Relevant bibliographies by topics / Atriale remodeling

Academic literature on the topic 'Atriale remodeling'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Atriale remodeling"

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Liu, Lei, Jianqiang Geng, Hongwei Zhao, Fengxiang Yun, Xiaoyu Wang, Sen Yan, Xue Ding, et al. "Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway." Cellular Physiology and Biochemistry 36, no. 5 (2015): 2039–50. http://dx.doi.org/10.1159/000430171.

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Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.
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Błaszczyk, Robert, and Mateusz Kłoda. "Genetic basis of atrial firbrillation – the role of microRNA." In a good rythm 3, no. 60 (December 30, 2021): 18–23. http://dx.doi.org/10.5604/01.3001.0015.7297.

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Atrial fibrillation is the most common arrhythmia in adults. In addition to the well-known cardiovascular risk factors, the role of genetic factors in the pathogenesis of atrial fibrillation is emphasized. MicroRNAs are a group of small, endogenous, single-stranded, non-coding RNAs, 20-22 nucleotides long, whose task is to regu­late gene expression at the post-transcriptional level. Changes in the expression of microRNAs in circulating blood and tissues lead to the development of cardiovascular diseases, including atrial fibrillation, leading to the remodeling of the heart muscle. Different types of remodeling, such as electrical remodelling, struc­tural remodeling, autonomic nerve remodelling, calcium handling abnormalities and single nucleotide polymorphisms in microRNA and related genes are responsible for the development and maintenance of atrial fibrillation. This paper presents the most important microRNAs that regulate genes that influence atrial fibrillation and thus may induce arrhythmia.
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Xie, Lai-Hua, Mayilvahanan Shanmugam, Ji Yeon Park, Zhenghang Zhao, Hairuo Wen, Bin Tian, Muthu Periasamy, and Gopal J. Babu. "Ablation of sarcolipin results in atrial remodeling." American Journal of Physiology-Cell Physiology 302, no. 12 (June 15, 2012): C1762—C1771. http://dx.doi.org/10.1152/ajpcell.00425.2011.

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Sarcolipin (SLN) is a key regulator of sarco(endo)plasmic reticulum (SR) Ca2+-ATPase (SERCA), and its expression is altered in diseased atrial myocardium. To determine the precise role of SLN in atrial Ca2+ homeostasis, we developed a SLN knockout ( sln−/−) mouse model and demonstrated that ablation of SLN enhances atrial SERCA pump activity. The present study is designed to determine the long-term effects of enhanced SERCA activity on atrial remodeling in the sln−/− mice. Calcium transient measurements show an increase in atrial SR Ca2+ load and twitch Ca2+ transients. Patch-clamping experiments demonstrate activation of the forward mode of sodium/calcium exchanger, increased L-type Ca2+ channel activity, and prolongation of action potential duration at 90% repolarization in the atrial myocytes of sln−/− mice. Spontaneous Ca2+ waves, delayed afterdepolarization, and triggered activities are frequent in the atrial myocytes of sln−/− mice. Furthermore, loss of SLN in atria is associated with increased interstitial fibrosis and altered expression of genes encoding collagen and other extracellular matrix proteins. Our results also show that the sln−/− mice are susceptible to atrial arrhythmias upon aging. Together, these findings indicate that ablation of SLN results in increased SERCA activity and SR Ca2+ load, which, in turn, could cause abnormal intracellular Ca2+ handling and atrial remodeling.
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Biliczki, Peter, Reinier A. Boon, Zenawit Girmatsion, Alicia Bukowska, Balázs Ördög, Bernhard M. Kaess, Stefan H. Hohnloser, et al. "Age-related regulation and region-specific distribution of ion channel subunits promoting atrial fibrillation in human left and right atria." EP Europace 21, no. 8 (May 25, 2019): 1261–69. http://dx.doi.org/10.1093/europace/euz135.

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Abstract Aims Age-induced changes and electrical remodelling are important components of the atrial fibrillation (AF) substrate. To study regional distribution and age-dependent changes in gene expression that may promote AF in human atria. Methods and results Human left atrial (LA) and right atrial (RA) tissue samples were obtained from donor hearts unsuitable for transplantation and from patients undergoing mitral valve repair. Atrial fibrillation was mimicked in vitro by tachypacing of human atrial tissue slices. Ionic currents were studied by the whole-cell patch-clamp technique; gene expression was analysed by real-time qPCR and immunoblotting. Both healthy RA and RA from older patients showed greater CACNA1c mRNA and CaV1.2 protein expression than LA. No age-dependent changes of Kir2.1 expression in both atria were seen. Remodelling occurred in a qualitatively similar manner in RA and LA. IK1 and Kir2.1 protein expression increased with AF. MiR-1, miR-26a, and miR-26b were down-regulated with AF in both atria. ICa,L was decreased. CACNA1c and CACNA2b expression decreased and miR-328 increased in RA and LA during AF. Ex vivo tachypacing of human atrial slices replicated these findings. There were age-dependent increases in miR-1 and miR-328, while miR-26a decreased with age in atrial tissues from healthy human donor hearts. Conclusion Features of electrical remodelling in man occur in a qualitatively similar manner in both human atria. Age-related miR-328 dysregulation and reduced ICa,L may contribute to increased AF susceptibility with age.
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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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Baba, Shigeo, Wen Dun, Masanori Hirose, and Penelope A. Boyden. "Sodium current function in adult and aged canine atrial cells." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 2 (August 2006): H756—H761. http://dx.doi.org/10.1152/ajpheart.00063.2006.

