Gustafsson, K., Stangl, V., Regitz-Zagrosek, V., Oertelt, S., Prescott, E., Franconi, F., Gerdts, E., Foryst-Ludwig, A., Maas, A.H.E.M., Kautzky-Willer, A., Knappe-Wegner, D., Kintscher, U., Ladwig, K.H., Schenck-Gustafsson, K., and Stangl, V.

Abstract

Item does not contain fulltext

Published
2016

46. HIT Poster session 1P154Preclinical diastolic dysfunction is related to impaired endothelial function in patients with chronic kidney diseaseP155Early detection of left atrial and left ventricular abnormalities in hypertensive and obese womenP156Right ventricle preserved systolic function irrespective of right ventricular hypertrophy and disease severity in anderson fabry diseaseP157Left atrial volume and function in patients undergoing percutaneous mitral valve repairP158Impact of left ventricular dysfunction on outcomes of patients undergoing direct TAVI with a self-expanding bioprosthesisP159Anatomic Doppler spectrum – retrospective spectral tissue Doppler from ultra high frame rate tissue Doppler imaging for evaluation of tissue deformationP160Phasic dynamics of ischaemic mitral regurgitation after primary coronary intervention in acute myocardial infarction: serial echocardiographic assessment from emergency room to long-term follow-upP161Reproducibility of 3DE RV volumes - novel insights at a regional levelP162Pulmonary vascular capacitance as assessed by echocardiography in pulmonary arterial hypertensionP163Three-dimensional endocardial area strain: a novel parameter for quantitative assessment of global left ventricular systolic functionP164Role of exercise hemodynamics assessed by echocardiography on symptom reduction after MitraClipP165Early identification of ventricular dysfunction in patients with juvenile systemic sclerosisP166Heart failure with and without preserved ejection fraction - the role of biomarkers in the aspect of global longitudinal strainP167Complex systolic deformation of aortic root: insights from two dimensional speckle tracking imageP168Volumetric and deformational imaging usind 2d strain and 3d echocardiography in patients with pulmonary hypertensionP169Influence of pressure load and right ventricular morphology and function on tricuspid regurgitation in pulmonary arterial hypertensionP170Left ventricular myocardial diastolic deformation analysis by 2D speckle tracking echocardiography and relationship with conventional diastolic parameters in chronic aortic regurgitationP171Extracellular volume, and not native T1 time, distinguishes diffuse fibrosis in dilated or hypertrophic cardiomyopathy at 3TP172Left atrial strain is significantly reduced in arterial hypertensionP173Symptomatic severe secondary mitral regurgitation: LV enddiastolic diameter (LVEDD) as preferable parameter for risk stratificationP174Left ventricular mechanics in isolated left bundle branch block at rest and when exercising: exploration of the concept of conductive cardiomyopathyP175Assessment of myocardial scar by 2D contrast echocardiographyP176Chronic pericarditis - expression of a rare disease: Erdheim Chester diseaseP177Aortic arch mechanics with two-dimensional speckle tracking echocardiography to estimate the left ventricular remodelling in hypertensive patientsP178Strain analysis by tissue doppler imaging: comparison of conventional manual measurement with a semi-automated approachP179Distribution of extravascular lung water in heart failure patients assessed by lung ultrasoudP180Surrogate markers for obstructive coronary artery diseaseP181LA deformation and LV longitudinal strain by two-dimensional speckle tracking echocardiography as predictors of postoperative AF development after aortic valve replacement in ASP182Left ventricular diastolic dysfunction in type 2 diabetic patients with non alcoholic fatty liver diseaseP183Myocardial strain by speckle-tracking and evaluation of 3D ejection fraction in drug-induced cardiotoxicity's approach in breast cancer

