Journal articles: '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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Ono, Katsushige. "Atrial Remodeling in Atrial Fibrillation." Japanese Journal of Electrocardiology 36, no. 2 (2016): 145–53. http://dx.doi.org/10.5105/jse.36.145.

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Nattel, Stanley, Brett Burstein, and Dobromir Dobrev. "Atrial Remodeling and Atrial Fibrillation." Circulation: Arrhythmia and Electrophysiology 1, no. 1 (April 2008): 62–73. http://dx.doi.org/10.1161/circep.107.754564.

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Nattel, Stanley, and Masahide Harada. "Atrial Remodeling and Atrial Fibrillation." Journal of the American College of Cardiology 63, no. 22 (June 2014): 2335–45. http://dx.doi.org/10.1016/j.jacc.2014.02.555.

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Sieweke, Jan-Thorben, Tobias Jonathan Pfeffer, Saskia Biber, Shambhabi Chatterjee, Karin Weissenborn, Gerrit M. Grosse, Jan Hagemus, et al. "miR−21 and NT-proBNP Correlate with Echocardiographic Parameters of Atrial Dysfunction and Predict Atrial Fibrillation." Journal of Clinical Medicine 9, no. 4 (April 14, 2020): 1118. http://dx.doi.org/10.3390/jcm9041118.

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This study aimed to investigate the association of circulating biomarkers with echocardiographic parameters of atrial remodelling and their potential for predicting atrial fibrillation (AF). In patients with and without AF (n = 21 and n = 60) the following serum biomarkers were determined: soluble ST2 (sST2), Galectin−3 (Gal-3), N-terminal pro-brain natriuretic peptide (NT-proBNP), microRNA (miR)−21, −29a, −133a, −146b and −328. Comprehensive transthoracic echocardiography was performed in all participants. Biomarkers were significantly altered in patients with AF. The echocardiographic parameter septal PA-TDI, indicating left atrial (LA) remodelling, correlated with concentrations of sST2 (r = 0.249, p = 0.048), miR−21 (r = −0.277, p = 0.012), miR−29a (r = −0.269, p = 0.015), miR−146b (r = −0.319, p = 0.004) and miR−328 (r = −0.296, p = 0.008). In particular, NT-proBNP showed a strong correlation with echocardiographic markers of LA remodelling and dysfunction (septal PA-TDI: r = 0.444, p < 0.001, LAVI/a’: r = 0.457, p = 0.001, SRa: r = 0.581, p < 0.001). Multivariate Cox regressions analysis highlighted miR−21 and NT-proBNP as predictive markers for AF (miR−21: hazard ratio (HR) 0.16; 95% confidence interval (CI) 0.04–0.7, p = 0.009; NT-proBNP: HR 1.002 95%CI 1.001–1.004, p = 0.006). Combination of NT-proBNP and miR−21 had the best accuracy to discriminate patients with AF from those without AF (area under the curve (AUC)= 0.843). Our findings indicate that miR−21 and NT-proBNP correlate with echocardiographic parameters of atrial remodeling and predict AF, in particular if combined.

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Suffee, Nadine, Thomas Moore-Morris, Bernd Jagla, Nathalie Mougenot, Gilles Dilanian, Myriam Berthet, Julie Proukhnitzky, et al. "Reactivation of the Epicardium at the Origin of Myocardial Fibro-Fatty Infiltration During the Atrial Cardiomyopathy." Circulation Research 126, no. 10 (May 8, 2020): 1330–42. http://dx.doi.org/10.1161/circresaha.119.316251.

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Rationale: Fibro-fatty infiltration of subepicardial layers of the atrial wall has been shown to contribute to the substrate of atrial fibrillation. Objective: Here, we examined if the epicardium that contains multipotent cells is involved in this remodeling process. Methods and Results: One hundred nine human surgical right atrial specimens were evaluated. There was a relatively greater extent of epicardial thickening and dense fibro-fatty infiltrates in atrial tissue sections from patients aged over 70 years who had mitral valve disease or atrial fibrillation when compared with patients aged less than 70 years with ischemic cardiomyopathy as indicated using logistic regression adjusted for age and gender. Cells coexpressing markers of epicardial progenitors and fibroblasts were detected in fibro-fatty infiltrates. Such epicardial remodeling was reproduced in an experimental model of atrial cardiomyopathy in rat and in Wilms tumor 1 (WT1) CreERT2/+ ;ROSA-tdT +/− mice. In the latter, genetic lineage tracing demonstrated the epicardial origin of fibroblasts within fibro-fatty infiltrates. A subpopulation of human adult epicardial-derived cells expressing PDGFR (platelet-derived growth factor receptor)-α were isolated and differentiated into myofibroblasts in the presence of Ang II (angiotensin II). Furthermore, single-cell RNA-sequencing analysis identified several clusters of adult epicardial-derived cells and revealed their specification from adipogenic to fibrogenic cells in the rat model of atrial cardiomyopathy. Conclusions: Epicardium is reactivated during the formation of the atrial cardiomyopathy. Subsets of adult epicardial-derived cells, preprogrammed towards a specific cell fate, contribute to fibro-fatty infiltration of subepicardium of diseased atria. Our study reveals the biological basis for chronic atrial myocardial remodeling that paves the way of atrial fibrillation.

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Lim, Wei-Wen, Melissa Neo, Shivshankar Thanigaimani, Pawel Kuklik, Anand N. Ganesan, Dennis H. Lau, Tatiana Tsoutsman, et al. "Electrophysiological and Structural Remodeling of the Atria in a Mouse Model of Troponin-I Mutation Linked Hypertrophic Cardiomyopathy: Implications for Atrial Fibrillation." International Journal of Molecular Sciences 22, no. 13 (June 28, 2021): 6941. http://dx.doi.org/10.3390/ijms22136941.