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The incidence of atrial fibrillation increases with age, but it is unknown whether there are changes in the intrinsic function of Na+ currents in cells of the aged atria. Thus, we studied right (RA) and left (LA) atrial cells from two groups of dogs, adult and aged (>8 yr), to determine the change in Na+ currents with age. In this study all dogs were in normal sinus rhythm. Whole cell voltage clamp techniques were used to compare the Na+ currents in the two cell groups. Immunocytochemical studies were completed for the Na+ channel protein Nav1.5 to determine whether there was structural remodeling of this protein with age. In cells from aged animals, we found that Na+ currents are similar to those we measured in adult atria. However, Na+ current ( INa) density of the aged atria differed depending on the atrial chamber with LA cell currents being larger than RA cell currents. Thus with age, the difference in INa density between atrial chambers remains. INa kinetic differences between aged and adult cells included a significant acceleration into the inactivated state and an enhanced use-dependent decrease in peak current in aged RA cells. Finally, there is no structural remodeling of the cardiac Na+ channel protein Nav1.5 in the aged atrial cell. In conclusion, with age there is no change in INa density, but there are subtle kinetic differences contributing to slight enhancement of use dependence. There is no structural remodeling of the fast Na+ current protein with age.
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Everett, Thomas H., Emily E. Wilson, Sander Verheule, Jose M. Guerra, Scott Foreman, and Jeffrey E. Olgin. "Structural atrial remodeling alters the substrate and spatiotemporal organization of atrial fibrillation: a comparison in canine models of structural and electrical atrial remodeling." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (December 2006): H2911—H2923. http://dx.doi.org/10.1152/ajpheart.01128.2005.

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Several animal models of atrial fibrillation (AF) have been developed that demonstrate either atrial structural remodeling or atrial electrical remodeling, but the characteristics and spatiotemporal organization of the AF between the models have not been compared. Thirty-nine dogs were divided into five groups: rapid atrial pacing (RAP), chronic mitral regurgitation (MR), congestive heart failure (CHF), methylcholine (Meth), and control. Right and left atria (RA and LA, respectively) were simultaneously mapped during episodes of AF in each animal using high-density (240 electrodes) epicardial arrays. Multiple 30-s AF epochs were recorded in each dog. Fast Fourier transform was calculated every 1 s over a sliding 2-s window, and dominant frequency (DF) was determined. Stable, discrete, high-frequency areas were seen in none of the RAP or control dogs, four of nine MR dogs, four of six CHF dogs, and seven of nine Meth dogs in either the RA or LA or both. Average DFs in the Meth model were significantly greater than in all other models in both LA and RA except LA DFs in the RAP model. The RAP model was the only one with a consistent LA-to-RA DF gradient (9.5 ± 0.2 vs. 8.3 ± 0.3 Hz, P < 0.00005). The Meth model had a higher spatial and temporal variance of DFs and lower measured organization levels compared with the other AF models, and it was the only model to show a linear relationship between the highest DF and dispersion ( R2 = 0.86). These data indicate that structural remodeling of atria (models known to have predominantly altered conduction) leads to an AF characterized by a stable high-frequency area, whereas electrical remodeling of atria (models known to have predominantly shortened refractoriness without significant conduction abnormalities) leads to an AF characterized by multiple high-frequency areas and multiple wavelets.
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Schotten, Ulrich, Sander Verheule, Paulus Kirchhof, and Andreas Goette. "Pathophysiological Mechanisms of Atrial Fibrillation: A Translational Appraisal." Physiological Reviews 91, no. 1 (January 2011): 265–325. http://dx.doi.org/10.1152/physrev.00031.2009.

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Atrial fibrillation (AF) is an arrhythmia that can occur as the result of numerous different pathophysiological processes in the atria. Some aspects of the morphological and electrophysiological alterations promoting AF have been studied extensively in animal models. Atrial tachycardia or AF itself shortens atrial refractoriness and causes loss of atrial contractility. Aging, neurohumoral activation, and chronic atrial stretch due to structural heart disease activate a variety of signaling pathways leading to histological changes in the atria including myocyte hypertrophy, fibroblast proliferation, and complex alterations of the extracellular matrix including tissue fibrosis. These changes in electrical, contractile, and structural properties of the atria have been called “atrial remodeling.” The resulting electrophysiological substrate is characterized by shortening of atrial refractoriness and reentrant wavelength or by local conduction heterogeneities caused by disruption of electrical interconnections between muscle bundles. Under these conditions, ectopic activity originating from the pulmonary veins or other sites is more likely to occur and to trigger longer episodes of AF. Many of these alterations also occur in patients with or at risk for AF, although the direct demonstration of these mechanisms is sometimes challenging. The diversity of etiological factors and electrophysiological mechanisms promoting AF in humans hampers the development of more effective therapy of AF. This review aims to give a translational overview on the biological basis of atrial remodeling and the proarrhythmic mechanisms involved in the fibrillation process. We pay attention to translation of pathophysiological insights gained from in vitro experiments and animal models to patients. Also, suggestions for future research objectives and therapeutical implications are discussed.
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Antipov, G. N., A. S. Postol, S. N. Kotov, M. O. Makarova, and Yu A. Shneider. "Atrial remodelling comparison after maze-3 and cryo-maze procedures in combined cardiac interventions: a retrospective study." Kuban Scientific Medical Bulletin 29, no. 2 (March 27, 2022): 14–27. http://dx.doi.org/10.25207/1608-6228-2022-29-2-14-27.

