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Добірка наукової літератури з теми "Atriale fibrosis"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Atriale fibrosis"

Gibson, Sarah E., Carol F. Farver, and 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 (February 1, 2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.

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Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.

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De Sensi, Francesco, Diego Penela, David Soto-Iglesias, Antonio Berruezo, and 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 (May 24, 2021): 2277. http://dx.doi.org/10.3390/jcm10112277.

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Atrial fibrillation (AF) is the most prevalent form of cardiac arrhythmia. It is often related to diverse pathological conditions affecting the atria and leading to remodeling processes including collagen accumulation, fatty infiltration, and amyloid deposition. All these events generate atrial fibrosis, which contribute to beget AF. In this scenario, cardiac imaging appears as a promising noninvasive tool for monitoring the presence and degree of LA fibrosis and remodeling. The aim of this review is to comprehensively examine the bench mechanisms of atrial fibrosis moving, then to describe the principal imaging techniques that characterize it, such as cardiac magnetic resonance (CMR) and multidetector cardiac computed tomography (MDCT), in order to tailor atrial fibrillation ablation to each individual.

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Villarroel-Ábrego, Hugo, Martha Reyes-Villatoro, and Camila Flores-Ventura. "Fibrosis atrial derecha y síndrome del nodo enfermo." Revista de Ecocardiografía Práctica y Otras Técnicas de Imagen Cardíaca 2, no. 1 (December 31, 2019): 30–33. http://dx.doi.org/10.37615/retic.v2n1a8.

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Varón de 57 años hipertenso y obeso consultó para valoración por disnea de esfuerzos. Se detectó leve hipertensión pulmonar por disfunción diastólica sin hipertrofia ventricular, incompetencia cronotrópica y fibrosis atrial derecha aislada por resonancia magnética. No había deterioro del strain del ventrículo dere-cho, pero sí de la aurícula derecha. Se implantó un marcapaso permanente. Se discute cómo, subyacente a la aparición de trastornos del automatismo y arritmias atriales, puede haber un sustrato de fibrosis no isquémica

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Aronis, Konstantinos N., Rheeda L. Ali, Jialiu A. Liang, Shijie Zhou, and Natalia A. Trayanova. "Understanding AF Mechanisms Through Computational Modelling and Simulations." Arrhythmia & Electrophysiology Review 8, no. 3 (August 9, 2019): 210–19. http://dx.doi.org/10.15420/aer.2019.28.2.

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AF is a progressive disease of the atria, involving complex mechanisms related to its initiation, maintenance and progression. Computational modelling provides a framework for integration of experimental and clinical findings, and has emerged as an essential part of mechanistic research in AF. The authors summarise recent advancements in development of multi-scale AF models and focus on the mechanistic links between alternations in atrial structure and electrophysiology with AF. Key AF mechanisms that have been explored using atrial modelling are pulmonary vein ectopy; atrial fibrosis and fibrosis distribution; atrial wall thickness heterogeneity; atrial adipose tissue infiltration; development of repolarisation alternans; cardiac ion channel mutations; and atrial stretch with mechano-electrical feedback. They review modelling approaches that capture variability at the cohort level and provide cohort-specific mechanistic insights. The authors conclude with a summary of future perspectives, as envisioned for the contributions of atrial modelling in the mechanistic understanding of AF.

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Pong, Terrence, Joy Aparicio-Valenzuela, Oluwatomisin Obafemi, Kevin Cyr, Cody Carlton, Calvin Taylor, and Anson Lee. "High-resolution spatiotemporal changes in dominant frequency and structural organization during persistent atrial fibrillation." PLOS ONE 18, no. 2 (February 14, 2023): e0271846. http://dx.doi.org/10.1371/journal.pone.0271846.

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Objective Analyze changes in frequency activity and structural organization that occur over time with persistent atrial fibrillation (AF) Background Little is known about the frequency characteristics of the epicardium during transition from paroxysmal to persistent AF. Accurate identification of areas of high dominant frequency (DF) is often hampered by limited spatial resolution. Improvements in electrode arrays provide high spatiotemporal resolution, allowing for characterization of the changes that occur during this transition. Methods AF was induced in adult Yorkshire swine by atrial tachypacing. DF mapping was performed using personalized mapping arrays. Histological analysis and late gadolinium enhanced magnetic resonance imaging were performed to determine structural differences in fibrosis. Results The left atrial epicardium was associated with a significant increase in DF in persistent AF (6.5 ± 0.2 vs. 7.4 ± 0.5 Hz, P = 0.03). The organization index (OI) significantly decreased during persistent AF in both the left atria (0.3 ± 0.03 vs. 0.2 ± 0.03, P = 0.01) and right atria (0.33 ± 0.04 vs. 0.23 ± 0.02, P = 0.02). MRI analysis demonstrated increased ECV values in persistent AF (0.19 vs 0.34, paroxysmal vs persistent, P = 0.05). Tissue sections from the atria showed increase in fibrosis in pigs with persistent AF compared to paroxysmal AF. Staining demonstrated decreased myocardial fiber alignment and loss of anisotropy in persistent AF tissue. Conclusions Changes in tissue organization and fibrosis are observed in the porcine model of persistent AF. Alterations in frequency activity and organization index can be captured with high resolution using flexible electrode arrays.

