Littérature scientifique sur le sujet « Atriale fibrosis »
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Articles de revues sur le sujet "Atriale fibrosis"
Gibson, Sarah E., Carol F. Farver et Richard A. Prayson. « Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy : An Autopsy Case and Review of the Literature ». Archives of Pathology & ; Laboratory Medicine 130, no 2 (1 février 2006) : 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.
Texte intégralDe Sensi, Francesco, Diego Penela, David Soto-Iglesias, Antonio Berruezo et Ugo Limbruno. « Imaging Techniques for the Study of Fibrosis in Atrial Fibrillation Ablation : From Molecular Mechanisms to Therapeutical Perspectives ». Journal of Clinical Medicine 10, no 11 (24 mai 2021) : 2277. http://dx.doi.org/10.3390/jcm10112277.
Texte intégralVillarroel-Ábrego, Hugo, Martha Reyes-Villatoro et Camila Flores-Ventura. « Fibrosis atrial derecha y síndrome del nodo enfermo ». Revista de Ecocardiografía Práctica y Otras Técnicas de Imagen Cardíaca 2, no 1 (31 décembre 2019) : 30–33. http://dx.doi.org/10.37615/retic.v2n1a8.
Texte intégralAronis, Konstantinos N., Rheeda L. Ali, Jialiu A. Liang, Shijie Zhou et Natalia A. Trayanova. « Understanding AF Mechanisms Through Computational Modelling and Simulations ». Arrhythmia & ; Electrophysiology Review 8, no 3 (9 août 2019) : 210–19. http://dx.doi.org/10.15420/aer.2019.28.2.
Texte intégralPong, Terrence, Joy Aparicio-Valenzuela, Oluwatomisin Obafemi, Kevin Cyr, Cody Carlton, Calvin Taylor et Anson Lee. « High-resolution spatiotemporal changes in dominant frequency and structural organization during persistent atrial fibrillation ». PLOS ONE 18, no 2 (14 février 2023) : e0271846. http://dx.doi.org/10.1371/journal.pone.0271846.
Texte intégralDosdall, Derek J., Ravi Ranjan, Koji Higuchi, Eugene Kholmovski, Nathan Angel, Li Li, Rob MacLeod et al. « Chronic atrial fibrillation causes left ventricular dysfunction in dogs but not goats : experience with dogs, goats, and pigs ». American Journal of Physiology-Heart and Circulatory Physiology 305, no 5 (1 septembre 2013) : H725—H731. http://dx.doi.org/10.1152/ajpheart.00440.2013.
Texte intégralLi, Guo-Liang, Guy Fontaine, Jine Wu, Shuanliang Fan, Chaofeng Sun et Ardan M. Saguner. « Atrial dysplasia in the atria of humans without cardiovascular disease ». Journal of Investigative Medicine 67, no 6 (14 février 2019) : 971–76. http://dx.doi.org/10.1136/jim-2018-000916.
Texte intégralSramko, Marek, et Josef Kautzner. « Atrial Fibrosis ». Journal of the American College of Cardiology 65, no 22 (juin 2015) : 2465. http://dx.doi.org/10.1016/j.jacc.2015.01.067.
Texte intégralNagel, Claudia, Giorgio Luongo, Luca Azzolin, Steffen Schuler, Olaf Dössel et Axel Loewe. « Non-Invasive and Quantitative Estimation of Left Atrial Fibrosis Based on P Waves of the 12-Lead ECG—A Large-Scale Computational Study Covering Anatomical Variability ». Journal of Clinical Medicine 10, no 8 (20 avril 2021) : 1797. http://dx.doi.org/10.3390/jcm10081797.
Texte intégralTandon, Karman, David Tirschwell, W. T. Longstreth, Bryn Smith et Nazem Akoum. « Embolic stroke of undetermined source correlates to atrial fibrosis without atrial fibrillation ». Neurology 93, no 4 (25 juin 2019) : e381-e387. http://dx.doi.org/10.1212/wnl.0000000000007827.
