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Journal articles on the topic 'Atrial electrical remodeling'

Author: Grafiati

Published: 14 March 2023

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1

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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2

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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3

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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4

Dobrev, Dobromir. "Electrical Remodeling in Atrial Fibrillation." Herz 31, no. 2 (April 2006): 108–12. http://dx.doi.org/10.1007/s00059-006-2787-9.

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5

Dun, Wen, and Penelope A. Boyden. "Aged atria: electrical remodeling conducive to atrial fibrillation." Journal of Interventional Cardiac Electrophysiology 25, no. 1 (March 12, 2009): 9–18. http://dx.doi.org/10.1007/s10840-008-9358-3.

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6

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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7

Tamargo, Juan, and Eva Delpón. "Vagal Stimulation and Atrial Electrical Remodeling." Revista Española de Cardiología (English Edition) 62, no. 7 (June 2009): 729–32. http://dx.doi.org/10.1016/s1885-5857(09)72352-7.

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8

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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9

Pang, Helen, Ricardo Ronderos, Andrés Ricardo Pérez-Riera, Francisco Femenía, and Adrian Baranchuk. "Reverse atrial electrical remodeling: A systematic review." Cardiology Journal 18, no. 6 (November 23, 2011): 625–31. http://dx.doi.org/10.5603/cj.2011.0025.

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10

Hou, Jian, Shaojie Huang, Yan Long, Jiaxing Huang, Song Yang, Jianping Yao, Guangxian Chen, et al. "DACT2 regulates structural and electrical atrial remodeling in atrial fibrillation." Journal of Thoracic Disease 12, no. 5 (May 2020): 2039–48. http://dx.doi.org/10.21037/jtd-19-4206.

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11

Takemoto, Yoshio, Rafael J. Ramirez, Kuljeet Kaur, Oscar Salvador-Montañés, Daniela Ponce-Balbuena, Roberto Ramos-Mondragón, Steven R. Ennis, Guadalupe Guerrero-Serna, Omer Berenfeld, and José Jalife. "Eplerenone Reduces Atrial Fibrillation Burden Without Preventing Atrial Electrical Remodeling." Journal of the American College of Cardiology 70, no. 23 (December 2017): 2893–905. http://dx.doi.org/10.1016/j.jacc.2017.10.014.

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12

EVERETT, THOMAS H., HUI LI, J. MICHAEL MANGRUM, CHRISTINA MASTRANGELO, and DAVID E. HAINES. "The Effects of Atrial Electrical Remodeling on Atrial Defibrillation Thresholds." Pacing and Clinical Electrophysiology 24, no. 8 (August 2001): 1208–15. http://dx.doi.org/10.1046/j.1460-9592.2001.01208.x.

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13

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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14

KALMAN, JONATHAN M., and PAUL B. SPARKS. "Electrical Remodeling of the Atria as a Consequence of Atrial Stretch." Journal of Cardiovascular Electrophysiology 12, no. 1 (January 2001): 51–55. http://dx.doi.org/10.1046/j.1540-8167.2001.00051.x.

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15

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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16

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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17

Cha, Yong-Mei, Petras P. Dzeja, Win K. Shen, Arshad Jahangir, Chari Y. T. Hart, Andre Terzic, and Margaret M. Redfield. "Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 4 (April 1, 2003): H1313—H1320. http://dx.doi.org/10.1152/ajpheart.00337.2002.

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The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined. Dogs with ( n = 6) and without ( n = 6) rapid pacing-induced CHF underwent echocardiography (conscious) and electrophysiological (under anesthesia) studies. CHF dogs had more pronounced mitral regurgitation, higher atrial pressure, larger atrial area, and increased atrial fibrosis. An enhanced propensity to sustain AF was observed in CHF, despite significant increases in atrial effective refractory period and wavelength. Profound deficits in atrial bioenergetics were present with reduced activities of the phosphotransfer enzymes CK and AK, depletion of high-energy phosphates (ATP and creatine phosphate), and reduction of cellular energetic potential (ATP-to-ADP and creatine phosphate-to-Cr ratios). AF duration correlated with left atrial area ( r = 0.73, P = 0.01) and inversely with atrial ATP concentration ( r = −0.75, P = 0.005), CK activity ( r = −0.57, P = 0.054), and AK activity ( r = −0.64, P = 0.02). Atrial levels of malondialdehyde, a marker of oxidative stress, were significantly increased in CHF. Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF.