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Dosdall, 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 (September 1, 2013): H725—H731. http://dx.doi.org/10.1152/ajpheart.00440.2013.

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Structural remodeling in chronic atrial fibrillation (AF) occurs over weeks to months. To study the electrophysiological, structural, and functional changes that occur in chronic AF, the selection of the best animal model is critical. AF was induced by rapid atrial pacing (50-Hz stimulation every other second) in pigs ( n = 4), dogs ( n = 8), and goats ( n = 9). Animals underwent MRIs at baseline and 6 mo to evaluate left ventricular (LV) ejection fraction (EF). Dogs were given metoprolol (50–100 mg po bid) and digoxin (0.0625–0.125 mg po bid) to limit the ventricular response rate to <180 beats/min and to mitigate the effects of heart failure. The pacing leads in pigs became entirely encapsulated and lost the ability to excite the heart, often before the onset of sustained AF. LV EF in dogs dropped from 54 ± 11% at baseline to 33 ± 7% at 6 mo ( P < 0.05), whereas LV EF in goats did not drop significantly (69 ± 8% at baseline vs. 60 ± 9% at 6 mo, P = not significant). After 6 mo of AF, fibrosis levels in dog atria and ventricles increased, whereas only atrial fibrosis levels increased in goats compared with control animals. In our experience, the pig model is not appropriate for chronic rapid atrial pacing-induced AF studies. Rate-controlled chronic AF in the dog model developed HF and LV fibrosis, whereas the goat model developed only atrial fibrosis without ventricular dysfunction and fibrosis. Both the dog and goat models are representative of segments of the patient population with chronic AF.

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Li, Guo-Liang, Guy Fontaine, Jine Wu, Shuanliang Fan, Chaofeng Sun, and Ardan M. Saguner. "Atrial dysplasia in the atria of humans without cardiovascular disease." Journal of Investigative Medicine 67, no. 6 (February 14, 2019): 971–76. http://dx.doi.org/10.1136/jim-2018-000916.

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Research on atrial histology of humans without cardiovascular disease is scarce. Therefore, our aim was to study human atrial histology in subjects without cardiovascular disease. Histology of the right atrium, left atrium or atrial septum was studied in eight patients (one newborn infant and seven adults) who died of a non-cardiac cause and who were not known to suffer from any cardiovascular pathology. Staining with hematoxylin phloxine saffron or Masson’s trichrome was performed to have a better identification of fibrosis and H&E for better identification of lymphocytes. Atrial histology was compared with the histology of the left ventricle and was taken from a collection of standard glass slides. Common light microscopic examination and numeric image processing was performed in all samples. Left atrial histology showed a substantial amount of adipocytes and interstitial fibrosis, associated with replacement fibrosis in some of these cases including one case of lymphocytic infiltrates, similar to the histologic changes of the right ventricle (RV) known in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD). Furthermore, we identified a perpendicular orientation of atrial myocardial fibres, which is also a feature of the thin RV free wall. A similar histologic substrate to the RV myocardium known in ARVD is found in the atria of humans without an overt cardiovascular pathology. This may explain the high prevalence of atrial fibrillation in the general population.

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Sramko, Marek, and Josef Kautzner. "Atrial Fibrosis." Journal of the American College of Cardiology 65, no. 22 (June 2015): 2465. http://dx.doi.org/10.1016/j.jacc.2015.01.067.

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Nagel, Claudia, Giorgio Luongo, Luca Azzolin, Steffen Schuler, Olaf Dössel, and 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 (April 20, 2021): 1797. http://dx.doi.org/10.3390/jcm10081797.

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The arrhythmogenesis of atrial fibrillation is associated with the presence of fibrotic atrial tissue. Not only fibrosis but also physiological anatomical variability of the atria and the thorax reflect in altered morphology of the P wave in the 12-lead electrocardiogram (ECG). Distinguishing between the effects on the P wave induced by local atrial substrate changes and those caused by healthy anatomical variations is important to gauge the potential of the 12-lead ECG as a non-invasive and cost-effective tool for the early detection of fibrotic atrial cardiomyopathy to stratify atrial fibrillation propensity. In this work, we realized 54,000 combinations of different atria and thorax geometries from statistical shape models capturing anatomical variability in the general population. For each atrial model, 10 different volume fractions (0–45%) were defined as fibrotic. Electrophysiological simulations in sinus rhythm were conducted for each model combination and the respective 12-lead ECGs were computed. P wave features (duration, amplitude, dispersion, terminal force in V1) were extracted and compared between the healthy and the diseased model cohorts. All investigated feature values systematically in- or decreased with the left atrial volume fraction covered by fibrotic tissue, however value ranges overlapped between the healthy and the diseased cohort. Using all extracted P wave features as input values, the amount of the fibrotic left atrial volume fraction was estimated by a neural network with an absolute root mean square error of 8.78%. Our simulation results suggest that although all investigated P wave features highly vary for different anatomical properties, the combination of these features can contribute to non-invasively estimate the volume fraction of atrial fibrosis using ECG-based machine learning approaches.