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Background. The maze procedure aims to eliminate atrial fibrillation (AF), restore sinus rhythm (SR) and atrial contractility. However, conflicting evidence exists regarding the extent of atrial remodelling in various techniques, which directed the focus of our study.Objectives. An atrial remodelling comparison after a cut-and-sew maze-3 surgery and its biatrial cryo-maze modification using 2D echocardiography.Methods. The study is a retrospective uncontrolled interrupted two-cohort time-series trial, with patients selected by pseudorandomisation according to a normal sinus rhythm-maintaining AF surgery method. A total of 217 maze-3 and 113 cryo-maze combined cardiac interventions have been performed within 2012–2021. The interventions included valve repair, coronary artery bypass grafting and their combination. Due to differences in long-term follow-up, the cohorts were pseudorandomised to select by 50 restored vs. maintained sinus rhythm patients using a nearest-neighbour classifier coupled with logistic regression. Mean follow-up period was 6 (1–17) months. The patients had paroxysmal, persistent and longstanding persistent AF. Echocardiography values prior to and long-term post-surgery were further analysed to determine the atrial remodelling dynamics. Results. A statistically significant atrial volume reduction is evident in a long-term within-cohort comparison. Meanwhile, a statistically more pronounced remodelling is observed between cohorts after maze-3 procedure. The cohort 1 vs. 2 estimates are: mean left atrial volume 120/125 mL3 (p = 0.011), left atrial size in apical view 52/53 mm (p = 0.023), right atrial size in apical view 58/62 mm (p = 0.004), right atrial size in parasternal short axis view 43/45 mm (p = 0.004), right atrial area in apical 4-chamber view 25/28 cm2 (p = 0.007). Maintained atrial pacing patients had positive systolic atrial function recovery rates (E/A ratio increased to average 1.5) in the long-term in both comparison cohorts.Conclusion. Remodelling is biatrial after all the maze procedures compared. A more pronounced atrial volume reduction occurs after maze-3 surgery. The presence of sinus rhythm is facilitated by cardiac conduction leading to mechanical and electrical remodelling of the atria.
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Etzion, Yoram, Michal Mor, Aryeh Shalev, Shani Dror, Ohad Etzion, Amir Dagan, Ofer Beharier, Arie Moran, and Amos Katz. "New insights into the atrial electrophysiology of rodents using a novel modality: the miniature-bipolar hook electrode." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1460—H1469. http://dx.doi.org/10.1152/ajpheart.00414.2008.

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Studies of atrial electrophysiology (EP) in rodents are challenging, and available data are sparse. Herein, we utilized a novel type of bipolar electrode to evaluate the atrial EP of rodents through small lateral thoracotomy. In anesthetized rats and mice, we attached two bipolar electrodes to the right atrium and a third to the right ventricle. This standard setup enabled high-resolution EP studies. Moreover, a permanent implantation procedure enabled EP studies in conscious freely moving rats. Atrial EP was evaluated in anesthetized rats, anesthetized mice (ICR and C57BL6 strains), and conscious rats. Signal resolution enabled atrial effective refractory period (AERP) measurements and first time evaluation of the failed 1:1 atrial capture, which was unexpectedly longer than the AERP recorded at near normal cycle length by 27.2 ± 2.3% in rats ( P < 0.0001; n = 35), 31.7 ± 8.3% in ICR mice ( P = 0.0001; n = 13), and 57.7 ± 13.7% in C57BL6 mice ( P = 0.015; n = 4). While AERP rate adaptation was noted when 10 S1s at near normal basic cycle lengths were followed by S2 at varying basic cycle length and S3 for AERP evaluation, such rate adaptation was absent using conventional S1S2 protocols. Atrial tachypacing in rats shortened the AERP values on a timescale of hours, but a reverse remodeling phase was noted thereafter. Comparison of left vs. right atrial pacing in rats was also feasible with the current technique, resulting in similar AERP values recorded in the low right atrium. In conclusion, our findings indicate that in vivo rate adaptation of the rodent atria is different than expected based on previous ex vivo recordings. In addition, atrial electrical remodeling of rats shows unique remodeling-reverse remodeling characteristics that are described here for the first time. Further understanding of these properties should help to determine the clinical relevance as well as limitations of atrial arrhythmia models in rodents.
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Dissertations / Theses on the topic "Atriale remodeling"

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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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Grabowski, Carsten [Verfasser], Andreas [Gutachter] Mügge, and Axel [Gutachter] Meissner. "Der Einfluss der Therapie mit kontinuierlich positivem Atemwegsdruck bei OSAS-Patienten auf das atriale Remodeling / Carsten Grabowski ; Gutachter: Andreas Mügge, Axel Meissner." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1136131841/34.

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Jesel-Morel, Laurence. "Sénescence, remodelage tissulaire et membranaire, risque thrombotique au cours de la fibrillation auriculaire." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ051/document.

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Nos travaux montrent qu’au cours de la fibrillation atriale (FA), les microparticules (MP) reflètent et contribuent à un état d’hypercoagulabilité et pro-inflammatoire. Leurs concentrations similaires dans les deux oreillettes de patients en FA témoignent d’une absence de différence de statut pro-thrombotique entre ces deux cavités cardiaques. Au cours des procédures d’ablation de FA, les concentrations de MP évoluent parallèlement à l’augmentation de l’activation cellulaire et plaquettaire. Nous avons également montré dans l'altération tissulaire des oreillettes en FA, l'importance de la sénescence qui évolue avec la progression du trouble du rythme. Nous avons caractérisé un modèle cellulaire de sénescence réplicative de cellules endothéliales auriculaires de porc permettant d'identifier l'apparition d'un phénotype pro-thrombotique, pro-inflammatoire, pro-adhésif et de mieux comprendre la physiologie de la cellule endothéliale atriale sénescente et le rôle majeur du système rénine-angiotensine dans ces mécanismes
Our data evidence that during atrial fibrillation (AF), microparticles (MP) contribute to an enhanced hypercoagulable and pro-inflammatory state. Similar concentrations of MP measured in left and right atria of AF patients highlight the absence of chamber-specific enhanced thrombogenic status. During AF ablation procedures, MP concentrations progress in parallel with cell and platelet activation. We also showed that AF progression is strongly related to human atrial senescence burden pointing toward a possible network that links in human atrium, senescence burden, endothelial dysfunction, thrombogenicity and atrial remodeling. We also developed a model of left atrium endothelial cell replicative senescence providing compelling evidences indicating that atrial endothelial senescence promotes thrombogenicity, inflammation and proteolysis. These data underline the major role of renin-angiotensin system in endothelial atrial cell senescence
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Cardin, Sophie. "Molecular mechanisms underlying atrial remodeling." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103457.