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Hypertrophic cardiomyopathy (HCM) is an inherited cardiac disorder affecting one in 500 of the general population. Atrial fibrillation (AF) is the most common arrhythmia in patients with HCM. We sought to characterize the atrial electrophysiological and structural substrate in young and aging Gly203Ser cardiac troponin-I transgenic (HCM) mice. At 30 weeks and 50 weeks of age (n = 6 per strain each group), the left atrium was excised and placed on a multi-electrode array (MEA) for electrophysiological study; subsequent histological analyses and plasma samples were analyzed for biomarkers of extracellular matrix remodeling and cell adhesion and inflammation. Wild-type mice of matched ages were included as controls. Young HCM mice demonstrated significantly shortened atrial action potential duration (APD), increased conduction heterogeneity index (CHI), increased myocyte size, and increased interstitial fibrosis without changes in effective refractory periods (ERP), conduction velocity (CV), inflammatory infiltrates, or circulating markers of extracellular matrix remodeling and inflammation. Aging HCM mice demonstrated aggravated changes in atria electrophysiology and structural remodeling as well as increased circulating matrix metalloproteinases (MMP)-2, MMP-3, and VCAM-1 levels. This model of HCM demonstrates an underlying atrial substrate that progresses with age and may in part be responsible for the greater propensity for AF in HCM.

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Carrascal, Yolanda. "Echocardiography Parameters Predicting Postoperative Atrial Fibrillation: their Influence on Early left Atrial Remodelling and Right Ventricular Function after Heart Valve Surgery." Clinical Cardiology and Cardiovascular Interventions 2, no. 1 (April 12, 2019): 01–05. http://dx.doi.org/10.31579/2641-0419/012.

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Kockskämper, Jens, and Florentina Pluteanu. "Left Atrial Myocardium in Arterial Hypertension." Cells 11, no. 19 (October 8, 2022): 3157. http://dx.doi.org/10.3390/cells11193157.

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Arterial hypertension affects ≈ 1 billion people worldwide. It is associated with increased morbidity and mortality and responsible for millions of deaths each year. Hypertension mediates damage of target organs including the heart. In addition to eliciting left ventricular hypertrophy, dysfunction and heart failure, hypertension also causes left atrial remodeling that may culminate in atrial contractile dysfunction and atrial fibrillation. Here, we will summarize data on the various aspects of left atrial remodeling in (essential) hypertension gathered from studies on patients with hypertension and from spontaneously hypertensive rats, an animal model that closely mimics cardiac remodeling in human hypertension. Analyzing the timeline of remodeling processes, i.e., distinguishing between alterations occurring in prehypertension, in early hypertension and during advanced hypertensive heart disease, we will derive the potential mechanisms underlying left atrial remodeling in (essential) hypertension. Finally, we will discuss the consequences of these remodeling processes for atrial and ventricular function. The data imply that left atrial remodeling is multifactorial, starts early in hypertension and is an important contributor to the progression of hypertensive heart disease, including the development of atrial fibrillation and heart failure.

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Heinzmann, David, Stefan Fuß, Saskia v. Ungern-Sternberg, Jürgen Schreieck, Meinrad Gawaz, Michael Gramlich, and Peter Seizer. "TGFβ Is Specifically Upregulated on Circulating CD14++ CD16+ and CD14+ CD16++ Monocytes in Patients with Atrial Fibrillation and Severe Atrial Fibrosis." Cellular Physiology and Biochemistry 49, no. 1 (2018): 226–34. http://dx.doi.org/10.1159/000492873.

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Background/Aims: Fibrotic remodeling of the atria plays a key role in the pathogenesis of atrial fibrillation (AF). As little is known about the contribution of circulating monocytes in atrial remodeling and the pathophysiology of AF, we investigated profibrotic factors in different subsets of circulating monocytes obtained from patients with atrial fibrillation undergoing catheter ablation. Methods: A 3D high density voltage mapping was performed in sinus rhythm to evaluate the extent of low-voltage areas (LVAs) in the atria of 71 patients with persistent AF. Low-voltage was defined as signals of < 0.5mV during sinus rhythm. Prior to ablation, blood was drawn and monocytes were analyzed by FACS. Based on the expression of CD14 and CD16, three subgroups including CD14++ CD16- (‘classical’), CD14++ CD16+ (‘intermediate’), and CD14+ CD16++ (‘non-classical’) were analyzed for the expression of TGFb, CD147, and MMP-9, representing pivotal profibrotic pathways in myocardial remodeling. Results: Expression of TGFb was increased in CD14+ monocytes of patients with extensive LVAs compared to patients with a low extend of LVAs. While CD14++ CD16- monocytes showed no difference, CD14++ CD16+ and CD14+ CD16++ monocytes showed a strong increase of TGFb abundance. Although CD147 and MMP-9 are strongly associated with myocardial fibrosis, we found no difference in expression between the two groups in any monocyte subsets. Conclusion: TGFb is specifically upregulated on CD14++ CD16+ and CD14+ CD16++ monocytes in patients with extensive LVAs undergoing catheter ablation.

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Wiersma, van Marion, Wüst, Houtkooper, Zhang, Groot, Henning, and Brundel. "Mitochondrial Dysfunction Underlies Cardiomyocyte Remodeling in Experimental and Clinical Atrial Fibrillation." Cells 8, no. 10 (October 5, 2019): 1202. http://dx.doi.org/10.3390/cells8101202.

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Atrial fibrillation (AF), the most common progressive tachyarrhythmia, results in structural remodeling which impairs electrical activation of the atria, rendering them increasingly permissive to the arrhythmia. Previously, we reported on endoplasmic reticulum stress and NAD+ depletion in AF, suggesting a role for mitochondrial dysfunction in AF progression. Here, we examined mitochondrial function in experimental model systems for AF (tachypaced HL-1 atrial cardiomyocytes and Drosophila melanogaster) and validated findings in clinical AF. Tachypacing of HL-1 cardiomyocytes progressively induces mitochondrial dysfunction, evidenced by impairment of mitochondrial Ca2+-handling, upregulation of mitochondrial stress chaperones and a decrease in the mitochondrial membrane potential, respiration and ATP production. Atrial biopsies from AF patients display mitochondrial dysfunction, evidenced by aberrant ATP levels, upregulation of a mitochondrial stress chaperone and fragmentation of the mitochondrial network. The pathophysiological role of mitochondrial dysfunction is substantiated by the attenuation of AF remodeling by preventing an increased mitochondrial Ca2+-influx through partial blocking or downregulation of the mitochondrial calcium uniporter, and by SS31, a compound that improves bioenergetics in mitochondria. Together, these results show that conservation of the mitochondrial function protects against tachypacing-induced cardiomyocyte remodeling and identify this organelle as a potential novel therapeutic target.

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Jalife, José, and Kuljeet Kaur. "Atrial remodeling, fibrosis, and atrial fibrillation." Trends in Cardiovascular Medicine 25, no. 6 (August 2015): 475–84. http://dx.doi.org/10.1016/j.tcm.2014.12.015.