Texte intégralThèses sur le sujet "Atriale fibrosis"
Guichard, Jean-Baptiste. « Déterminants du remodelage atrial et de son effet pro-arythmique dans la fibrillation atriale ». Thesis, Lyon, 2019. http://hdl.handle.net/1866/24623.
Texte intégralRational and objective - Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Atrial remodeling, whether electrical or structural, leads to the development of atrial cardiomyopathy. The atrial cardiomyopathy results in various complications: on one hand, mechanical with an increased thromboembolic risk and heart failure, and on the other hand electrical prdeisposing to atrial arrhythmias including AF. The aim of the thesis was to characterize the determinants of atrial remodeling, and their proarrhythmic effect in AF. Main results - The first part of the thesis focused on the characterization of the atrial remodeling induced by sustained atrial flutter (AFL) in a chronic canine model in order to characterize the interrelationship between AF and AFL. AFL caused electrical remodeling, including increased AF vulnerability and decreased effective refractory periods (ERPs). However, failed to influence AF duration, atrial conduction velocities and fibrosis. Chronic AF in the presence of an anatomical substrate for AFL led to specific AF characteristics, in terms of cycle length and its variability. In addition, AFL ablation significantly reduced arrhythmia duration but not AF vulnerability. The second part of the thesis characterized the differential role of atrial arrhythmia and ventricular response in AF-induced atrial remodeling. We characterized the atrial remodeling induced by lone atrial arrhythmia in AF, with AV-block to prevent high ventricular rate: on the one hand electrical via decreased ERP, reduced expression of sodium channels and gap junctions, which increased AF vulnerability; on the other hand, structural fibrosis which contributed to conduction slowing. Lone high-rate ventricular response also induced atrial remodeling involving increased AF vulnerability, decreased atrial conduction velocities, moderate abnormalities of fibrosis and sodium channel downregulation. In addition, there was a synergistic effect on atrial remodeling of combined atrial arrhythmia and high ventricular rate, especially regarding fibrosis. Thus, atrial tachyarrhythmia and rapid ventricular response during AF produce distinct atrial remodeling; both can contribute to the arrhythmogenic substrate. These results provide new insights into the determinants of AF-related remodeling and provide novel considerations for ventricular rate-control. The third part of the thesis studies the ability of cilnidipine, an N- and L-type calcium channel blocker, to alter autonomic, electrical and structural remodeling associated with chronic AF, in a subacute and chronic dog model. We found that the cilnidipine inhibits the electrophysiological, autonomic and structural consequences of AF-related remodeling and the AF-associated increase in AF-vulnerability and AF-duration; in contrast, the highly selective L-type calcium channel blocker nifedipine had no protective effects. The protective effects of cilnidipine on the remodeling consequences of short-term AF were principally manifested by reductions in AF-induced ERP-abbreviation. With longer-term AF, cilnidipine also attenuated conduction-velocity reductions, protecting against AF-induced fibrosis and downregulation of sodium-channel and connexin subunits. Cilnidipine’s anti-remodeling properties were associated with suppression of the changes in autonomic tone caused by AF. Conclusion - Thus, we have shown 1) the distinct remodeling phenotypes produced by the closely related atrial re-entrant arrhythmias AFL and AF, as well as the interaction when they co-exist; 2) the specific contributions of the atrial rhythm and ventricular rate consequences of AF and how they interact; and 3) the ability of autonomic outflow inhibition by blocking N-type Ca2+-channels to prevent both electrical and structural components of AF-induced profibrillatory remodeling. This work provides new insights into the mechanisms involved in AF-related atrial remodeling and introduces novel preventive approaches.
Rahhal, Amer. « Identification and Quantification of Fibrosis and Adipose Tissue of the Atrial Myocardium using Cardiac Magnetic Resonance Imaging ». Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS588.