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18

LO, LI-WEI, CHING-TAI TAI, YENN-JIANG LIN, SHIH-LIN CHANG, WANWARANG WONGCHAROEN, and SHIH-ANN CHEN. "Reverse Atrial Electrical Remodeling After Catheter Ablation of Persistent Atrial Fibrillation." Journal of Cardiovascular Electrophysiology 17, no. 7 (July 2006): 798–99. http://dx.doi.org/10.1111/j.1540-8167.2006.00470.x.

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19

Neuberger, Hans-Ruprecht, Ulrich Schotten, Yuri Blaauw, Dirk Vollmann, Sabine Eijsbouts, Arne van Hunnik, and Maurits Allessie. "Chronic Atrial Dilation, Electrical Remodeling, and Atrial Fibrillation in the Goat." Journal of the American College of Cardiology 47, no. 3 (February 2006): 644–53. http://dx.doi.org/10.1016/j.jacc.2005.09.041.

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20

MANGRUM, J. MICHAEL, THOMAS H. EVERETT, MARK A. MITCHELL, IAN D. MCRURY, HUI LI, and DAVID E. HAINES. "The Effects of Reverse Atrial Electrical Remodeling on Atrial Defibrillation Thresholds." Pacing and Clinical Electrophysiology 25, no. 4 (April 2002): 470–76. http://dx.doi.org/10.1046/j.1460-9592.2002.00470.x.

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21

Aguilar, M., X. Qi, H. Huang, P. Comtois, and S. Nattel. "Effect of Fibroblast Electrical Remodeling on Atrial Arrhythmogenesis in Atrial Fibrillation." Canadian Journal of Cardiology 29, no. 10 (October 2013): S108—S109. http://dx.doi.org/10.1016/j.cjca.2013.07.139.

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22

Healey, Jeff S., Carsten W. Israel, Stuart J. Connolly, Stefan H. Hohnloser, Girish M. Nair, Syamkumar Divakaramenon, Alessandro Capucci, et al. "Relevance of Electrical Remodeling in Human Atrial Fibrillation." Circulation: Arrhythmia and Electrophysiology 5, no. 4 (August 2012): 626–31. http://dx.doi.org/10.1161/circep.112.970442.

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23

Bollmann, A. "Quantification of electrical remodeling in human atrial fibrillation." Cardiovascular Research 47, no. 2 (August 2000): 207–9. http://dx.doi.org/10.1016/s0008-6363(00)00133-4.

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24

Allessie, M. "Electrical, contractile and structural remodeling during atrial fibrillation." Cardiovascular Research 54, no. 2 (May 2002): 230–46. http://dx.doi.org/10.1016/s0008-6363(02)00258-4.

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25

Srivastava, Ujala, Aparajita Bhattacharya, Mohamed Boutjdir, and Ademuyiwa S. Aromolaran. "Mechanisms of Atrial Electrical Remodeling in Obese Heart." Biophysical Journal 114, no. 3 (February 2018): 383a. http://dx.doi.org/10.1016/j.bpj.2017.11.2118.

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26

Van Wagoner, David R., and Jeanne M. Nerbonne. "Molecular Basis of Electrical Remodeling in Atrial Fibrillation." Journal of Molecular and Cellular Cardiology 32, no. 6 (June 2000): 1101–17. http://dx.doi.org/10.1006/jmcc.2000.1147.

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27

Simard, Christophe, Virginie Ferchaud, Laurent Sallé, Paul Milliez, Alain Manrique, Joachim Alexandre, and Romain Guinamard. "TRPM4 Participates in Aldosterone-Salt-Induced Electrical Atrial Remodeling in Mice." Cells 10, no. 3 (March 12, 2021): 636. http://dx.doi.org/10.3390/cells10030636.