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Neumann, T., and H. Hölschermann. "Atriales Remodeling und Anti-Remodeling-Therapie bei Vorhofflimmern." DMW - Deutsche Medizinische Wochenschrift 131, no. 16 (April 2006): 884–87. http://dx.doi.org/10.1055/s-2006-939863.

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Sato, Satsuki, Jinya Suzuki, Masamichi Hirose, Mika Yamada, Yasuo Zenimaru, Takahiro Nakaya, Mai Ichikawa, et al. "Cardiac overexpression of perilipin 2 induces atrial steatosis, connexin 43 remodeling, and atrial fibrillation in aged mice." American Journal of Physiology-Endocrinology and Metabolism 317, no. 6 (December 1, 2019): E1193—E1204. http://dx.doi.org/10.1152/ajpendo.00227.2019.

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Atrial fibrillation (AF) is prevalent in patients with obesity and diabetes, and such patients often exhibit cardiac steatosis. Since the role of cardiac steatosis per se in the induction of AF has not been elucidated, the present study was designed to explore the relation between cardiac steatosis and AF. Transgenic (Tg) mice with cardiac-specific overexpression of perilipin 2 (PLIN2) were housed in the laboratory for more than 12 mo before the study. Electron microscopy of the atria of PLIN2-Tg mice showed accumulation of small lipid droplets around mitochondrial chains, and five- to ninefold greater atrial triacylglycerol (TAG) content compared with wild-type (WT) mice. Electrocardiography showed significantly longer RR intervals in PLIN2-Tg mice than in WT mice. Transesophageal electrical burst pacing resulted in significantly higher prevalence of sustained (>5 min) AF (69%) in PLIN2-Tg mice than in WT mice (24%), although it was comparable in younger (4-mo-old) mice. Connexin 43 (Cx43), a gap junction protein, was localized at the intercalated disks in WT atria but was heterogeneously distributed on the lateral side of cardiomyocytes in PLIN2-Tg atria. Langendorff-perfused hearts using the optical mapping technique showed slower and heterogeneous impulse propagation in PLIN2-Tg atria compared with WT atria. Cardiac overexpression of hormone-sensitive lipase in PLIN2-Tg mice resulted in atrial TAG depletion and amelioration of AF susceptibility. The results suggest that PLIN2-induced steatosis is associated with Cx43 remodeling, impaired conduction propagation, and higher incidence of AF in aged mice. Therapies targeting cardiac steatosis could be potentially beneficial against AF in patients with obesity or diabetes.

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D’Andrea, Antonello, Eduardo Bossone, Juri Radmilovic, Lucia Riegler, Enrica Pezzullo, Raffaella Scarafile, Maria Giovanna Russo, Maurizio Galderisi, and Raffaele Calabrò. "Exercise-Induced Atrial Remodeling." Cardiology Clinics 34, no. 4 (November 2016): 557–65. http://dx.doi.org/10.1016/j.ccl.2016.06.005.

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Thomas, Liza, and Walter P. Abhayaratna. "Left Atrial Reverse Remodeling." JACC: Cardiovascular Imaging 10, no. 1 (January 2017): 65–77. http://dx.doi.org/10.1016/j.jcmg.2016.11.003.

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Girmatsion, Zenawit, and Joachim R. Ehrlich. "Implications of Remodelling in Atrial Fibrillation Therapy." European Cardiology Review 6, no. 3 (2010): 39. http://dx.doi.org/10.15420/ecr.2010.6.3.39.

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Atrial fibrillation (AF) is a common arrhythmia that in most cases occurs secondary to other (mostly cardiac) disorders. AF itself has a prominent tendency to alter various properties of the human heart that eventually stabilise the arrhythmia and may lead to complications of the disease. Due to its great prevalence and rising incidence, improved treatment options for AF are eminent targets of basic and clinical research and industrial development. This article covers the consequences in terms of electrical, structural and endothelial/inflammatory remodelling associated with AF and respective therapeutic options arising from such alterations. For instance, atrial-specific antiarrhythmic drugs have been found to exploit properties of electrically remodelled atria, early antifibrotic therapy with angiotensin-converting enzyme inhibitors may be beneficial in preventing structural changes and reversal of endothelial dysfunction may be helpful in reducing AF-associated complications. Research during the past two decades has provided profound, novel insights that might turn into therapeutic benefit for affected patients in the near future.

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Yoo, Shin, Anna Pfenniger, Jacob Hoffman, Wenwei Zhang, Jason Ng, Amy Burrell, David A. Johnson, et al. "Attenuation of Oxidative Injury With Targeted Expression of NADPH Oxidase 2 Short Hairpin RNA Prevents Onset and Maintenance of Electrical Remodeling in the Canine Atrium." Circulation 142, no. 13 (September 29, 2020): 1261–78. http://dx.doi.org/10.1161/circulationaha.119.044127.

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Background: Atrial fibrillation (AF) is the most common heart rhythm disorder in adults and a major cause of stroke. Unfortunately, current treatments of AF are suboptimal because they are not targeted to the molecular mechanisms underlying AF. Using a highly novel gene therapy approach in a canine, rapid atrial pacing model of AF, we demonstrate that NADPH oxidase 2 (NOX2) generated oxidative injury causes upregulation of a constitutively active form of acetylcholine-dependent K + current ( I KACh ), called I KH ; this is an important mechanism underlying not only the genesis, but also the perpetuation of electric remodeling in the intact, fibrillating atrium. Methods: To understand the mechanism by which oxidative injury promotes the genesis and maintenance of AF, we performed targeted injection of NOX2 short hairpin RNA (followed by electroporation to facilitate gene delivery) in atria of healthy dogs followed by rapid atrial pacing. We used in vivo high-density electric mapping, isolation of atrial myocytes, whole-cell patch clamping, in vitro tachypacing of atrial myocytes, lucigenin chemiluminescence assay, immunoblotting, real-time polymerase chain reaction, immunohistochemistry, and Masson trichrome staining. Results: First, we demonstrate that generation of oxidative injury in atrial myocytes is a frequency-dependent process, with rapid pacing in canine atrial myocytes inducing oxidative injury through the induction of NOX2 and the generation of mitochondrial reactive oxygen species. We show that oxidative injury likely contributes to electric remodeling in AF by upregulating I KACh by a mechanism involving frequency-dependent activation of PKC ε (protein kinase C epsilon). The time to onset of nonsustained AF increased by >5-fold in NOX2 short hairpin RNA–treated dogs. Furthermore, animals treated with NOX2 short hairpin RNA did not develop sustained AF for up to 12 weeks. The electrophysiological mechanism underlying AF prevention was prolongation of atrial effective refractory periods, at least in part attributable to the attenuation of I KACh . Attenuated membrane translocation of PKC ε appeared to be a likely molecular mechanism underlying this beneficial electrophysiological remodeling. Conclusions: NOX2 oxidative injury (1) underlies the onset, and the maintenance of electric remodeling in AF, as well, and (2) can be successfully prevented with a novel, gene-based approach. Future optimization of this approach may lead to a novel, mechanism-guided therapy for AF.