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Tandon, Karman, David Tirschwell, W. T. Longstreth, Bryn Smith, and Nazem Akoum. "Embolic stroke of undetermined source correlates to atrial fibrosis without atrial fibrillation." Neurology 93, no. 4 (June 25, 2019): e381-e387. http://dx.doi.org/10.1212/wnl.0000000000007827.

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ObjectiveTo examine the hypothesis that atrial fibrosis and associated atrial cardiopathy may be in the causal pathway of cardioembolic stroke independently of atrial fibrillation (AF) by comparing atrial fibrosis burden between patients with embolic stroke of undetermined source (ESUS), patients with AF, and healthy controls.MethodsWe used late-gadolinium-enhancement MRI to compare atrial fibrosis in 10 patients with ESUS against 10 controls (no stroke, no AF) and 10 patients with AF. Fibrosis was compared between groups, controlling for stroke risk factors.ResultsMean age was 51 ± 15 years, and 43% of participants were female. Patients with ESUS had more atrial fibrosis than controls (16.8 ± 5.7% vs 10.6 ± 5.7%, p = 0.019) and similar fibrosis compared to patients with AF (17.8 ± 4.8%, p = 0.65). Odds ratios of ESUS per quartile of fibrosis were 3.22 (95% CI [CI] 1.11–9.32, p = 0.031, unadjusted) and 3.17 (95% CI 1.05–9.52, p = 0.041, CHA2DVASc score adjusted). Patients with >12% fibrosis had a higher percentage of ESUS (77.8% vs 27.3%, p = 0.02), and patients with >20% fibrosis had the highest proportion of ESUS (4 of 5).ConclusionsPatients with ESUS exhibit similar atrial fibrosis compared to patients with AF and more fibrosis than healthy controls. Fibrosis is associated with ESUS after controlling for stroke risk factors, supporting the hypothesis that fibrosis is in the causal pathway of cardioembolic stroke independently of AF. Prospective studies are needed to assess the role of anticoagulation in primary and secondary stroke prevention in patients with high atrial fibrosis.

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Більше джерел

Дисертації з теми "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.

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Rationnel et objectif - La fibrillation atriale (FA) est la pathologie rythmique supra-ventriculaire la plus fréquemment diagnostiquée. Le remodelage atrial, qu’il soit électrique ou structurel, conduit à la mise en place et au développement de la cardiomyopathie atriale. La cardiomyopathie atriale est responsable de différentes complications : d’une part mécaniques conduisant à l’augmentation du risque thrombo-embolique et de l’insuffisance cardiaque, d’autre part électriques conduisant à différentes arythmies atriales dont la FA. L’objectif du présent travail est de caractériser les déterminants du remodelage atrial et de leur effet pro-arythmique à l’étage supra-ventriculaire dans la FA. Principaux résultats – Le premier axe de recherche a permis d’objectiver le remodelage induit par le flutter atrial (FLA) chronique à l’aide d’un modèle chronique canin. Le FLA est à l’origine d’un remodelage atrial électrique avec une augmentation de la vulnérabilité à développer de la FA et une diminution des périodes réfractaires effectives (PRE). Cependant, le FLA n’induit pas de remodelage structurel avec notamment l’absence d’augmentation de la durée de FA, de diminution des vitesses de conduction et d’augmentation du processus fibrotique atrial. À noter que la FA chronique, en présence d’un substrat anatomique de FLA, présente des caractéristiques électrophysiologiques originales, en terme de durée de cycle et de d’arythmie et de sa stabilité. De plus, l’ablation du FLA permet de diminuer significativement la durée mais pas la vulnérabilité à présenter des arythmies supra-ventriculaires. Le second axe de recherche a permis de caractériser le rôle différentiel de l’arythmie atriale de la réponse ventriculaire rapide en cas de FA dans le développement du remodelage atrial. Nos travaux ont caractérisé le remodelage atrial induit par l’arythmie atriale isolée en cas de FA : d’une part électrique via la diminution des PRE et l’augmentation de la vulnérabilité ; d’autre part structurel via la diminution des vitesses de conduction et les anomalies des canaux sodiques, des jonctions communicantes et du processus fibrotique. La réponse ventriculaire rapide isolée induit également un remodelage atrial à type d’augmentation de la vulnérabilité, de diminution des vitesses de conduction, d’anomalies modérées du processus fibrotique et des canaux sodiques. À noter une dégradation modérée de la fonction systolique ventriculaire gauche. Cependant, ce remodelage atrial est significativement différent du remodelage induit par l’insuffisance cardiaque. De plus, il existe un effet synergique au niveau du remodelage atrial de l’arythmie atriale et de la fréquence ventriculaire élevée en cas de FA, au niveau du processus fibrotique notamment. Le troisième axe de recherche a permis d’objectiver le rôle de la cilnidipine, un inhibiteur calcique de type N et L, dans la limitation du remodelage atrial en cas de FA chronique, à l’aide d’un modèle aigü et chronique canin. Nos travaux ont caractérisé l’action anti-remodelante de la cilnidipine au niveau électrique, via la limitation de la diminution des PRE, de l’augmentation de la vulnérabilité atriale et de la durée de FA. D’autre part, la cilnidipine semble limiter le remodelage atrial, ce qui est objectivé par la normalisation des vitesses de conduction, de l’expression des canaux sodiques, des jonctions communicantes et de la fibrose tissulaire. La cilnidipine, contrairement aux inhibiteurs calciques de type L tels que la nifédipine, possède une activité anti-remodelante via la modulation de l’activité du système nerveux autonome. Conclusion – Différents facteurs, tels que le flutter atrial, les fréquences atriales et ventriculaires en cas de FA, ont été caractérisés comme déterminants du développement du remodelage atrial. A contrario, la modulation d’un des déterminants du remodelage atrial, le système nerveux autonome via la cilnidipine, permet de de limiter le remodelage atrial secondaire à la FA. Ce travail fournit de nouvelles données sur les mécanismes impliqués dans le remodelage atrial lié à la FA et introduit de nouvelles approches préventives au développement de la FA.
Rational 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.