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Atrial fibrillation (AF) is the most sustained arrhythmia in the population and is associated with increased morbidity and mortality. A variety of cardiac disease entities, including valve disease, cardiomyopathies, hypertension and diabetes increase the risk of AF. However, present drug therapies are ineffective and can even increase the risk of dangerous ventricular tachyarrhythmias. Studies in animal models show that AF is associated with atrial remodeling that favors AF induction and maintenance. The mechanisms of atrial remodeling depend on the underlying pathology. Atrial remodeling caused by atrial tachycardia or AF itself is primarily electrical, associated with changes in the expression and function of ion channels. These changes are reflected in decreased atrial refractory periods, impaired refractoriness adaptation to rate and conduction slowing. Together, these electrical changes increase the incidence of AF. Heart failure (HF), an important cause of AF, induces another type of atrial remodeling. HF-remodeling is characterized by conduction heterogeneity and altered atrial structural properties. In particular, interstitial fibrosis plays a major role in the stabilization of reentry circuits and prolongation of AF duration.Although many studies have described a large number of the changes associated with each form of remodeling, the underlying mechanisms remain poorly understood. The goal of this thesis was to clarify the molecular mechanisms underlying the atrial remodeling associated with AF. In my first study, I put forward the hypothesis that atrial remodeling caused by atrial tachycardia and that resulting from HF differ in terms of the time course and nature of underlying changes in cardiac gene expression. I indeed discovered that the changes in gene expression induced by atrial tachycardia and HF were qualitatively different and evolved differently over time. The changes by atrial tachycardia were limited and showed time-dependent adaptation, whereas the changes induced by HF were qualitatively greater and more varied, and showed qualitative evolution with the development of the pathology. In my second study, I put forward the hypothesis that HF caused by ventricular "tachycardiomyopathy" causes differential gene-expression changes in atria versus ventricles and that these changes evolve over time. This study highlighted the signaling pathways implicated in atrial remodeling like those of MAP kinases, ubiquitin/proteasome systems and apoptosis, along with specific metabolic pathways like the electron-chain transport system and Krebs cycle at the ventricular level.Even though the large-scale study of gene-expression changes allowed us to identify certain signaling systems, they do not detect post-translational alterations. In our third study, I put forward the hypothesis that tachycardia-induced HF causes progressive changes in the proteins involved in different functional groups that play an important role in atrial pathophysiology. My results highlighted proteins linked to oxidative stress, metabolism and contractile proteins.In my final study, I decided to explore a new therapeutic avenue for AF prevention based on the molecular pathophysiology of AF. I had identified the MAP kinase ERK as a particularly important molecule in atrial remodeling caused by myocardial infarction in the rat and I had obtained results implicating a microRNA (miR21) in signaling leading to pathological ERK hyperphosphorylation. I therefore suggested that atrial interstitial fibrosis could be prevented by targeting underlying microRNA-related mechanisms and thereby reduce the inducibility and maintenance of AF caused by HF. My study is not yet completed but the preliminary results suggest beneficial effects of anti-miR21 treatment in preventing AF. In conclusion, my studies indicate the molecular pathophysiology underlying AF and suggest that it can be exploited to develop new therapeutic approaches.
La fibrillation auriculaire est l'arythmie supra-ventriculaire soutenue la plus commune et est associée à un taux élevé de morbidité et de mortalité. Les traitements pharmacologique actuels demeurent inefficaces et entraînent parfois même une augmentation du risque d'arythmies ventriculaires. Les études effectuées sur différents modèles animaux ont démontré que la fibrillation auriculaire était associée à un remodelage auriculaire qui favorisait son induction et son incidence. Les mécanismes de remodelage auriculaire diffèrent selon la pathologie sous-jascente. Le remodelage auriculaire induit par une tachycardie auriculaire ou une fibrillation auriculaire est principalement électrique, associé à l'altération de l'expression et de la fonction de canaux ioniques. Ces changements se reflète par un raccourcissement des périodes réfractaires, une diminution d'adaptation au rythme et un ralentissement de la vélocité de conduction, augmentant ainsi l'incidence de la fibrillation auriculaire. L'insuffisance cardiaque, induit un remodelage auriculaire principalement caractérisé par une hétérogénéité de conduction associée à une altération des propriétés structurelles de l'oreillette. Notamment, la fibrose interstitielle joue un rôle majeur dans la stabilisation de circuits de réentrée et la prolongation de la durée de la fibrillation auriculaire. Bien que plusieurs études aient décrit un grand nombre de changements associés à chacun de ces types de remodelage, les mécanismes qui sous-tendent ces changements demeurent mal connus. Dans notre première étude, nous avons émis l'hypothèse selon laquelle le remodelage auriculaire induit par la tachycardie auriculaire et celui induit par une défaillance cardiaque diffèreraient au point de vue de l'évolution temporelle et de la nature des changements au niveau génomique. Nous avons constaté que les changements d'expression génique induits par la tachycardie auriculaire et par la tachycardie ventriculaire étaient qualitativement différents et évoluaient de façon différente dans le temps. Comparativement aux changements survenant au niveau auriculaire, les changements ventriculaires observés au point de vue biochimique et histopathologique différaient en terme d'intensité et de progression temporelle. Dans notre deuxième étude, nous avons émis l'hypothèse que l'insuffisance cardiaque induite par une tachycardie soutenue entraînait des changements d'expression génique qui diffèreraient entre les oreillettes et les ventricules et ces changements seraient évolutifs. Cette étude nous a permis de mettre en évidence l'implication des voies de signalisations telles que la voie des MAP kinases, l'apoptose et le système ubiquitine/protéosome au niveau auriculaire et certaines voies métaboliques au niveau ventriculaire. Bien que l'étude des changements d'expression génique nous permette de mettre en évidence certaines voies de signalisation, les changements survenant au niveau post-transcriptionel ne sont pas toujours détectables par une approche génomique. Dans notre troisième étude, nous avons donc émis l'hypothèse que l'insuffisance cardiaque induite par une tachycardie ventriculaire entraînait un remodelage auriculaire qui impliquerait des changements évolutifs importants d'expression de protéines de différents groupes fonctionnels. Nos résultats ont montré un changement au niveau de protéines liées au stress oxydatif, au métabolisme et aux protéines contractiles. Dans notre dernière étude, nous avons exploré une nouvelle avenue thérapeutique dans le traitement préventif de la fibrillation auriculaire. Nous avons suggéré que la fibrose interstitielle pourrait être prévenue par la modulation de mécanismes de régulation de l'expression de gènes par des microARN, qui réduirait l'inductibilité et le maintien de FA en contexte d'insuffisance cardiaque. Nos résultats préliminaires suggèrent un effet bénéfique du traitement anti-miR21 pour réduire la fibrillation auriculaire.
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Khoo, Chee Wah. "The relationship between left atrial remodelling, atrial fibrillation burden and thrombogenesis." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6847/.