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Lader, Joshua M., Carolina Vasquez, Li Bao, Karen Maass, Jiaxiang Qu, Eirini Kefalogianni, Glenn I. Fishman, William A. Coetzee, and Gregory E. Morley. "Remodeling of atrial ATP-sensitive K+ channels in a model of salt-induced elevated blood pressure." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 2011): H964—H974. http://dx.doi.org/10.1152/ajpheart.00410.2011.

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Hypertension is associated with the development of atrial fibrillation; however, the electrophysiological consequences of this condition remain poorly understood. ATP-sensitive K+ (KATP) channels, which contribute to ventricular arrhythmias, are also expressed in the atria. We hypothesized that salt-induced elevated blood pressure (BP) leads to atrial KATP channel activation and increased arrhythmia inducibility. Elevated BP was induced in mice with a high-salt diet (HS) for 4 wk. High-resolution optical mapping was used to measure atrial arrhythmia inducibility, effective refractory period (ERP), and action potential duration at 90% repolarization (APD90). Excised patch clamping was performed to quantify KATP channel properties and density. KATP channel protein expression was also evaluated. Atrial arrhythmia inducibility was 22% higher in HS hearts compared with control hearts. ERP and APD90 were significantly shorter in the right atrial appendage and left atrial appendage of HS hearts compared with control hearts. Perfusion with 1 μM glibenclamide or 300 μM tolbutamide significantly decreased arrhythmia inducibility and prolonged APD90 in HS hearts compared with untreated HS hearts. KATP channel density was 156% higher in myocytes isolated from HS animals compared with control animals. Sulfonylurea receptor 1 protein expression was increased in the left atrial appendage and right atrial appendage of HS animals (415% and 372% of NS animals, respectively). In conclusion, KATP channel activation provides a mechanistic link between salt-induced elevated BP and increased atrial arrhythmia inducibility. The findings of this study have important implications for the treatment and prevention of atrial arrhythmias in the setting of hypertensive heart disease and may lead to new therapeutic approaches.

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Kugler, Szilvia, Gábor Duray, and István Préda. "Új felismerések a pitvarfibrilláció genezisében és fenntartásában: az egyénre szabott kezelés lehetőségei." Orvosi Hetilap 159, no. 28 (July 2018): 1135–45. http://dx.doi.org/10.1556/650.2018.31087.

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Abstract: Atrial fibrillation affects approximately three percent of the adults. Ablation strategies targeting the isolation of the pulmonary veins are the up-to-date cornerstones for atrial fibrillation ablations. However, a one-year success rate of repeated interventions is not more than 70%. Long-term efficacy of catheter ablation is presumably limited by electrical and structural remodeling of the atria, which results in a progressive increase in the duration of atrial fibrillation to become sustained. The potential pathophysiological importance of the epicardial adipose tissue, atrial fibrosis, autonomic nervous system and arrhythmogenic foci are documented by several studies. Increased volume, inflammation induced transformation to fibrosis and myocardial infiltration of atrial subepicardial fat in obese patients result in higher risk of atrial fibrillation development. Changes in atrial autonomic innervation under some conditions including regular physical exercise strongly promote arrhythmogenesis via the mechanism of enhanced triggered activity or abbreviated atrial refractoriness. Individualized management of possible trigger and substrate mechanisms are proposed to provide a novel basis for the effective treatment of atrial fibrillation. Pro-fibrotic signalling pathways can be inhibited by the suppression of renin-angiotensin-aldosterone system. Neuromodulation strategies include renal sympathetic denervation and ganglionic plexi ablation. Anticoagulation therapy has also been shown to reduce the burden of abnormal atrial remodeling. Possible novel catheter ablation techniques are used for right or left atrial linear lesions, scar homogenization and catheter ablation of complex fractionated atrial electrograms, rotors or ectopic foci. Beside these new management strategies, clinical consideration of factors of particular risks as obesity, hyperlipidaemia, hypertension, diabetes and obstructive sleep apnoe are also essential. Orv Hetil. 2018; 159(28): 1135–1145.

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Zhang, Yun-Long, Hua-Jun Cao, Xiao Han, Fei Teng, Chen Chen, Jie Yang, Xiao Yan, et al. "Chemokine Receptor CXCR-2 Initiates Atrial Fibrillation by Triggering Monocyte Mobilization in Mice." Hypertension 76, no. 2 (August 2020): 381–92. http://dx.doi.org/10.1161/hypertensionaha.120.14698.

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Atrial fibrillation (AF) is frequently associated with increased inflammatory response characterized by infiltration of monocytes/macrophages. The chemokine receptor CXCR-2 is a critical regulator of monocyte mobilization in hypertension and cardiac remodeling, but it is not known whether CXCR-2 is involved in the development of hypertensive AF. AF was induced by infusion of Ang II (angiotensin II; 2000 ng/kg per minute) for 3 weeks in male C57BL/6 wild-type mice, CXCR-2 knockout mice, bone marrow-reconstituted chimeric mice, and mice treated with the CXCR-2 inhibitor SB225002. Microarray analysis revealed that 4 chemokine ligands of CXCR-2 were significantly upregulated in the atria during 3 weeks of Ang II infusion. CXCR-2 expression and the number of CXCR2 + immune cells markedly increased in Ang II–infused atria in a time-dependent manner. Moreover, Ang II–infused wild-type mice had increased blood pressure, AF inducibility, atrial diameter, fibrosis, infiltration of macrophages, and superoxide production compared with saline-treated wild-type mice, whereas these effects were significantly attenuated in CXCR-2 knockout mice and wild-type mice transplanted with CXCR-2-deficient bone marrow cells or treated with SB225002. Moreover, circulating blood CXCL-1 levels and CXCR2 + monocyte counts were higher and associated with AF in human patients (n=31) compared with sinus rhythm controls (n=31). In summary, this study identified a novel role for CXCR-2 in driving monocyte infiltration of the atria, which accelerates atrial remodeling and AF after hypertension. Blocking CXCR-2 activation may serve as a new therapeutic strategy for AF.