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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.

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La fibrillation auriculaire est le plus souvent associée à une cardiomyopathie atriale composée de fibrose et d’infiltrats fibro-adipeux. L’identification de cette myopathie atrial en clinique est difficile, l’IRM qui permet l’imagerie tissulaire pourrait être un précieux outil diagnostic de la cardiomyopathie atriale. Méthodes: Etude de la déformation de la paroi libre de l’oreillette gauche (OG) par technique de « tracking IRM » (PLA) réalisée chez 13 patients, 24 heures avant une intervention de chirurgie valvulaire mitrale. 13 patients contrôles ont été inclus. Au cours de l’intervention, un échantillon de paroi libre de l’OG a été recueilli fixé dans le para formaldéhyde puis étudié à l’aide de technique d’histologie et par ex vitro par imagerie IRM. Résultats: La première étude a porté sur la corrélation entre les PLA et l’histologie auriculaire. Un PLA bas a été retrouvé chez les patients porteur d’un valvulopathie mitrale avec une OG remodelée par rapport à la population contrôle (P<0.001). Une corrélation significative a été observée entre la valeur du PLA et le dégrée d’infiltration fibro-adipeux du myocarde auriculaire (r=0.75, P=0.017). La deuxième étude a étudié la capacité de l’imagerie IRM d’analyser les différentes composantes histologiques du myocarde auriculaire. Nous avons établi les différentes séquences d’analyse d’image T2, Dixon qui permettent d’identifié: la fibrose, le myocarde et le tissu adipeux Conclusion : La déformation du myocarde auriculaire est liée au remodelage tissulaire et est un bon biomarqueur de la myopathie atriale. L’imagerie IRM est capable ex vivo d’identifier les différentes composantes histologiques du myocarde auriculaire
Introduction: 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

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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.

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Introduction: Cardiac fibrosis is a pathological response that causes abnormalities in cardiac conduction and mechanical function, thereby contributing to the pathophysiology of a variety of cardiac conditions, including hypertrophy, failure, and arrhythmias. Atrial fibrillation (AF) is the most common sustained clinical arrhythmia and is a major cause of population morbidity and mortality. Recent studies have demonstrated that structural remodeling, involving prominent fibrotic changes, is a fundamental determinant of the perpetuation of AF, and contributes synergistically with electrical remodeling to the AF substrate. Atrial fibrosis is a hallmark feature of arrhythmogenic structural remodeling in clinical AF. Increased amounts of fibrous tissue occur not only in AF patients with identifiable cardiac diseases, but also in those with lone AF.There is a positive correlation between the amount of fibrosis and the persistence of AF,7 suggesting that AF may itself cause structural remodeling that in turn promotes AF. Evidence supporting this idea comes from animal studies showing that even when the ventricular rate is well-controlled, rapid atrial activation causes atrial fibrosis,9 and from work indicating that rapidly-activated atrial-derived cardiomyocytes secrete substances that enhance collagen synthesis by atrial fibroblasts. Methods We studied 60 male adult inbred Fisher rats. We divided the animals in 3 groups of 20 rats each. The first group received vagal stimulation and induce atrial fibrillation protocol (AF + VNS) and follow for 60 days, after 24 h 10 rats were treated with angiotensin II drugs for 60 days (AF + VNS + Ang II). The second group received vagal stimulation (VNS) and follow for 60 days, after after 24 h 10 rats were treated with angiotensin II drugs for 60 days (VNS + Ang II). The third group received induce atrial fibrillation protocol (AF) and follow for 60 days, after 24 h 10 rats were treated with angiotensin II drugs for 60 days (AF + Ang II). Results α1(I) and α1(III) procollagen mRNA levels increased statistically significant in the groups with atrial fibrillation associated or not with VNS in contrast with the group in sinus rhythm. The treatment with Angiotensin II receptor antagonist decrease proportionally in all groups the expression of mRNA levels for ventricular and atrial α1(I) and α1(III) procollagen. The VNS increase the expression of mRNA levels for ventricular and atrial α1(I) and α1(III) procollagen statistically significant between the two group in atrial fibrillation but not statistically significant when the group were treated with Angiotensin II receptor antagonist. The level of right ventricle was almost two time compare with both atria analysis or left ventricle analysis, the VNS increase the level of of mRNA levels for ventricular and atrial α1 (I) and α1(III) procollagen in the right ventricle also in the sinus rhythm group (p=0.5). Conclusion The study demonstrates that long-term VNS in the rats with permanent atria fibrillation induce an increase in cardiac procollagen mRNAs, cardiac fibrosis histologically evident with the presence of inflammatory cells and myocyte necrosis in both groups with atrial fibrillation with statistically significant of the increases in case of VNS; the highest increases of the cardiac procollagen mRNAs was observed in the right ventricle more that in the both atria, this increase was prevented from angiotensine II antagonist receptor therapy. We showed that VNS increased the inducibility of AF. We observed moreover the VNS associates with atrial fibrillation decrease significant the rate ventricular response.