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Aldosterone plays a major role in atrial structural and electrical remodeling, in particular through Ca2+-transient perturbations and shortening of the action potential. The Ca2+-activated non-selective cation channel Transient Receptor Potential Melastatin 4 (TRPM4) participates in atrial action potential. The aim of our study was to elucidate the interactions between aldosterone and TRPM4 in atrial remodeling and arrhythmias susceptibility. Hyperaldosteronemia, combined with a high salt diet, was induced in mice by subcutaneously implanted osmotic pumps during 4 weeks, delivering aldosterone or physiological serum for control animals. The experiments were conducted in wild type animals (Trpm4+/+) as well as Trpm4 knock-out animals (Trpm4-/-). The atrial diameter measured by echocardiography was higher in Trpm4-/- compared to Trpm4+/+ animals, and hyperaldosteronemia-salt produced a dilatation in both groups. Action potentials duration and triggered arrhythmias were measured using intracellular microelectrodes on the isolated left atrium. Hyperaldosteronemia-salt prolong action potential in Trpm4-/- mice but had no effect on Trpm4+/+ mice. In the control group (no aldosterone-salt treatment), no triggered arrythmias were recorded in Trpm4+/+ mice, but a high level was detected in Trpm4-/- mice. Hyperaldosteronemia-salt enhanced the occurrence of arrhythmias (early as well as delayed-afterdepolarization) in Trpm4+/+ mice but decreased it in Trpm4-/- animals. Atrial connexin43 immunolabelling indicated their disorganization at the intercalated disks and a redistribution at the lateral side induced by hyperaldosteronemia-salt but also by Trpm4 disruption. In addition, hyperaldosteronemia-salt produced pronounced atrial endothelial thickening in both groups. Altogether, our results indicated that hyperaldosteronemia-salt and TRPM4 participate in atrial electrical and structural remodeling. It appears that TRPM4 is involved in aldosterone-induced atrial action potential shortening. In addition, TRPM4 may promote aldosterone-induced atrial arrhythmias, however, the underlying mechanisms remain to be explored.

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28

Nam, Gi-Byoung, Dong-Woon Kim, Chengri Che, Seogjae Lee, Jong-Myeon Hong, Seung-Woon Lim, Ki-Jeong Na, and Myeong-Chan Cho. "Pacing-induced Atrial Electrical Remodeling and its Recovery in Conscious Dog Atria." Korean Circulation Journal 28, no. 6 (1998): 961. http://dx.doi.org/10.4070/kcj.1998.28.6.961.

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29

Sparks, Paul B., Shenthar Jayaprakash, Jitendra K. Vohra, and Jonathan M. Kalman. "Electrical Remodeling of the Atria Associated With Paroxysmal and Chronic Atrial Flutter." Circulation 102, no. 15 (October 10, 2000): 1807–13. http://dx.doi.org/10.1161/01.cir.102.15.1807.

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30

LAU, CHU-PAK, HUNG-FAT TSE, CHUNG-WAH SIU, and DAVID GBADEBO. "Atrial Electrical and Structural Remodeling: Implications for Racial Differences in Atrial Fibrillation." Journal of Cardiovascular Electrophysiology 23 (November 2012): s36—s40. http://dx.doi.org/10.1111/jce.12022.

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31

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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32

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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33

Nakashima, Hideko, Koichiro Kumagai, Hidenori Urata, Naoki Gondo, Munehito Ideishi, and Kikuo Arakawa. "Angiotensin II Antagonist Prevents Electrical Remodeling in Atrial Fibrillation." Circulation 101, no. 22 (June 6, 2000): 2612–17. http://dx.doi.org/10.1161/01.cir.101.22.2612.

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34

Bosch, R. "Ionic mechanisms of electrical remodeling in human atrial fibrillation." Cardiovascular Research 44, no. 1 (October 1999): 121–31. http://dx.doi.org/10.1016/s0008-6363(99)00178-9.

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35

YANG, Z., W. SHEN, J. ROTTMAN, J. WIKSWO, and K. MURRAY. "Rapid stimulation causes electrical remodeling in cultured atrial myocytes." Journal of Molecular and Cellular Cardiology 38, no. 2 (February 2005): 299–308. http://dx.doi.org/10.1016/j.yjmcc.2004.11.015.

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36

Alexander, Bryce, Fariha Sadiq, Kousha Azimi, Benedict Glover, Pavel Antiperovitch, Wilma M. Hopman, Zardasht Jaff, and Adrian Baranchuk. "Reverse atrial electrical remodeling induced by cardiac resynchronization therapy." Journal of Electrocardiology 50, no. 5 (September 2017): 610–14. http://dx.doi.org/10.1016/j.jelectrocard.2017.04.015.

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37

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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BALAN, Alkora Ioana, Irina PINTILIE, Cristina SOMKEREKI, Marcel PERIAN, Laura CHINEZU, Claudia BANESCU, Razvan Constantin SERBAN, and Alina SCRIDON. "Role of Preexisting Proarrhythmic Atrial Remodeling in Post-Coronary Artery Bypass Grafting Atrial Fibrillation." Romanian Journal of Cardiology 31, no. 3 (September 24, 2021): 597–607. http://dx.doi.org/10.47803/rjc.2021.31.3.597.