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COSIO, FRANCISCO G., and ERNESTO CASTILLO. "Left Atrial Anatomic Remodeling in Atrial Fibrillation." Journal of Cardiovascular Electrophysiology 18, no. 1 (January 2007): 53–54. http://dx.doi.org/10.1111/j.1540-8167.2006.00701.x.

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Schmitt, Nicole, Morten Grunnet, and Søren-Peter Olesen. "Cardiac Potassium Channel Subtypes: New Roles in Repolarization and Arrhythmia." Physiological Reviews 94, no. 2 (April 2014): 609–53. http://dx.doi.org/10.1152/physrev.00022.2013.

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About 10 distinct potassium channels in the heart are involved in shaping the action potential. Some of the K+channels are primarily responsible for early repolarization, whereas others drive late repolarization and still others are open throughout the cardiac cycle. Three main K+channels drive the late repolarization of the ventricle with some redundancy, and in atria this repolarization reserve is supplemented by the fairly atrial-specific KV1.5, Kir3, KCa, and K2Pchannels. The role of the latter two subtypes in atria is currently being clarified, and several findings indicate that they could constitute targets for new pharmacological treatment of atrial fibrillation. The interplay between the different K+channel subtypes in both atria and ventricle is dynamic, and a significant up- and downregulation occurs in disease states such as atrial fibrillation or heart failure. The underlying posttranscriptional and posttranslational remodeling of the individual K+channels changes their activity and significance relative to each other, and they must be viewed together to understand their role in keeping a stable heart rhythm, also under menacing conditions like attacks of reentry arrhythmia.

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Opie, Lionel H. "Tedisamil in Coronary Disease: Additional Benefits in the Therapy of Atrial Fibrillation?" Journal of Cardiovascular Pharmacology and Therapeutics 8, no. 1_suppl (March 2003): S33—S37. http://dx.doi.org/10.1177/107424840300800105.

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Atrial fibrillation has recently come into clinical and research focus. In particular, ventricular rate control has been carefully compared with atrial rhythm control. Additionally, the recent discovery of atrial stunning has initiated clinical and research interest in atrial remodeling. Atrial fibrillation is more likely to occur when the atria are damaged by increased fibrosis. The ideal way to prevent atrial fibrillation and the risk of repetition is by tackling the root causes, such as ischemic heart disease, heart failure, and left ventricular hypertrophy. Tedisamil is an unusual antifibrillatory compound that has a novel mechanism of action by inhibiting the transient outward current (Ito) and the repolarizing potassium currents in the sinoatrial node. Tedisamil works acutely against atrial fibrillation. Importantly, atrial fibrillation is often caused by or related to cardiac ischemia, and conversely, ischemia is caused by the increased oxygen demand of atrial fibrillation. Hence, the double properties of tedisamil as a drug that both inhibits atrial fibrillation and acts in an anti-ischemic mode are an attractive basis for future clinical research.

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Grigoryan, S. V., L. G. Azarapetyan, and K. G. Adamyan. "Comparative evaluation of markers of inflammation and fibrosis in patients with various clinical forms of atrial fibrillation." Cardiovascular Therapy and Prevention 17, no. 6 (December 20, 2018): 26–31. http://dx.doi.org/10.15829/1728-8800-2018-6-26-31.

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Aim. To identify and assess the significance of clinical and functional data characterizing cardiac remodeling, as well as inflammatory and fibrosis markers in patients with various clinical forms that promote the progression of atrial fibrillation (AF).Material and methods. We observed 213 patients with arterial hypertension or in combination with coronary artery disease, who were diagnosed with AF. For the clinical and functional assessment of various clinical forms of AF, the significance of certain clinical, hemodynamic, structural, functional, and immunological risk factors for AF was studied. We used the method of binary logistic regression and calculated the significance of the risk factors odds ratio (OR).Results. We made a database consisting of 33 indicators characterizing the clinical, hemodynamic and structural-functional heart condition, inflammatory and fibrosis markers, the significance of which was ambiguous in various clinical groups of AF patients. We identified enough informativeness of the OR significance for indicators of atrial electrical remodeling, which significantly increases from the paroxysmal AF to the persistent form. It confirms a significant role for the heterogeneity of pulses in the atria during the progression of AF. The degree of structural remodeling of both the atria and ventricles also significantly increases with the progression of AF. We also noted that inflammatory markers have statistically significant role with paroxysmal AF. With persistent AF, the significance of OR for inflammatory markers increases, and with permanent AF, their significance decreases. The significance of the OR in fibrosis marker is significantly high with AF and in the further AF progression, and it significantly increases with the persistent AF form.Conclusion. We determined different degrees of electrical and structural remodeling of the atria and ventricles in patients with various clinical forms of AF. At the same time, there is an increase in the reliability of OR in inflammatory and fibrosis markers. However, in patients with persistent AF, the duration of AF and increase in the significance of the OR in fibrosis marker come to the fore.

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Dilaveris, Polychronis, Christos-Konstantinos Antoniou, Panagiota Manolakou, Eleftherios Tsiamis, Konstantinos Gatzoulis, and Dimitris Tousoulis. "Biomarkers Associated with Atrial Fibrosis and Remodeling." Current Medicinal Chemistry 26, no. 5 (April 22, 2019): 780–802. http://dx.doi.org/10.2174/0929867324666170918122502.

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Atrial fibrillation is the most common rhythm disturbance encountered in clinical practice. Although often considered as solely arrhythmic in nature, current evidence has established that atrial myopathy constitutes both the substrate and the outcome of atrial fibrillation, thus initiating a vicious, self-perpetuating cycle. This myopathy is triggered by stress-induced (including pressure/volume overload, inflammation, oxidative stress) responses of atrial tissue, which in the long term become maladaptive, and combine elements of both structural, especially fibrosis, and electrical remodeling, with contemporary approaches yielding potentially useful biomarkers of these processes. Biomarker value becomes greater given the fact that they can both predict atrial fibrillation occurrence and treatment outcome. This mini-review will focus on the biomarkers of atrial remodeling (both electrical and structural) and fibrosis that have been validated in human studies, including biochemical, histological and imaging approaches.