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Contemporary pacemakers allow quantification of atrial high-rate episodes (AHREs) and atrial fibrillation burden (AFB) accurately. It is generally believed that left atrial (LA) remodelling may precede the development of atrial arrhythmias (AA), and AHRE precede the clinical manifestation of atrial flutter or fibrillation. However, the relationship between LA remodelling with AHRE has not been studied. Furthermore, the relationship of AFB to progressive LA remodelling and how this relates to indices of thrombogenesis is unclear. The aim of my study is to investigate the inter-relationship between LA remodelling, AA burden and indices of thrombogenesis in patients with pacemakers. My findings suggest that the incidence of AHRE was 35%. Increased frequency of right ventricular pacing is associated with LA enlargement and reduced global left and right ventricular function. However, there was no clear association between the right atrial pacing with cardiac remodelling. The cumulative percentage right ventricular pacing and increased LA volume are associated with the development of AHREs, but AFB is independently associated with changes in LA function, left ventricular diastolic function and indices of platelet activation and thrombosis. In addition, I demonstrated the feasibility and reproducibility of a novel method of IACT measurement in patients with permanent pacemakers.
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Clauß, Sebastian [Verfasser]. "Proarrhythmic atrial remodeling mechanisms leading to arrhythmias / Sebastian Clauß." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1228271046/34.

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Hodzic, Amir. "Exploration du coeur d'athlète à l'aide d'outils échocardiographiques d'analyse de la déformation myocardique, des volumes ventriculaires et des flux intra cavitaires Accuracy of speckle tracking in the context of stress echocardiography in short axis view: an in vitro validation study Analysis of inter-system variability of systolic and diastolic intraventricular pressure gradients derived from color Doppler M-mode echocardiography Echocardiographic evidence of left ventricular untwisting-filling interplay Cardiovascular adaptations in American-style football players in response to the inter- season training Right ventricular global and regional remodeling in American-style-football athletes: a longitudinal 3D echocardiographic study." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC428.