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Moubarak, 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.

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L'ANP est une hormone cardiaque libérée lors de l'insuffisance cardiaque. Les fibroblastes cardiaques, responsables de la synthèse des composants de la matrice extracellulaire (MEC), acquièrent dans les conditions pathologiques la capacité de se différencier en myofibroblastes, conduisant ainsi à une fibrose cardiaque. Les mécanismes de régulation impliquant l'ANP et ses récepteurs (NPR) restent peu connus et font l'objet de ce travail. Les fibroblastes ventriculaires ont été isolés à partir de coeurs de rats Wistar et mis en culture afin d'induire leur différenciation. Les cultures ont ensuite été soumises à différents traitements impliqués dans la voie ANP/NPR. L'ANP diminue le taux de prolifération, la migration cellulaire, et la sécrétion de collagène des myofibroblastes. Cet effet est mimé par le 8-Br-GMPc. L'analyse protéomique et génomique a permis de confirmer la présence des récepteurs natriurétiques A et B dans nos cellules. Par ailleurs, l'expression de dix isoformes de phosphodiestérases dans les myofibroblastes a été révélée par un criblage génomique. L'inhibition non sélective de ces phosphodiestérases provoque une diminution de la prolifération et de la sécrétion de collagène. Enfin, les concentrations intracellulaires de GMPc et d'AMPc ont été trouvées augmentées en présence de l'ANP. En parallèle, la caractérisation des courants ioniques présents sur les myofibroblastes a montré une absence des courants sodique rapide et potassique ATP-dépendant. Cette étude montre le rôle de la voie ANP/NPR/GMPc dans la modulation des propriétés fibroblastiques et illustre la complexité des processus de différenciation cellulaire au cours de la fibrogenèse cardiaque
ANP 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

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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/.

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La tesi descrive il T1 mapping, un metodo diagnostico non invasivo emergente per l’identificazione e la quantificazione della fibrosi atriale. Nel primo capitolo ci si è soffermati sulle caratteristiche del tessuto fibrotico e sulle cause che generano tale patologia tra cui la fibrillazione atriale. Nel secondo capitolo vengono descritte le tecniche non invasive comunemente più utilizzate per la valutazione della fibrosi tra cui: sistemi di mappaggio elettronanatomico e risonanza magnetica cardiaca con l’uso di mezzo di contrasto. Nel terzo capitolo sono approfondite tutte le sequenze necessarie per la costruzione di mappe di tempi T1 indagando anche sui fattori a cui la tecnica è più sensibile. Infine è stato dedicato ampio spazio a ricerche mediche sulla correlazione tra i tempi T1 delle camere cardiache, i potenziali elettroanatomici delle stesse e la probabilità di sviluppare fibrillazioni atriali recidive in alcuni pazienti sottoposti ad ablazione transcatetere.

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Leonardi, 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/.

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Questo lavoro di tesi si è svolto in collaborazione con le Unità Operative di Cardiologia e di Radiologia dell’ospedale “M. Bufalini” di Cesena e della St. Jude Medical, Inc., con l’obiettivo di sviluppare e implementare un metodo per l’identificazione e la valutazione della fibrosi atriale mediante risonanza magnetica in pazienti con fibrillazione atriale, candidati a procedura di ablazione. I pazienti sono stati sottoposti all’esame di risonanza magnetica (RM) angio per la valutazione della morfologia atriale e alla DE-MRI per l’identificazione e la visualizzazione delle zone di alto enhancement sulla struttura 3D dell’atrio sinistro, ossia le zone di alta intensità corrispondenti alla fibrosi. La struttura anatomica è utile all’elettrofisiologo per conoscere la morfologia dell’atrio e delle vene polmonari, permettendo quindi di minimizzare l’uso della fluoroscopia durante la procedura di ablazione. La conoscenza dei siti e della quantificazione della fibrosi è vantaggiosa per il medico per la pianificazione preoperatoria, in quanto nei pazienti con molta fibrosi non è sufficiente l’isolamento delle vene polmonari, ma si ottengono risultati migliori effettuando un’ablazione estensiva della parete atriale. Inoltre gli studi in letteratura hanno dimostrato che i pazienti con un’estensione di fibrosi superiore al 35% della superficie atriale, hanno una probabilità superiore al 50% di soffrire nuovamente di fibrillazione atriale dopo la procedura di ablazione; lo studio della fibrosi atriale vuole quindi essere un metodo per predire se l’ablazione avrà successo, oppure se è preferibile seguire indicazioni terapeutiche diverse. Il primo passo di questo lavoro è stata la registrazione delle immagini angio-RM e DE-MR mediante il software VolView. Successivamente si è implementato un programma in Matlab per segmentare in modo automatico l’atrio sinistro e si è visualizzata la struttura tridimensionale con la mappa cromatica della fibrosi utilizzando il software ParaView. Infine per validare questo lavoro si è effettuato un confronto qualitativo dei risultati ottenuti con il mappaggio elettro-anatomico acquisito mediante il sistema EnSite Velocity della St. Jude Medical, Inc. durante la procedura di ablazione transcatetere. Per eseguire questo confronto è stato necessario interfacciare il nostro lavoro con il sistema EnSite Velocity, con lo scopo di riuscire a visualizzare le mappe elettro-anatomiche sul nostro sistema e di importare la nostra struttura anatomica nel loro.