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Takawale, Abhijit, Martin Aguilar, Yasmina Bouchrit, and Roddy Hiram. "Mechanisms and Management of Thyroid Disease and Atrial Fibrillation: Impact of Atrial Electrical Remodeling and Cardiac Fibrosis." Cells 11, no. 24 (December 14, 2022): 4047. http://dx.doi.org/10.3390/cells11244047.

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Atrial fibrillation (AF) is the most common cardiac arrhythmia associated with increased cardiovascular morbidity and mortality. The pathophysiology of AF is characterized by electrical and structural remodeling occurring in the atrial myocardium. As a source of production of various hormones such as angiotensin-2, calcitonin, and atrial natriuretic peptide, the atria are a target for endocrine regulation. Studies have shown that disorders associated with endocrine dysregulation are potential underlying causes of AF. The thyroid gland is an endocrine organ that secretes three hormones: triiodothyronine (T3), thyroxine (T4) and calcitonin. Thyroid dysregulation affects the cardiovascular system. Although there is a well-established relationship between thyroid disease (especially hyperthyroidism) and AF, the underlying biochemical mechanisms leading to atrial fibrosis and atrial arrhythmias are poorly understood in thyrotoxicosis. Various animal models and cellular studies demonstrated that thyroid hormones are involved in promoting AF substrate. This review explores the recent clinical and experimental evidence of the association between thyroid disease and AF. We highlight the current knowledge on the potential mechanisms underlying the pathophysiological impact of thyroid hormones T3 and T4 dysregulation, in the development of the atrial arrhythmogenic substrate. Finally, we review the available therapeutic strategies to treat AF in the context of thyroid disease.

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Si, Man, Krystle Trosclair, Kathryn A. Hamilton, and Edward Glasscock. "Genetic ablation or pharmacological inhibition of Kv1.1 potassium channel subunits impairs atrial repolarization in mice." American Journal of Physiology-Cell Physiology 316, no. 2 (February 1, 2019): C154—C161. http://dx.doi.org/10.1152/ajpcell.00335.2018.

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Voltage-gated Kv1.1 potassium channel α-subunits, encoded by the Kcna1 gene, have traditionally been regarded as neural-specific with no expression or function in the heart. However, recent data revealed that Kv1.1 subunits are expressed in atria where they may have an overlooked role in controlling repolarization and arrhythmia susceptibility independent of the nervous system. To explore this concept in more detail and to identify functional and molecular effects of Kv1.1 channel impairment in the heart, atrial cardiomyocyte patch-clamp electrophysiology and gene expression analyses were performed using Kcna1 knockout ( Kcna1−/−) mice. Specifically, we hypothesized that Kv1.1 subunits contribute to outward repolarizing K+ currents in mouse atria and that their absence prolongs cardiac action potentials. In voltage-clamp experiments, dendrotoxin-K (DTX-K), a Kv1.1-specific inhibitor, significantly reduced peak outward K+ currents in wild-type (WT) atrial cells but not Kcna1−/− cells, demonstrating an important contribution by Kv1.1-containing channels to mouse atrial repolarizing currents. In current-clamp recordings, Kcna1−/− atrial myocytes exhibited significant action potential prolongation which was exacerbated in right atria, effects that were partially recapitulated in WT cells by application of DTX-K. Quantitative RT-PCR measurements showed mRNA expression remodeling in Kcna1−/− atria for several ion channel genes that contribute to the atrial action potential including the Kcna5, Kcnh2, and Kcnj2 potassium channel genes and the Scn5a sodium channel gene. This study demonstrates a previously undescribed heart-intrinsic role for Kv1.1 subunits in mediating atrial repolarization, thereby adding a new member to the already diverse collection of known K+ channels in the heart.

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Saygili, Erol, Obaida R. Rana, Esra Saygili, Hannes Reuter, Konrad Frank, Robert H. G. Schwinger, Jochen Müller-Ehmsen, and Carsten Zobel. "Losartan prevents stretch-induced electrical remodeling in cultured atrial neonatal myocytes." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (June 2007): H2898—H2905. http://dx.doi.org/10.1152/ajpheart.00546.2006.

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Atrial fibrillation (AF) is the most frequent arrhythmia found in clinical practice. In recent studies, a decrease in the development or recurrence of AF was found in hypertensive patients treated with angiotensin-converting enzyme inhibitors or angiotensin receptor-blocking agents. Hypertension is related to an increased wall tension in the atria, resulting in increased stretch of the individual myocyte, which is one of the major stimuli for the remodeling process. In the present study, we used a model of cultured atrial neonatal rat cardiomyocytes under conditions of stretch to provide insight into the mechanisms of the preventive effect of the angiotensin receptor-blocking agent losartan against AF on a molecular level. Stretch significantly increased protein-to-DNA ratio and atrial natriuretic factor mRNA expression, indicating hypertrophy. Expression of genes encoding for the inward rectifier K+current ( IK1), Kir2.1, and Kir2.3, as well as the gene encoding for the ultrarapid delayed rectifier K+current ( IKur), Kv1.5, was significantly increased. In contrast, mRNA expression of Kv4.2 was significantly reduced in stretched myocytes. Alterations of gene expression correlated with the corresponding current densities: IK1and IKurdensities were significantly increased in stretched myocytes, whereas transient outward K+current ( Ito) density was reduced. These alterations resulted in a significant abbreviation of the action potential duration. Losartan (1 μM) prevented stretch-induced increases in the protein-to-DNA ratio and atrial natriuretic peptide mRNA expression in stretched myocytes. Concomitantly, losartan attenuated stretch-induced alterations in IK1, IKur, and Itodensity and gene expression. This prevented the stretch-induced abbreviation of action potential duration. Prevention of stretch-induced electrical remodeling might contribute to the clinical effects of losartan against AF.

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Odeh, Ameer, Gabriel D. Dungan, Amir Darki, Debra Hoppensteadt, Fakiha Siddiqui, Bulent Kantarcioglu, Jawed Fareed, and Mushabbar A. Syed. "Collagen Remodeling and Fatty Acid Regulation Biomarkers in Understanding the Molecular Pathogenesis of Atrial Fibrillation." Clinical and Applied Thrombosis/Hemostasis 28 (January 2022): 107602962211451. http://dx.doi.org/10.1177/10760296221145181.