Author

Gevaert, AB, primary, Borizanova, A, primary, Graziani, F, primary, Galuszka, O M, primary, Stathogiannis, K, primary, Lervik Nilsen, L C, primary, Nishino, S, primary, Willis, J, primary, Venner, C, primary, Luo, XX, primary, Van De Heyning, C M, primary, Castaldi, B, primary, Michalski, BW, primary, Wang, TL, primary, Aktemur, T, primary, Dorlet, S, primary, Verseckaite, R, primary, Amzulescu, MS, primary, Brecht, A, primary, Brand, M, primary, Galli, E, primary, Murzilli, R, primary, Bica, R, primary, Teixeira, R, primary, Schmid, J, primary, Miglioranza, MH, primary, Cherneva, ZH, primary, Gheghici, S, primary, Pernigo, M, primary, Rafael, D, primary, Van Craenenbroeck, AH, additional, Shivalkar, B, additional, Lemmens, K, additional, Vrints, CJ, additional, Van Craenenbroeck, EM, additional, Somleva, D, additional, Zlatareva- Gronkova, N, additional, Kinova, E, additional, Goudev, A, additional, Camporeale, A, additional, Pieroni, M, additional, Pedicino, D, additional, Laurito, MP, additional, Verrecchia, E, additional, Lanza, GA, additional, Manna, R, additional, Crea, F, additional, Reinthaler, M, additional, Rutschow, S, additional, Gross, M, additional, Landmesser, U, additional, Kasner, M, additional, Toutouzas, K, additional, Drakopoulou, M, additional, Latsios, G, additional, Synetos, A, additional, Kaitozis, O, additional, Trantalis, G, additional, Mastrokostopoulos, A, additional, Kotronias, R, additional, Tousoulis, D, additional, Brekke, BB, additional, Aase, SA, additional, Lonnebakken, MT, additional, Stensvag, D, additional, Amundsen, B, additional, Torp, H, additional, Stoylen, A, additional, Watanabe, N, additional, Kimura, T, additional, Nakama, T, additional, Furugen, M, additional, Koiwaya, H, additional, Ashikaga, K, additional, Kuriyama, N, additional, Shibata, Y, additional, Augustine, DX, additional, Knight, D, additional, Sparey, J, additional, Coghlan, G, additional, Easaw, J, additional, Huttin, O, additional, Voilliot, D, additional, Mercy, M, additional, Villemin, T, additional, Olivier, A, additional, Mandry, D, additional, Chaouat, A, additional, Juilliere, Y, additional, Selton-Suty, C, additional, Fang, F, additional, Li, S, additional, Zhang, ZH, additional, Yu, CM, additional, Bertrand, PB, additional, De Maeyer, C, additional, De Bock, D, additional, Paelinck, BP, additional, Claeys, MJ, additional, Reffo, E, additional, Balzarin, M, additional, Zulian, F, additional, Milanesi, O, additional, Miskowiec, D, additional, Kupczynska, K, additional, Peczek, L, additional, Nawrot, B, additional, Lipiec, P, additional, Kasprzak, JD, additional, Li, H, additional, Jin, XY, additional, Poci, N, additional, Kaymaz, C, additional, Venner, C, additional, Manenti, V, additional, Carillo, S, additional, Chabot, F, additional, Mizariene, V, additional, Rimkeviciute, D, additional, Bieseviciene, M, additional, Jonkaitiene, R, additional, Jurkevicius, R, additional, Roy, C, additional, Slimani, A, additional, Boileau, L, additional, De Meester, C, additional, Vancraeynest, D, additional, Pasquet, A, additional, Vanoverschelde, JL, additional, Pouleur, AC, additional, Gerber, BL, additional, Oertelt-Prigione, S, additional, Seeland, U, additional, Ruecke, M, additional, Regitz-Zagrosek, V, additional, Stangl, V, additional, Knebel, F, additional, Laux, D, additional, Roeing, J, additional, Butz, T, additional, Christ, M, additional, Grett, M, additional, Wennemann, R, additional, Trappe, H- J, additional, Fournet, M, additional, Leclercq, C, additional, Samset, E, additional, Daubert, J-C, additional, Donal, E, additional, Leo, LA, additional, Pasotti, E, additional, Klersy, C, additional, Moccetti, T, additional, Faletra, FF, additional, Dobre, D, additional, Darmon, S, additional, Dumitrescu, S, additional, Calistru, P, additional, Monteiro, R, additional, Ribeiro, M, additional, Garcia, J, additional, Cardim, N, additional, Goncalves, L, additional, Kaufmann, R, additional, Grubler, MR, additional, Verheyen, N, additional, Weidemann, F, additional, Binder, JS, additional, Santanna, RT, additional, Rover, MM, additional, Leiria, T, additional, Kalil, R, additional, Picano, E, additional, Gargani, L, additional, Kuneva, ZK, additional, Vasilev, DV, additional, Ianula, R, additional, Dasoveanu, M, additional, Calin, C, additional, Homentcovsci, C, additional, Siliste, R, additional, Bergamini, C, additional, Mantovani, A, additional, Bonapace, S, additional, Lipari, P, additional, Barbieri, E, additional, Bonora, E, additional, Targher, G, additional, Camarozano, AC, additional, Pereira Da Cunha, CL, additional, Padilha, SL, additional, Souza, AM, additional, and Freitas, AKE, additional

Published
2015
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47. Secretory products from human adipocytes impair endothelial function via nuclear factor kappa B

Author

Kralisch, S., Sommer, G., Stangl, V., Köhler, U., Kratzsch, J., Stephan, H., Faber, R., Schubert, A., Lössner, U., Vietzke, A., Bluher, M., Stumvoll, M., Fasshauer, M., and Publica

Subjects
obesity, Adipokine, Fett, adipocyte, endothelial dysfunction
Abstract

Hyperplasia and hypertrophy of fat cells can be found in obesity, and increased adiposity is associated with endothelial dysfunction as an early event of atherosclerosis. However, it is unclear whether human adipocytes directly influence endothelial function. To study the crosstalk between fat and endothelial cells, human umbilical venous endothelial cells (HUVECs), and human coronary artery endothelial cells (HCAECs) were cultured in infranatants (Adipo) of primary differentiated human adipocytes. Interestingly, incubation of HUVECs and HCAECs with Adipo significantly increased monocyte adhesion 7.3 and 2.2-fold, respectively. VCAM-1, ICAM-1, and E-selectin in HUVECs were upregulated 3.9, 3.0, and 9.5-fold, respectively, under these conditions. Furthermore, Adipo significantly stimulated NF kappaB activity 1.9-fold. The NF kappaB inhibitor MG-132 and heat inactivation significantly reversed Adipo-stimulated monocyte adhesion. TNF alpha-neutralizing antibodies partly reversed Adipo-induced monocyte adhesion. In contrast, thiazolidinedione-pretreatment of human adipocytes did not alter the effects of Adipo. Adipo did not show cytotoxic effects. Taken together, we demonstrate that endothelial dysfunction is induced by adipocyte-secreted factors via NF kappaB partly dependent on TNF alpha.

Published
2008

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