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Margara, 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/.

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La Fibrillazione Atriale (FA) è una delle aritmie più frequentemente riscontrate nella pratica clinica, ma i meccanismi che la generano e che la sostengono non sono ancora oggi ben chiari. L’obiettivo di questo lavoro di tesi è indagare il substrato aritmogeno della FA con particolare attenzione al legame tra rimodellamento elettrico e strutturale. La tecnica di riferimento per la valutazione della fibrosi è la risonanza magnetica con iniezione di mezzo di contrasto e acquisizione ritardata. Tipicamente, però, la presenza di fibrosi viene valutata durante la procedura di ablazione transcatetere mediante l’analisi dei potenziali elettrici rilevati, considerando le zone a basso potenziale indicative della presenza di alterazioni strutturali. In questo lavoro sono stati elaborati dati di Risonanza Magnetica (RM), in particolare sequenze Angio-RM e DE-RM. Dalle sequenze Angio-RM è stato ricostruito un modello 3D paziente-specifico dell’atrio, mentre dalle sequenze DE-RM sono state ricavate informazioni relative alla presenza di tessuto atriale fibrotico. Al modello 3D è stata poi sovrapposta l’informazione sull’intensità di grigio del dato DE-RM per poter visualizzare la localizzazione delle zone di fibrosi sulla superficie 3D dell’atrio.  Sono stati anche esportati dal sistema di mappaggio elettroanatomico EnSite NavX (St. Jude Medical) i dati relativi alla geometria dell’atrio e ai potenziali registrati durante lo svolgimento della procedura di ablazione. Da questi dati è stato possibile ricostruire in ambiente Matlab le mappe di voltaggio raffiguranti i potenziali registrati durante la procedura. Per poter studiare e valutare il legame esistente tra rimodellamento elettrico e strutturale, sono state confrontate le mappe di voltaggio e le superfici raffiguranti fibrosi.  Questo lavoro di tesi è stato svolto in collaborazione con l’U.O. di Cardiologia dell’Ospedale Bufalini di Cesena e la St. Jude Medical.

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Onofri, 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/.

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In questo studio si è sviluppato un nuovo algoritmo per la segmentazione dell'endocardio atriale sinistro, per pazienti affetti da fibrillazione atriale. A differenza delle convenzionali tecniche di segmentazione, si è fatto uso di una rete neurale convoluzionale chiamata U-Net, che è stata appositamente addestrata in modo supervisionato e testata, con dati MRI-GE e relativa etichetta di segmentazione binaria, dei volumi appartenenti a 154 pazienti diversi. Per l'addestramento si è fatto uso dei volumi di 123 pazienti (80%) e 31 pazienti sono dedicati al test (20%). Le CNN richiedono molto tempo per l'addestramento (ore) mentre hanno un funzionamento feed-foreward, con velocità di calcolo algebrico nella fase di test. I dati grezzi in uscita dalla rete, sono stati post-elaborati al fine di ottenere una purificazione dalle formazioni di volume spurio, ossia non connessi con il volume endocardico atriale sinistro (LAE). In questo studio si disponeva anche della segmentazione semantica binaria manuale delle immagini di test, le quali sono state considerate il gold standard di riferimento. Si è visualizzata la registrazione tra il volume binario di riferimento ed il volume in uscita della rete purificato per un confronto qualitativo e per l'applicazione di metriche per eseguire una analisi quantitativa, come il coefficiente di Dice e la distanza di Hausdorff. Queste misure vengono estratte e se ne produce una tabella. Sulla base di questi risultati si è potuto eseguire un'analisi statistica per esaminare il funzionamento globale della rete sulla base di variabili statistiche come la media e deviazione standard, pesati sulla base della dimensione del volume di ogni paziente e calcolati sull'errore inteso come differenza tra i due volumi. In termini globali la rete ha generalizzato bene per tutti i pazienti. Con una media di 12,2 cm^3 ed una deviazione standard 11,7 cm^3 la rete ha dimostrato di avere una tendenza a sovrastimare il d

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Cacciatore, Angela [Verfasser], and 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.

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Baliga, 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.

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Thesis (Ph. D.)--Ohio State University, 2004.
Document 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.