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Introduction Atrial Fibrillation (AF) is the most common cardiac arrythmia in the world. Structural remodeling and fatty acid metabolism dysregulation are believed to play a role in the development of AF. This study explored different biomarkers in the blood of AF patients and a control population to determine if there was a significant difference between the two groups. Material and Methods Plasma samples were collected from 73 patients with confirmed diagnosis of AF from Loyola University Clinic. Control group represented commercially available plasma ( n = 50). Sandwich ELISA kits were used to quantify the collagen remodeling proteins and liver type fatty acid binding protein (L-FABP) in the AF population and the control population. Non-esterified fatty acids (NEFAs) were measured using an enzymatic colorimetric kit from Wako Diagnostics. Statistical analyses were performed using GraphPad Prism. Results All the collagen remodeling biomarkers were significantly higher in AF patients compared to the control group. The fatty acid dysregulation biomarkers were elevated in the AF patients. Spearman correlation analyses yielded significant correlations between L-FABP and TIMP-1 ( r = 0.47, P < 0.001), NEFA and TIMP-2 ( r = 0.41, P = 0.002), NEFA and ICTP ( r = 0.41, P =0 .002), and NEFA and PIIINP ( r = 0.61, P < 0.0001). Summary and Conclusions The elevation of collagen remodeling biomarkers suggests an upregulation of these biomarkers and their potential role in AF, which may contribute to atrial fibrosis. L-FABP and NEFAs were elevated in AF patients. The correlations between the collagen remodeling and fatty acid dysregulation biomarkers may be due to their involvement in structural remodeling of the atria.

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Garratt, C. J., and S. P. Fynn. "Atrial electrical remodelling and atrial fibrillation." QJM: An International Journal of Medicine 93, no. 9 (September 2000): 563–65. http://dx.doi.org/10.1093/qjmed/93.9.563.

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Sharikov, Nikita L., S. M. Chibisov, O. N. Ragozin, and S. Sh Gasimova. "Variants of the anatomical structure of the coronary arteries and the left atrium remodeling in patients with different forms of atrial fibrillation." Clinical Medicine (Russian Journal) 96, no. 9 (December 30, 2018): 809–13. http://dx.doi.org/10.18821/0023-2149-2018-96-9-809-813.

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One of the reasons leading to dilatation of the left atrium is atrial fibrillation. A retrospective analysis of 136 case histories of patients with various forms of “non-valvular” atrial fibrillation was performed, depending on the shape of atrial fibrillation, the patients were divided into 3 groups. In patients with atrial fibrillation in 62.5%, the source of the atrial branches was the envelope branch of the left coronary artery. Atrial branches originating from the right coronary artery system were identified in 35.8%. In men, atrial arteries occur significantly more often. The results differ from publications, according to which the blood supply of the atria and sinoatrial node from 60 to 75% is carried out by branches departing from the basin of the right coronary artery. The degree of dilatation of the left atrium does not depend on the source of blood supply, but a correlation between the size of the left atrium and the diameter of the branches of the artery of the sinatrial node in the group of patients with paroxysmal atrial fibrillation is traced.

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Lee, Hsiang-Chun, and Yi-Hsiung Lin. "The Pathogenic Role of Very Low Density Lipoprotein on Atrial Remodeling in the Metabolic Syndrome." International Journal of Molecular Sciences 21, no. 3 (January 30, 2020): 891. http://dx.doi.org/10.3390/ijms21030891.

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Atrial fibrillation (AF) is the most common persistent arrhythmia, and can lead to systemic thromboembolism and heart failure. Aging and metabolic syndrome (MetS) are major risks for AF. One of the most important manifestations of MetS is dyslipidemia, but its correlation with AF is ambiguous in clinical observational studies. Although there is a paradoxical relationship between fasting cholesterol and AF incidence, the beneficial benefit from lipid lowering therapy in reduction of AF is significant. Here, we reviewed the health burden from AF and MetS, the association between two disease entities, and the metabolism of triglyceride, which is elevated in MetS. We also reviewed scientific evidence for the mechanistic links between very low density lipoproteins (VLDL), which primarily carry circulatory triglyceride, to atrial cardiomyopathy and development of AF. The effects of VLDL to atria suggesting pathogenic to atrial cardiomyopathy and AF include excess lipid accumulation, direct cytotoxicity, abbreviated action potentials, disturbed calcium regulation, delayed conduction velocities, modulated gap junctions, and sarcomere protein derangements. The electrical remodeling and structural changes in concert promote development of atrial cardiomyopathy in MetS and ultimately lead to vulnerability to AF. As VLDL plays a major role in lipid metabolism after meals (rather than fasting state), further human studies that focus on the effects/correlation of postprandial lipids to atrial remodeling are required to determine whether VLDL-targeted therapy can reduce MetS-related AF. On the basis of our scientific evidence, we propose a pivotal role of VLDL in MetS-related atrial cardiomyopathy and vulnerability to AF.

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Rizvi, Farhan, Alessandra DeFranco, Ramail Siddiqui, Ulugbek Negmadjanov, Larisa Emelyanova, Alisher Holmuhamedov, Gracious Ross, et al. "Chamber-specific differences in human cardiac fibroblast proliferation and responsiveness toward simvastatin." American Journal of Physiology-Cell Physiology 311, no. 2 (August 1, 2016): C330—C339. http://dx.doi.org/10.1152/ajpcell.00056.2016.

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Fibroblasts, the most abundant cells in the heart, contribute to cardiac fibrosis, the substrate for the development of arrythmogenesis, and therefore are potential targets for preventing arrhythmic cardiac remodeling. A chamber-specific difference in the responsiveness of fibroblasts from the atria and ventricles toward cytokine and growth factors has been described in animal models, but it is unclear whether similar differences exist in human cardiac fibroblasts (HCFs) and whether drugs affect their proliferation differentially. Using cardiac fibroblasts from humans, differences between atrial and ventricular fibroblasts in serum-induced proliferation, DNA synthesis, cell cycle progression, cyclin gene expression, and their inhibition by simvastatin were determined. The serum-induced proliferation rate of human atrial fibroblasts was more than threefold greater than ventricular fibroblasts with faster DNA synthesis and higher mRNA levels of cyclin genes. Simvastatin predominantly decreased the rate of proliferation of atrial fibroblasts, with inhibition of cell cycle progression and an increase in the G0/G1 phase in atrial fibroblasts with a higher sensitivity toward inhibition compared with ventricular fibroblasts. The DNA synthesis and mRNA levels of cyclin A, D, and E were significantly reduced by simvastatin in atrial but not in ventricular fibroblasts. The inhibitory effect of simvastatin on atrial fibroblasts was abrogated by mevalonic acid (500 μM) that bypasses 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition. Chamber-specific differences exist in the human heart because atrial fibroblasts have a higher proliferative capacity and are more sensitive to simvastatin-mediated inhibition through HMG-CoA reductase pathway. This mechanism may be useful in selectively preventing excessive atrial fibrosis without inhibiting adaptive ventricular remodeling during cardiac injury.