Texte intégralIntroduction: Atrial fibrillation is associated with an atrial cardiomyopathy composed mainly of fibrosis and adipose tissue accumulation. However, its detection is difficult in clinical practice. Notably, there is controversy on the ability of MRI to quantify these components as well as the clinical significance of this parameter. Methods: LA strain (PLAS) was evaluated with MRI feature tracking in 13 patients 24 hours before mitral valve surgery and 13 healthy controls. Histologic correlation biopsies was available in 10 patients. Atrial samples were collected from patients who underwent cardiac surgery. Samples were fixed in formaldehyde and analyzed using 3D MRI acquisitions including T1 mapping and DIXON imaging. Samples were histologically analyzed in the same orientation used for MRI study. Results: We first studied the correlation between PLAS and atrial remodeling. PLAS was lower in patients with mitral regurgitation than in healthy subjects (P˂0.001). A strong association was found between PLAS and the degree of fibrofatty replacement evaluated by histologic analysis (r=-0.75, P=0.017). In a second study, we studied the ability of MRI to discriminate the various atrial components. High correlation was observed between T1 Mapping and histology for total r=0.93, interstitial r=0.93, and fatty fibrosis r=0.96. High correlation between DIXON and histology were found in fat r=0.98. Conclusion: PLAS correlates with the degree of fibrofatty infiltration which could be used as an imaging biomarker for the atrial cardiomyopathy. High field ex vivo MRI is able to identify the various components of the atrial myocardium; however, in vivo application remains a challenge
ASMUNDIS, C. DE. « RUOLO DELLA STIMOLAZIONE VAGALE SULLA PROLIFERAZIONE DEI FIBROBLASTI CARDIACI IN VIVO IN MODELLO ANIMALE DI FIBRILLAZIONE ATRIALE ». Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150146.
Texte intégralMoubarak, Majed. « Étude des effets du peptide natriurétique atrial sur les fibroblastes : implication physiopathologique dans le remodelage cardiaque ». Thesis, Poitiers, 2014. http://www.theses.fr/2014POIT2312/document.
Texte intégralANP is a cardiac hormone released during heart failure and acts as a regulator of the extracellular matrix (ECM). Cardiac fibroblasts are responsible for the synthesis of ECM components and acquire under pathological conditions the capacity to differentiate into myofibroblasts, leading to cardiac fibrosis. Regulatory mechanisms involving ANP and its receptors (NPR) are poorly known and make the subject of our work. Ventricular fibroblasts were isolated from Wistar rat hearts and cultured to induce differentiation. The cultures were then subjected to various treatments involved in the ANP/NPR pathway. ANP decreases the proliferation rate, cell migration and collagen secretion. This effect was mimicked by 8-Br-cGMP. In addition, genomic and proteomic analysis confirmed the presence of the natriuretic receptor A and B in our cells. Furthermore, the expression of ten phosphodiesterases isoforms in the myofibroblasts was revealed by genomic screening. The non-selective inhibition of these phosphodiesterases causes a decrease in the proliferation and secretion of collagen. Finally, the intracellular concentrations of cAMP and cGMP were increased in the presence of ANP. In parallel, the characterization of ionic currents present in myofibroblasts revealed the absence of rapid sodium and potassium ATP-dependent currents. This study shows the role of the ANP/NPR/cGMP pathway in modulating fibroblast properties and exposes the complexity of the cell differentiation process during cardiac fibrogenesis
Mastrorilli, Antonio Pio. « Mappaggio t1 in risonanza magnetica per la quantificazione della fibrosi atriale ». Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amslaurea.unibo.it/9991/.
Texte intégralLeonardi, Roberta. « Segmentazione automatica dell'atrio sinistro e valutazione della fibrosi atriale in risonanza magnetica ». Master's thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amslaurea.unibo.it/6427/.
Texte intégralMargara, Francesca. « Studio e valutazione del legame tra rimodellamento elettrico e strutturale in Fibrillazione Atriale ». Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amslaurea.unibo.it/9619/.