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Книги з теми "Atriale fibrosis"

Haugaa, Kristina H., Francesco Faletra, and João L. Cavalcante. Cardiac rhythm disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0063.

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Cardiac rhythm disorders require diagnostic, prognostic, and guidance of therapeutic procedures by echocardiography. The most common sustained cardiac arrhythmia is atrial fibrillation (AF) leading to an increased risk for mortality, heart failure, and thromboembolic events. Echocardiography is performed to assess the aetiology of AF which most commonly is associated with diseases leading to enlarged atria. Furthermore, echocardiography is crucial to evaluate thromboembolic risk by assessing the morphology and function of the left atrial appendage among other parameters. Non-invasive imaging modalities including two-dimensional transthoracic (TTE) and transoesophageal echocardiography (TOE) with three-dimensional imaging are often indicated. Finally, TOE can help in the preprocedural planning and providing guidance for interventions such as pulmonary vein ablation and percutaneous left atrial appendage closure. In patients with ventricular arrhythmias, TTE is the first-line diagnostic tool for assessing the aetiology of ventricular arrhythmias. Ischaemic heart disease, either acute or chronic fibrosis, is the most common causes of ventricular tachycardias. Left ventricular ejection fraction remains the most important parameter for indication of an implantable cardioverter defibrillator for primary prevention therapy, although newer strain echocardiographic measures may add incremental prognostic information.

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Sánchez-Quintana, Damián, and José Angel Cabrera. Normal atrial and ventricular myocardial structures. Edited by Yen Ho. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0014.

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The heart functions by means of a three-dimensional arrangement of myofibres supported by an extracellular matrix which plays an important role in maintaining the size and shape of the heart. In both atria, the structure of the walls and the atrial septum confers a three-dimensional arrangement of muscle bundles and myoarchitecture that allows preferential electrical intra- and interatrial conduction which is important for a better understanding of atrial activation and arrhythmias. The myoarchitecture within the ventricular walls has a three-dimensional arrangement of myofibres, within a supporting matrix of fibrous tissue, which changes orientation from being oblique in the subepicardium to circumferential in the middle and to longitudinal in the subendocardium, allowing the chambers to change in shape and size through the cardiac cycle. Within each ventricle, the circumferential portion is the thickest transmurally, with the longitudinal portion the thinnest. The three-dimensional arrangement of the ventricular mesh serves to realign the myocytes during ventricular contraction, accounting for the extent of systolic mural thickening. Abnormal myoarchitecture in combination with alterations in the connective tissue matrix provide the structural basis for abnormalities in myocardial function.

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Частини книг з теми "Atriale fibrosis"

Kottkamp, Hans, Andreas Rieger, Fabian Moser, and Christian Poenisch. "Fibrotic Atrial Cardiomyopathy." In Cardiac Mapping, 628–34. Chichester, UK: John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119152637.ch50.

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Navaravong, Leenhapong, and Nassir F. Marrouche. "Magnetic Resonance Imaging Mapping of Atrial Fibrosis and Atrial Fibrillation." In Cardiac Mapping, 618–27. Chichester, UK: John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119152637.ch49.

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Zhao, Jichao, Robert S. Stephenson, Greg B. Sands, Ian J. LeGrice, Henggui Zhang, Jonathan C. Jarvis, and Bruce H. Smaill. "Atrial Fibrosis and Atrial Fibrillation: A Computer Simulation in the Posterior Left Atrium." In 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.

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Wu, Fuping, Lei Li, Guang Yang, Tom Wong, Raad Mohiaddin, David Firmin, Jennifer Keegan, Lingchao Xu, and Xiahai Zhuang. "Atrial Fibrosis Quantification Based on Maximum Likelihood Estimator of Multivariate Images." In 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.

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Ramirez, Alexies, and Nassir F. Marrouche. "Role of Late Gadolinium-Enhanced Magnetic Resonance Imaging in Detection and Quantification of Atrial Fibrosis." In Cardiac Mapping, 656–63. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118481585.ch60.

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Palacio, Laura C., Juan P. Ugarte, Javier Saiz, and Catalina Tobón. "Genesis of Atrial Fibrillation Under Different Diffuse Fibrosis Density Related with Atmospheric Pollution. In-Silico Study." In 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.

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Yang, 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." In 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.

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Huang, Chao, Stephen L. Wasmund, Takanori Yamaguchi, Nathan Knighton, Robert W. Hitchcock, Irina A. Polejaeva, Kenneth L. White, Nassir F. Marrouche, and Frank B. Sachse. "Towards Automated Quantification of Atrial Fibrosis in Images from Catheterized Fiber-Optics Confocal Microscopy Using Convolutional Neural Networks." In 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.

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Rosenberg, Michael A. "Circulating Fibrosis Biomarkers and Cardiovascular Health: Disease-Focused Approach in Heart Failure, Arrhythmias, Sudden Cardiac Death, and Atrial Fibrillation." In Biomarkers in Cardiovascular Disease, 1–34. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7741-5_48-1.

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Van Wagoner, David R. "Mechanisms of atrial remodelling." In ESC CardioMed, 2125–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0498.