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Jandrić-Kočič, Marijana. "The incidence of atrial fibrillation in type 2 diabetes mellitus patients." Sestrinska rec 23, no. 81 (2020): 20–24. http://dx.doi.org/10.5937/sestrec2081020j.

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Goal: Diabetes mellitus type 2 is a metabolic syndrome with systemic disorders of carbohydrate metabolism, fat and protein due to the absolute or relative lack of biologically active insulin. Atrial fibrillation is characterized by high frequency excitation of atria, consequent asynchronous atrial contraction, and irregular ventricular excitation. Diabetes predisposes fibrillation through metabolic abnormalities, structural, electrical, electromechanical, and autonomic remodeling of atrias. The study had to examine the incidence of atrial fibrillation in type 2 diabetes mellitus patients and to investigate the effect of continuous anti-diabetic therapy on the frequency of atrial fibrillation. Materials and methods: The test was conducted from 01. 10. 2017 to 01.01.2019. 106 patients with type 2 diabetes mellitus were evaluated. The data were collected on the basis of history, available medical documentation, laboratory analyzes and electrocardiograms. Data processing is done using standard statistical methods. Results: The survey covered 10 (9%) men and 96 (91%) women. The age of the respondents was 30-44 years (5 subjects, 4.7%), 44-59 years (38 subjects, 35.8%), 60 years and more (63 respondents, 59.5%). The therapeutic modalities included metformin (24 subjects, 22.6%), metformin and insulin (35 subjects, 33%), insulin (8 subjects, 7.5%), metformin and sulfonylurea derivatives (39 subjects, 36.9%). Diabetes in subjects was up to 5 years (8 subjects, 7.5%), 5-10 years (26 subjects, 24.5%), 10-15 years (32 subjects, 30.2%), over 15 years (40 respondents, 37.8% ). A healthy electrocardiogram had 83 (78.3%) subjects, atrial fibrillation 21 (19.8%) subjects, other rhythm disorders 2 (1.9%) subjects. The frequency of fibrillation within the therapeutic modality was: metformin therapy, 1 (4.2%) subjects, metformin and insulin therapy, 9 (25.7%) subjects, insulin therapy, 3 (37.5%) subjects, metformin therapy and sulfonillureas 9 (20.5%) respondents. Conclusion: Type 2 diabetes mellitus patients have high incidence of atrial fibrillation (19.8%). Continuous metformin therapy results in statistically significantly lower incidence of atrial fibrillation compared to other therapeutic modalities (p <0.001). Early detection, metformin administration, and diet regimen can significantly reduce the incidence of atrial fibrillation in patients.

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Dordevic, Aleksandar, Martin Genger, Carsten Schwarz, Cesare Cuspidi, Elvis Tahirovic, Burkert Pieske, Hans-Dirk Düngen, and Marijana Tadic. "Biatrial Remodeling in Patients with Cystic Fibrosis." Journal of Clinical Medicine 8, no. 8 (July 31, 2019): 1141. http://dx.doi.org/10.3390/jcm8081141.

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Background: Previous studies have focused on left and right ventricular remodeling in cystic fibrosis (CF), whereas atrial function has not been assessed in detail so far. We sought to investigate left and right atrial (LA and RA) function in patients with CF. Methods: This retrospective investigation included 82 CF patients (64 survivors and 18 non-survivors) who were referred to CF department over the period of four years, as well as 32 control subjects matched by age and gender. All participants underwent an echocardiographic examination including a strain analysis, which was performed offline and blinded for groups. Results: LA and RA volume indexes were significantly higher in CF patients than in controls and were particularly high in CF non-survivors. LA conduit and reservoir functions were significantly worse in CF survivors and non-survivors, compared with control subjects. RA phasic function was not different between controls, CF survivors and non-survivors. The parameters of lung function (forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1)) and the LA and RA volume indexes were predictors of mortality in CF patients. However, in a multivariate analysis, only FVC was an independent predictor of mortality in CF patients. Conclusions: Our results suggest that both atria are enlarged, but only LA function is impaired in CF patients. LA reservoir and conduit function is particularly deteriorated in CF patients. Though statistical significance was not reached due to our limited sample size, there was a trend of deterioration of LA and RA function from controls across CF survivors to CF non-survivors. LA and RA enlargement represented predictors of mortality in CF patients.

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Corradi, Domenico, Sergio Callegari, Roberta Maestri, Stefano Benussi, and Ottavio Alfieri. "Structural remodeling in atrial fibrillation." Nature Clinical Practice Cardiovascular Medicine 5, no. 12 (October 14, 2008): 782–96. http://dx.doi.org/10.1038/ncpcardio1370.

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Maruyama, Toru. "Remodeling Induced by Atrial Fibrillation." Circulation Journal 76, no. 4 (2012): 812–13. http://dx.doi.org/10.1253/circj.cj-12-0155.

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Goette, Andreas, Clegg Honeycutt, and Jonathan J. Langberg. "Electrical Remodeling in Atrial Fibrillation." Circulation 94, no. 11 (December 1996): 2968–74. http://dx.doi.org/10.1161/01.cir.94.11.2968.

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Fujiki, Akira. "Electrical remodeling in atrial fibrillation." Journal of Molecular and Cellular Cardiology 45, no. 4 (October 2008): S3—S4. http://dx.doi.org/10.1016/j.yjmcc.2008.09.600.

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Ferrantini, Cecilia, Josè Manuel Pioner, Francesca Gentile, Raffaele Coppini, Cristina Morelli, Nicoletta Piroddi, Beatrice Scellini, et al. "Atrial Remodeling in Hypertrophic Cardiomyopathy." Biophysical Journal 112, no. 3 (February 2017): 556a. http://dx.doi.org/10.1016/j.bpj.2016.11.3000.

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Journal articles on the topic 'Atriale remodeling'

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