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Introduction: Due to its deleterious effects, early identifi cation of patients at risk of postoperative AF (POAF) is of critical importance. Preexisting proarrhythmic atrial remodeling could contribute to this increased risk. Therefore, we aimed to evaluate the presence of preexisting proarrhythmic atrial remodeling and its impact on POAF occurrence in patients undergoing coronary artery bypass grafting (CABG). Methods: Data regarding atrial structural (atrial size and histology), electrical (P-wave and atrial action potential parameters, mRNA expression of several AF-related genes), and autonomic (heart rate variability parameters) proarrhythmic remodeling were compared between patients with (AF; n=11) and without (no-AF; n=19) POAF. Impact of POAF on postoperative outcomes was also evaluated. Results: No signifi cant difference was observed in atrial electrical parameters between the two groups (all p>0.05). However, compared with no-AF, AF patients had more important subepicardial adipose infi ltration (p=0.02) and higher markers of parasympathetic and sympathetic modulation (both p=0.03). Patients with POAF had longer hospital stay and more often presented postoperative renal dysfunction (both p=0.04). Conclusion: These fi ndings suggest that preexisting atrial structural (i.e., increased atrial subepicardial adiposity) and autonomic (i.e., sympatho-vagal coactivation) alterations could favor the occurrence of POAF. At its turn, POAF was associated with altered postoperative outcomes in CABG patients.

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Zhao, Hongyan, Tiankai Li, Guangzhong Liu, Li Zhang, Guangnan Li, Jia Yu, Qi Lou, et al. "Chronic B-Type Natriuretic Peptide Therapy Prevents Atrial Electrical Remodeling in a Rabbit Model of Atrial Fibrillation." Journal of Cardiovascular Pharmacology and Therapeutics 24, no. 6 (June 3, 2019): 575–85. http://dx.doi.org/10.1177/1074248419854749.

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Background: Atrial fibrillation (AF) is an important and growing clinical problem. Current pharmacological treatments are unsatisfactory. Electrical remodeling has been identified as one of the principal pathophysiological mechanisms that promote AF, but there are no effective therapies to prevent or correct electrical remodeling in patients with AF. In AF, cardiac production and circulating levels of B-type natriuretic peptide (BNP) are increased. However, its functional significance in AF remains to be determined. We assessed the hypotheses that chronic BNP treatment may prevent the altered electrophysiology in AF, and preventing AF-induced activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) may play a role. Methods and Results: Forty-four rabbits were randomly divided into sham, rapid atrial pacing (RAP at 600 beats/min for 3 weeks), RAP/BNP, and sham/BNP groups. Rabbits in the RAP/BNP and sham/BNP groups received subcutaneous BNP (20 μg/kg twice daily) during the 3-week study period. HL-1 cells were subjected to rapid field stimulation for 24 hours in the presence or absence of BNP, KN-93 (a CaMKII inhibitor), or KN-92 (a nonactive analog of KN-93). We compared atrial electrical remodeling-related alterations in the ion channel/function/expression of these animals. We found that only in the RAP group, AF inducibility was significantly increased, atrial effective refractory periods and action potential duration were reduced, and the density of I Ca, L and I to decreased, while I K1 increased. The changes in the expressions of Cav1.2, Kv4.3, and Kir2.1 and currents showed a similar trend. In addition, in the RAP group, the activation of CaMKIIδ and phosphorylation of ryanodine receptor 2 and phospholamban significantly increased. Importantly, these changes were prevented in the RAP/BNP group, which were further validated by in vitro studies. Conclusions: Chronic BNP therapy prevents atrial electrical remodeling in AF. Inhibition of CaMKII activation plays an important role to its anti-AF efficacy in this model.

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40

Ramirez, Rafael J., Stanley Nattel, and Marc Courtemanche. "Mathematical analysis of canine atrial action potentials: rate, regional factors, and electrical remodeling." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (October 1, 2000): H1767—H1785. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1767.