Texte intégralOnofri, Claudio. « Design e sviluppo di un nuovo algoritmo di segmentazione basato su CNN per la stima della volumetria atriale sinistra in pazienti con fibrillazione atriale ». Master's thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amslaurea.unibo.it/25390/.
Texte intégralCacciatore, Angela [Verfasser], et Hans-Ruprecht [Akademischer Betreuer] Neuberger. « Prokollagen Propeptide : Marker für atriale Fibrose und Vorhofflimmern ? / Angela Cacciatore. Betreuer : Hans-Ruprecht Neuberger ». Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2013. http://d-nb.info/1052907148/34.
Texte intégralBaliga, Reshma S. « Roles and mechanisms of oxidant stress in cardiovascular disease ». Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1092841524.
Texte intégralDocument formatted into pages. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 Aug. 18.
Livres sur le sujet "Atriale fibrosis"
Haugaa, Kristina H., Francesco Faletra et João L. Cavalcante. Cardiac rhythm disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0063.
Texte intégralSánchez-Quintana, Damián, et José Angel Cabrera. Normal atrial and ventricular myocardial structures. Sous la direction de Yen Ho. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0014.
Texte intégralChapitres de livres sur le sujet "Atriale fibrosis"
Kottkamp, Hans, Andreas Rieger, Fabian Moser et Christian Poenisch. « Fibrotic Atrial Cardiomyopathy ». Dans Cardiac Mapping, 628–34. Chichester, UK : John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119152637.ch50.
Texte intégralNavaravong, Leenhapong, et Nassir F. Marrouche. « Magnetic Resonance Imaging Mapping of Atrial Fibrosis and Atrial Fibrillation ». Dans Cardiac Mapping, 618–27. Chichester, UK : John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119152637.ch49.
Texte intégralZhao, Jichao, Robert S. Stephenson, Greg B. Sands, Ian J. LeGrice, Henggui Zhang, Jonathan C. Jarvis et Bruce H. Smaill. « Atrial Fibrosis and Atrial Fibrillation : A Computer Simulation in the Posterior Left Atrium ». Dans Functional Imaging and Modeling of the Heart, 400–408. Berlin, Heidelberg : Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-38899-6_47.
Texte intégralWu, Fuping, Lei Li, Guang Yang, Tom Wong, Raad Mohiaddin, David Firmin, Jennifer Keegan, Lingchao Xu et Xiahai Zhuang. « Atrial Fibrosis Quantification Based on Maximum Likelihood Estimator of Multivariate Images ». Dans Medical Image Computing and Computer Assisted Intervention – MICCAI 2018, 604–12. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00937-3_69.
Texte intégralRamirez, Alexies, et Nassir F. Marrouche. « Role of Late Gadolinium-Enhanced Magnetic Resonance Imaging in Detection and Quantification of Atrial Fibrosis ». Dans Cardiac Mapping, 656–63. Oxford, UK : Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481585.ch60.
Texte intégralPalacio, Laura C., Juan P. Ugarte, Javier Saiz et Catalina Tobón. « Genesis of Atrial Fibrillation Under Different Diffuse Fibrosis Density Related with Atmospheric Pollution. In-Silico Study ». Dans Communications in Computer and Information Science, 291–301. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-61834-6_25.
Texte intégralYang, Guang, Xiahai Zhuang, Habib Khan, Shouvik Haldar, Eva Nyktari, Xujiong Ye, Greg Slabaugh et al. « Segmenting Atrial Fibrosis from Late Gadolinium-Enhanced Cardiac MRI by Deep-Learned Features with Stacked Sparse Auto-Encoders ». Dans Communications in Computer and Information Science, 195–206. Cham : Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60964-5_17.