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L’athlète entrainé est un modèle physiologique d’adaptation cardiaque extrême où il est parfois difficile de faire la distinction entre le remodelage cardiaque adaptatif induit par l’exercice physique et certaines cardiomyopathies débutantes. L’échocardiographie est l’examen d’imagerie de premier choix pour l’étude du cœur d’athlète au repos et à l’effort. Les développements semi-récents du speckle tracking et de l’imagerie tridimensionnelle (3D) ont montré un intérêt clinique dans la description de la réponse cardiaque à l’exercice. Toutefois certains aspects techniques nécessitent d’être investigués. De plus, les outils de post-traitement actuels ne permettent qu’une évaluation incomplète de l’hémodynamique cardiaque et de l’analyse morphofonctionnelle régionale. Dans un premier temps, à l’aide d’un modèle expérimental mimant l’échocardiographie de stress, nous avons démontré la validité du speckle tracking pour l’étude de la déformation régionale dans une large gamme de fréquences de déformation en comparaison à la technique de référence par sonomicrométrie. Secondairement, nous avons étudié chez des sujets volontaires sans cardiopathie avérée (athlètes et non athlètes) une méthode de quantification non invasive des gradients de pressions intraventriculaires (GPIVs) pour l’évaluation de la fonction systolique et diastolique ventriculaire gauche (VG), qui est basée sur le post-traitement des données de vitesses de flux intra cavitaires acquises en mode TM Doppler couleur. Nous avons montré que cet indice hémodynamique était facilement accessible, et bien corrélé au mécanisme de succion VG. L’analyse des mesures de GPIVs a mis en évidence une variabilité inter-constructeur qui était principalement liée aux différences de résolution de l’image Doppler couleur. Enfin, en utilisant une approche échocardiographique multiparamétrique (speckle tracking, GPIV, et volumes 3D), nous nous sommes intéressés à caractériser la relation physiologique entre le type d’entrainement physique et le remodelage cardiaque gauche et droit au sein d’une équipe de footballeurs canadiens suivie de manière longitudinale. L’analyse régionale des modifications morphologiques et fonctionnelles du ventricule droit (VD) induites par l’exercice chronique a été réalisée à l’aide d’un nouvel algorithme de post- traitement des acquisitions 3D permettant une segmentation tripartite (apex, chambre d’admission, chambre d’éjection) des volumes VD en échocardiographie. En conclusion, les outils de post-traitement échocardiographique étudiés dans ce travail pour l’analyse globale et régionale de la fonction et de la morphologie cardiaques semblent applicables au cœur d’athlète et pourraient avoir un intérêt dans la caractérisation du remodelage cardiaque physiologique à l’exercice
The trained athlete is a physiological model of extreme cardiac adaptation for whom the distinction between adaptive cardiac remodeling induced by chronic exercise and certain early cardiomyopathies can be difficult to assess. Echocardiography is the first-choice imaging modality to evaluate the athlete’s heart at rest and during exercise. Semi-recent developments in speckle tracking and 3D ultrasound imaging have shown clinical interest in the echocardiographic description of the athlete’s heart. However, some technical aspects require further investigation. Moreover, current post-treatment tools provide only a partial analysis of cardiac hemodynamics and regional myocardial function. Using an experimental model mimicking stress echocardiography, we first demonstrated the validity of speckle tracking in comparison to sonomicrometry to measure regional deformation in a large range of deformation rates. Secondly, we studied in volunteers without heart disease (athletes and non- athletes) the reliability of a method to assess non-invasively the left ventricular (LV) systolic and diastolic intraventricular pressure gradients (IVPGs) based on post-processing of intracardiac flow velocity data acquired using color Doppler M-mode. This hemodynamic index was highly feasible and well correlated with LV suction. Analysis of IVPG measurements revealed inter-vendor variability which was mainly related to differences in color Doppler image resolution. Finally, using a multiparametric echocardiographic approach (speckle tracking, IVPGs, and 3D volumes), we studied the physiological relationship between the type of exercise training and the left and right cardiac remodeling among a Canadian football team followed longitudinally. The regional analysis of right ventricular (RV) morphological and functional changes induced by chronic exercise was performed using a new computational method based on 3D echocardiography that volumetrically parcellated the RV into three segments (apex, outlet, and inlet). In conclusion, our workhas shown that the echocardiographic post-processing tools studied for the global and regional analysis of cardiac function and morphology apply to the athlete’s heart and could be useful in the characterization of the exercise-induced cardiac remodeling
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Colman, Michael Alan. "Development of a biophysically detailed model of the human atria for the investigation of the mechanisms of atrial arrhythmias." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/development-of-a-biophysically-detailed-model-of-the-human-atria-for-the-investigation-of-the-mechanisms-of-atrial-arrhythmias(29e4f51f-6ead-43e4-8574-eae9e4e1eb26).html.

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Atrial arrhythmias are the most prevalent sustained cardiac arrhythmias. Rates of hospitalisation and costs incurred to healthcare organisations are increasing in epidemic proportions. Despite this, the mechanisms of the transition from sinus rhythm to arrhythmic states are not well understood. The high level of regional electrical heterogeneity observed in the atria is thought to contribute towards the high prevalence of atrial arrhythmias. However, current computer models of the intact human atria only account for a small degree of this regional electrical heterogeneity, and do not include descriptions of the pacemaker regions of the sinoatrial node and the atrioventricular node. In this project, a new computational model of the intact 3D human atria is developed. First, a new single cell model to simulate the electrical action potential of the human atrial myocyte is developed. This model more accurately simulated the experimentally observed properties of human atrial action potentials than previous models. A family of electrically heterogeneous models describing the major regions within the atria is then developed, including those of the sinoatrial- and atrioventricular- nodes. This set of regional cell models represents the most expansive and complete set currently available. It is demonstrated that the large range of different electrical properties results in a large range of action potential morphology and duration within the atria. Models of the effect of sympathetic and parasympathetic regulation on the electrical AP of the models of the atrial working myocardium and the pacemaker regions were also incorporated. This demonstrated that sympathetic regulation can increase the pacing rate of the sinoatrial node and the atrio-ventricular node, and has a complex dose dependent effect on the atrial working myocardium. Four distinct models of the effects of atrial fibrillation induced remodelling on the atrial working myocardium are developed. These characterised the effect of remodelling of IKur on the overall changes in action potential morphology and duration observed. It is shown that the presence or absence of remodelling of this channel accounts for two distinct observed morphologies. A previous 3D anatomical model of the human atria is improved. First, detailed anatomical models for the sinoatrial node and the atrioventricular node are incorporated into the model. Second, it is further segmented to include regions for the pulmonary veins, atrio-ventricular ring, atrial septum and sinoatrial node block zone. This model is used to investigate the effects of sympathetic and parasympathetic regulation in the 3D atria. Finally, a detailed investigation of the underlying mechanisms of atrial fibrillation in the 3D atria, and the effect of electrical remodelling on the behaviour of atrial fibrillation, is performed using the detailed 3D model. This work represents a significant advance in 3D human atrial modelling. The anatomical model incorporates a greater level of complexity than previous models, and for the first time allowed investigation of the pacemaking mechanisms in the 3D intact human atria. The atrial fibrillation protocols are more physiologically relevant than previous models and have elucidated the roles that electrophysiological remodelling, electrical heterogeneity and structural anisotropy play in the development and maintenance of atrial fibrillation.
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Drahn, Steven [Verfasser]. "Bedeutung von mikroRNA-1 und -328 für atriales Remodeling bei Vorhofflimmern / Steven Drahn." Greifswald : Universitätsbibliothek Greifswald, 2015. http://d-nb.info/1070926280/34.