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The atria serve a combination of reservoir, sensor, and neuroendocrine roles that help the heart to adapt to variations in blood volume, heart rate, and ventricular filling. When stressed by high-rate activity or increased haemodynamic load (due to hypertension, valve disease, or heart failure), the atria respond with increased oxidant production (oxidative stress) that promotes transcriptional changes that reversibly remodel electromechanical activity, with shortened action potential duration and effective refractory period, slowed and heterogeneous conduction, and impaired contractility. When the stresses persistent, the atria undergo persistent structural changes including chamber dilatation and increased interstitial fibrosis. The combination of electrical and structural remodelling leads to increased risk and persistence of atrial fibrillation and stroke. Accumulation of dysfunctional proteins that are normally recycled by the proteasome may contribute to the susceptibility to development of atrial fibrillation. Changes in ion channel expression are most often associated with the development of persistent atrial fibrillation. While many atrial fibrillation therapies have focused on targeting of atrial ion channels, efforts to target atrial proteostasis may have promise as a therapeutic atrial fibrillation treatment or prevention strategy.

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Тези доповідей конференцій з теми "Atriale fibrosis"

Tang, Xin, Piyush Bajaj, Rashid Bashir, and Taher Saif. "Mechanical Communication Between Cardiac Cell Leads to Synchrony in Beating." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80937.

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It is generally understood that cardiac cells synchronize their beating through electro-chemical signalling. Here we show, theoretically and experimentally, that isolated cardiac cells can communicate with each other through an intervening deformable media. Such communication leads to coupled dynamics and emergence of synchronous beating. The interaction between the cells depends inversely with the elastic modulus of the media, and the distance between them. This finding may explain asynchronous beating of the atrium in patients with atrial fibrillation where the stiffness of the atrial wall becomes significantly harder due to fibrosis [1].

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Di Martino, Elena S., Chiara Bellini, Dale J. Ward, Nicolas Brown, and David Schwartzman. "Porcine Left Atrial Wall Stress After Ventricular Tachypacing Mimicking the Effects of Early Atrial Fibrillation." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19528.

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Atrial Fibrillation (AF) is the cardiac arrhythmia most commonly encountered in clinical practice. Current statistics referring to the US population indicate a prevalence of AF up to 2.2 million people, projected to increase to 2.66 million by the end of 2010. AF has a high impact on society in terms of human costs, with an annual mortality rate of 11,438 patients. AF also increases the risk of ischemic stroke at least by a factor of 4 and it is responsible for at least 15% of all ischemic strokes, which represent the main cause of long-term disability and one of the main contributors to health care costs [1]. AF results from the synergic action of electrophysiological, biochemical and structural remodeling. Ventricular tachypacing (VTP) has been successfully used in animal models to reproduce relevant features observed in patients suffering from AF, such as ion-channel alterations, fibrosis development and atrial dilatation [2] [3].

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Schiatti, "Teresa, Marilu Casini, Thomas Hutschalik, Manuel Koch, Ramona Emig, Remi Peyronnet, and Ursula Ravens." "Impact of Mechanically-Induced Fibrosis on Atrial Electromechanical Function." In 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.426.

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Ogbomo-Harmitt, "Shaheim, Ahmed Qureshi, Andrew P. King, and Oleg Aslanidi." "Impact of Fibrosis Border Zone Characterisation on Fibrosis-Substrate Isolation Ablation Outcome for Atrial Fibrillation." In 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.218.

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Ranjan, Ravi, Elyar Ghafoori, Roya Kamali, Eugene Kwan, Kennosuke Yamashita, Rob MacLeod, and Derek Dosdall. "Regions of High Dominant Frequency in Chronic Atrial Fibrillation Anchored to Areas of Atrial Fibrosis." In 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.403.

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Riccio, Jennifer, Sara Rocher, Laura Martinez, Alejandro Alcaine, Javier Saiz, Juan Pablo Martínez, and Pablo Laguna. "Unipolar Electrogram Eigenvalue Distribution Analysis for the Identification of Atrial Fibrosis." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.434.

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Roney, Caroline, Jason Bayer, R�mi Dubois, Marianna Meo, Hubert Cochet, Pierre Ja�s, and Edward Vigmond. "The Combination of Pulmonary Vein Electrophysiology and Atrial Fibrosis Determines Driver Location." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.374-228.

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van Montfoort, "Margot, Victor G. Marques, Ozan Özgül, Ali Gharaviri, Simone Pezzuto, Angelo Auricchio, Pietro Bonizzi, Ulrich Schotten, and Stef Zeemering." "Fibrosis Reduces the Coincidence of Repetitive Activations Patterns between the Coronary Sinus and Atrial Regions in Simulated Atrial Fibrillation." In 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.155.

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Pelloni, Samuele, Michela Mase, Alessandro Cristoforetti, and Flavia Ravelli. "Modeling fibrosis distribution for the study of wave propagation patterns during atrial fibrillation." In 2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2014. http://dx.doi.org/10.1109/esgco.2014.6847528.

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Gharaviri, Ali, Mark Potse, Sander Verheule, Rolf Krause, Angelo Auricchio, and Ulrich Schotten. "Epicardial Fibrosis Explains Increased Transmural Conduction in a Computer Model of Atrial Fibrillation." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.071-216.

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