Texte intégralHuang, Chao, Stephen L. Wasmund, Takanori Yamaguchi, Nathan Knighton, Robert W. Hitchcock, Irina A. Polejaeva, Kenneth L. White, Nassir F. Marrouche et Frank B. Sachse. « Towards Automated Quantification of Atrial Fibrosis in Images from Catheterized Fiber-Optics Confocal Microscopy Using Convolutional Neural Networks ». Dans Functional Imaging and Modeling of the Heart, 168–76. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21949-9_19.
Texte intégralRosenberg, Michael A. « Circulating Fibrosis Biomarkers and Cardiovascular Health : Disease-Focused Approach in Heart Failure, Arrhythmias, Sudden Cardiac Death, and Atrial Fibrillation ». Dans Biomarkers in Cardiovascular Disease, 1–34. Dordrecht : Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7741-5_48-1.
Texte intégralVan Wagoner, David R. « Mechanisms of atrial remodelling ». Dans ESC CardioMed, 2125–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0498.
Texte intégralActes de conférences sur le sujet "Atriale fibrosis"
Tang, Xin, Piyush Bajaj, Rashid Bashir et Taher Saif. « Mechanical Communication Between Cardiac Cell Leads to Synchrony in Beating ». Dans ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80937.
Texte intégralDi Martino, Elena S., Chiara Bellini, Dale J. Ward, Nicolas Brown et David Schwartzman. « Porcine Left Atrial Wall Stress After Ventricular Tachypacing Mimicking the Effects of Early Atrial Fibrillation ». Dans ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19528.
Texte intégralSchiatti, "Teresa, Marilu Casini, Thomas Hutschalik, Manuel Koch, Ramona Emig, Remi Peyronnet et Ursula Ravens". « Impact of Mechanically-Induced Fibrosis on Atrial Electromechanical Function ». Dans 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.426.
Texte intégralOgbomo-Harmitt, "Shaheim, Ahmed Qureshi, Andrew P. King et Oleg Aslanidi". « Impact of Fibrosis Border Zone Characterisation on Fibrosis-Substrate Isolation Ablation Outcome for Atrial Fibrillation ». Dans 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.218.
Texte intégralRanjan, Ravi, Elyar Ghafoori, Roya Kamali, Eugene Kwan, Kennosuke Yamashita, Rob MacLeod et Derek Dosdall. « Regions of High Dominant Frequency in Chronic Atrial Fibrillation Anchored to Areas of Atrial Fibrosis ». Dans 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.403.
Texte intégralRiccio, Jennifer, Sara Rocher, Laura Martinez, Alejandro Alcaine, Javier Saiz, Juan Pablo Martínez et Pablo Laguna. « Unipolar Electrogram Eigenvalue Distribution Analysis for the Identification of Atrial Fibrosis ». Dans 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.434.
Texte intégralRoney, Caroline, Jason Bayer, R�mi Dubois, Marianna Meo, Hubert Cochet, Pierre Ja�s et Edward Vigmond. « The Combination of Pulmonary Vein Electrophysiology and Atrial Fibrosis Determines Driver Location ». Dans 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.374-228.
Texte intégralvan Montfoort, "Margot, Victor G. Marques, Ozan Özgül, Ali Gharaviri, Simone Pezzuto, Angelo Auricchio, Pietro Bonizzi, Ulrich Schotten et Stef Zeemering". « Fibrosis Reduces the Coincidence of Repetitive Activations Patterns between the Coronary Sinus and Atrial Regions in Simulated Atrial Fibrillation ». Dans 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.155.
Texte intégralPelloni, Samuele, Michela Mase, Alessandro Cristoforetti et Flavia Ravelli. « Modeling fibrosis distribution for the study of wave propagation patterns during atrial fibrillation ». Dans 2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2014. http://dx.doi.org/10.1109/esgco.2014.6847528.
Texte intégralGharaviri, Ali, Mark Potse, Sander Verheule, Rolf Krause, Angelo Auricchio et Ulrich Schotten. « Epicardial Fibrosis Explains Increased Transmural Conduction in a Computer Model of Atrial Fibrillation ». Dans 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.071-216.
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