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Tsuneyoshi, Hiroshi. "Atrial natriuretic peptide (ANP) helps prevent late remodeling after left ventricular aneurysm repair." Kyoto University, 2005. http://hdl.handle.net/2433/144751.

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Books on the topic "Atriale remodeling"

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Khan, Anjum. Atrial remodeling in congestive heart failure. Ottawa: National Library of Canada, 2002.

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Chauhan, Vijay S., Sanjiv M. Narayan, and Atul Verma, eds. Electrical and Structural Remodelling in Atrial Fibrillation: Phenotypes for Personalized Therapy. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-082-9.

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Billman, George E., ed. Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-647-0.

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Lancellotti, Patrizio, and Bernard Cosyns. Assessment of the Left Ventricular Systolic Function. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0004.

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Evaluation of ventricular systolic function and cavity dimensions is an essential part of the echocardiographic examination. Treatment strategy and decisionmaking for a patient’s condition is affected by systolic function. Echocardiography plays a major in monitoring the effects of therapy. Appropriate knowledge about how to assess left ventricular size, shape and function is thus crucial. This chapter demonstrates left chamber quantification through various measurements of left ventricular size and dimensions, left ventricular mass, left ventricularglobal function, regional wall motion, left ventricular segmentation, global left ventricular remodelling, and left atrial measurements. Techniques, advantages, and limitations of different methods and echocardiographic examinations are given throughout.
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Rosca, Monica, Sergio Mondillo, and Kim O’Connor. Left atrium. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0022.

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The left atrium (LA) in a close interdependence with the left ventricle plays an essential role in the overall cardiovascular performance. The impact of LA remodelling on prognosis and risk stratification has gathered increasing evidence. With advances in imaging technology, the assessment of LA size and function become more accessible and precise. LA volume provides the most accurate estimate of LA size and superior prognostic information. Accounting for complex geometry and motion, three-dimensional echocardiography emerges as the preferred technique for the assessment of dynamic changes in LA volume. The assessment of LA function, providing important pathophysiological information, can add consistency in establishing the clinical role of LA remodelling. It is essential to fully understand the strengths and weaknesses of conventional and new echocardiographic techniques used to evaluate LA function. Atrial strain and strain rate parameters are less load dependent and have higher sensitivity in assessing LA function than conventional parameters. However, the lack of standardization and incomplete data regarding their prognostic value limits their routine use in current clinical practice.
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D’Andrea, Antonello, André La Gerche, and Christine Selton-Suty. Systemic disease and other conditions: athlete’s heart. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0055.

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The term ‘athlete’s heart’ refers to the structural, functional, and electrical adaptations that occur as a result of habitual exercise training. It is characterized by an increase of the internal chamber dimensions and wall thickness of both atria and ventricles. The athlete’s right ventricle also undergoes structural, functional, and electrical remodelling as a result of intense exercise training. Some research suggests that the haemodynamic stress of intense exercise is greater for the right heart and, as a result, right heart remodelling is slightly more profound when compared with the left heart. Echocardiography is the primary tool for the assessment of morphological and functional features of athlete’s heart and facilitates differentiation between physiological and pathological LV hypertrophy. Doppler myocardial and strain imaging can give additional information to the standard indices of global systolic and diastolic function and in selected cases cardiac magnetic resonance imaging may help in the diagnosis of specific myocardial diseases among athletes such as hypertrophic cardiomyopathy, dilated cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy.
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Rigo, Fausto, Covadonga Fernández-Golfín, and Bruno Pinamonti. Dilated cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0043.

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Dilated cardiomyopathy (DCM) is characterized by a globally dilated and dysfunctioning left ventricle (LV). Therefore, echocardiographic diagnostic criteria for DCM are a LV end-diastolic diameter greater than 117% predicted value corrected for age and body surface area and a LV ejection fraction less than 45% (and/or fractional shortening less than 25%). Usually, the LV is also characterized by a normal or mildly increased wall thickness with eccentric hypertrophy and increased mass, a spherical geometry (the so-called LV remodelling), a dyssynchronous contraction (typically with left bundle branch block), and diastolic dysfunction with elevated LV filling pressure. Other typical echocardiographic features of DCM include functional mitral and tricuspid regurgitation, right ventricular dysfunction, atrial dilatation, and secondary pulmonary hypertension. Several echocardiographic parameters, measured both at baseline and at follow-up, are valuable for prognostic stratification of DCM patients. Furthermore, re-evaluation of echocardiographic parameters during the disease course under optimal medical therapy is valuable for tailoring medical treatment and confirming indications for invasive treatments at follow-up. The stress echo can play a pivotal role in the different phases of DCM helping us in stratifying the prognosis of these patients. Finally, familial screening is an important tool for early diagnosis of DCM in asymptomatic patients.
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Book chapters on the topic "Atriale remodeling"

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Szekeres, László. "On Atrial Remodeling and Drug Treatment of Atrial Fibrillation." In Cardiac Remodeling and Failure, 319–30. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9262-8_22.

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Wagoner, David R. Van. "Electrical and Structural Remodeling in Atrial Fibrillation." In Atrial Fibrillation, 57–68. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-163-5_5.

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Everett, Thomas H., and Jeffrey E. Olgin. "Remodeling in Atrial Fibrillation." In Cardiac Mapping, 604–17. Chichester, UK: John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119152637.ch48.

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Jalife, José, and Omer Berenfeld. "Dominant Frequency Mapping to Assess the Consequences of Remodeling in the Mechanism of Atrial Fibrillation." In Atrial Fibrillation, 77–100. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-163-5_7.

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Cui, Jiaxin, Mariluz Rojo Domingo, Ryan Konno, Claudia A. Manetti, George Kagugube, Oscar Odeigah, and Joakim Sundnes. "Impact of Pathological Vascular Remodelling on Right Ventricular Mechanics." In Computational Physiology, 91–109. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_7.

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AbstractPulmonary arterial hypertension (PAH) is a rare disorder characterized by elevated blood pressure and pulmonary vascular resistance, often followed by right ventricular hypertrophy and heart failure. The effect of PAH and its treatments on the mechanics, function, and remodelling of the right ventricle (RV) is currently not well understood. To study cardiac biomechanics and functionality as PAH progresses, we implemented a computational model of the heart simulating right ventricular maladaptive remodelling. Our Windkessel-based model, which accounts for direct ventricular interaction and the presence of the pericardium, is utilized to simulate various disease stages of PAH. We find that the pericardium has a larger effect on heart performance than ventricular interaction through the septum.We also examined the effectiveness of two treatments, ventricular assist device (RVAD) and atrial septostomy, on diseased hearts. We show that while both pulsatile and continuous RVADs restore cardiac function, pulsatile RVAD improves cardiac output 29.4% more than continuous RVAD. We also demonstrate that atrial septostomy improves cardiac output by 19.5%. Our model can be further extended by simulating the heart&#x2019;s response to other treatments such as extracorporeal membrane oxygenation (ECMO), and by incorporating ventricular remodelling growth simulations and finite-element ventricular modelling.
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Brundel, B. J. J. M., R. H. Henning, H. H. Kampinga, I. C. Van Gelder, and H. J. G. M. Crijns. "Molecular Mechanisms of Remodeling in Human Atrial Fibrillation." In Cardiovascular Genomics: New Pathophysiological Concepts, 199–212. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1005-5_17.

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Yang, Qunhui, Gaofeng Wu, Limei Han, Ying Feng, Shumei Lin, Qiufeng Lv, Jiancheng Yang, and Jianmin Hu. "Taurine Reverses Atrial Structural Remodeling in Ach-Cacl2 Induced Atrial Fibrillation Rats." In Advances in Experimental Medicine and Biology, 831–41. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1079-2_65.

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Slotwiner, David J., and Jonathan S. Steinberg. "Limited ablation for persistent atrial fibrillation using preprocedure reverse remodeling." In Practical Guide to Catheter Ablation of Atrial Fibrillation, 303–14. Chichester, UK: John Wiley & Sons Ltd, 2015. http://dx.doi.org/10.1002/9781118658369.ch21.

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Disertori, M., and M. Marini. "Does Early Echocardiography-Guided Cardioversion of Atrial Fibrillation Prevent Electrical/Mechanical Remodeling of the Atria?" In Cardiac Arrhythmias 2001, 373–77. Milano: Springer Milan, 2002. http://dx.doi.org/10.1007/978-88-470-2103-7_57.

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Franz, Michael R. "Excitable Gap, Antiarrhythmic Actions, Electrical Remodeling: The Role Of MAP Recording in Atrial Fibrillation And Other Atrial Tachyarrhythmias." In Monophasic Action Potentials, 126–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60851-3_9.

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Conference papers on the topic "Atriale remodeling"

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Bai, Jieyun, Yaosheng Lu, Andy C.Y. Lo, and Jichao Zhao. "PITX2 Overexpression Leads to Atrial Electrical Remodeling Linked to Atrial Fibrillation." In 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.002.

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CRIJNS, HJGM. "ION CHANNEL REMODELING AND ATRIAL FIBRILLATION: CLINICAL ASPECTS." In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0002.

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Razeghi, Orod, Rashed Karim, John Whitaker, Catalina Tobon Gomez, and Steven Niederer. "A Platform for Quantifying Atrial Structural Remodelling." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.047-306.

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Salzmann-Djufri, M., T. Giessler, S. Rohrbach, F. Knapp, L. Ling, S. Vogt, N. Mirow, A. Böning, and B. Niemann. "New-Onset Atrial Fibrillation—Metabolic Markers, Cytokines, and Remodeling Anticipating Paroxysmal Atrial Fibrillation." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705421.

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IMANAGA, ISSEI, LIN HAI, and KOICHI OGAWA. "REMODELING OF GAP JUNCTION CONNEXIN IN ATRIAL AND VENTRICULAR FIBRILLATION." In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0059.

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Nesterova, T., D. Shmarko, K. Ushenin, and O. Solovyova. "Age-dependent effects of chronic atrial fibrillation remodeling in population of human atrial cardiomyocyte models." In THE VII INTERNATIONAL YOUNG RESEARCHERS’ CONFERENCE – PHYSICS, TECHNOLOGY, INNOVATIONS (PTI-2020). AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0033019.

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Drager, LF, LA Bortolotto, RP Pedrosa, EM Krieger, and G. Lorenzi-Filho. "Left Atrial Remodeling and Arterial Stiffness in Patients with Obstructive Sleep Apnea:Implications for Atrial Fibrillation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3987.

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Popovic, N., P. Haemers, R. Willems, and P. Claus. "Combined reconstruction of atrial morphology and paracardial fat depositions to study remodeling in atrial fibrillation." In 2016 38th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2016. http://dx.doi.org/10.1109/embc.2016.7590745.

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Niemann, B., H. L. Wißbrock, L. Li, S. Jackson, P. Schleichert, A. Böning, and S. Rohrbach. "Control of Atrial Remodeling by miRNA Modulation as an Additive Strategy in Surgical Atrial Fibrillation Ablation." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725715.

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Valinoti, Maddalena, Graziano Vito Lozupone, Paolo Sabbatani, Roberto Mantovan, Stefano Severi, and Cristiana Corsi. "Analysis of the electrical patterns and structural remodeling in atrial fibrillation." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7320012.

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