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Dogs have been used extensively to study atrial arrhythmias, but there are no published mathematical models of the canine atrial action potential (AP). To obtain insights into the ionic mechanisms governing canine atrial AP properties, we incorporated formulations of K+, Na+, Ca2+, and Cl− currents, based on measurements in canine atrial myocytes, into a mathematical model of the AP. The rate-dependent behavior of model APs corresponded to experimental measurements and pointed to a central role for L-type Ca2+ current inactivation in rate adaptation. Incorporating previously described regional ionic current variations into the model largely reproduced AP forms characteristic of the corresponding right atrial regions (appendage, pectinate muscle, crista terminalis, and atrioventricular ring). When ionic alterations induced by tachycardia-dependent remodeling were incorporated, the model reproduced qualitatively the AP features constituting the cellular substrate for atrial fibrillation. We conclude that this ionic model of the canine atrial AP agrees well with experimental measurements and gives potential insights into mechanisms underlying functionally important electrophysiological phenomena in canine atrium.

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41

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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42

Todd, Derick M., Simon P. Fynn, Andrew P. Walden, W. Julian Hobbs, Sanjay Arya, and Clifford J. Garratt. "Repetitive 4-Week Periods of Atrial Electrical Remodeling Promote Stability of Atrial Fibrillation." Circulation 109, no. 11 (March 23, 2004): 1434–39. http://dx.doi.org/10.1161/01.cir.0000124006.84596.d9.

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Hobbs, W. Julian C., Simon Fynn, Derick M. Todd, Peter Wolfson, Mike Galloway, and Clifford J. Garratt. "Reversal of Atrial Electrical Remodeling After Cardioversion of Persistent Atrial Fibrillation in Humans." Circulation 101, no. 10 (March 14, 2000): 1145–51. http://dx.doi.org/10.1161/01.cir.101.10.1145.

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44

Yamada, Hirotsugu, Yong Jin Kim, Tomotsugu Tabata, Neil L. Greenberg, Erwan Donal, Deborah A. Agler, Junko Watanabe, et al. "Correlation of left atrial mechanical and electrical remodeling following short duration atrial fibrillation." Journal of the American College of Cardiology 39 (March 2002): 376. http://dx.doi.org/10.1016/s0735-1097(02)81689-8.

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45

Xu, Qiang, and Huan Lan. "GW27-e1201 MiR-101 is involved in atrial electrical remodeling in atrial fibrillation." Journal of the American College of Cardiology 68, no. 16 (October 2016): C44. http://dx.doi.org/10.1016/j.jacc.2016.07.162.

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46

Abed, H., P. Kuklik, D. Kelly, A. Nelson, S. Worthley, W. Abhayaratna, G. Wittert, and P. Sanders. "Obesity Results in Progressive Atrial Electrical and Structural Remodeling: Implications for Atrial Fibrillation." Heart, Lung and Circulation 20 (January 2011): S2. http://dx.doi.org/10.1016/j.hlc.2011.05.006.

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47

Abed, Hany S., Chrishan S. Samuel, Dennis H. Lau, Darren J. Kelly, Simon G. Royce, Muayad Alasady, Rajiv Mahajan, et al. "Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation." Heart Rhythm 10, no. 1 (January 2013): 90–100. http://dx.doi.org/10.1016/j.hrthm.2012.08.043.

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48

Doñate Puertas, Rosa, Gilles Millat, Isabelle Ernens, Vincent Gache, Samuel Chauveau, Elodie Morel, Emilie Christin, Nathalie Couturier, Yvan Devaux, and Philippe Chevalier. "Atrial Structural Remodeling Gene Variants in Patients with Atrial Fibrillation." BioMed Research International 2018 (September 10, 2018): 1–12. http://dx.doi.org/10.1155/2018/4862480.

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Atrial fibrillation (AF) is a common arrhythmia for which the genetic studies mainly focused on the genes involved in electrical remodeling, rather than left atrial muscle remodeling. To identify rare variants involved in atrial myopathy using mutational screening, a high-throughput next-generation sequencing (NGS) workflow was developed based on a custom AmpliSeq™ panel of 55 genes potentially involved in atrial myopathy. This workflow was applied to a cohort of 94 patients with AF, 76 with atrial dilatation and 18 without. Bioinformatic analyses used NextGENe® software and in silico tools for variant interpretation. The AmpliSeq custom-made panel efficiently explored 96.58% of the targeted sequences. Based on in silico analysis, 11 potentially pathogenic missense variants were identified that were not previously associated with AF. These variants were located in genes involved in atrial tissue structural remodeling. Three patients were also carriers of potential variants in prevalent arrhythmia-causing genes, usually associated with AF. Most of the variants were found in patients with atrial dilatation (n=9, 82%). This NGS approach was a sensitive and specific method that identified 11 potentially pathogenic variants, which are likely to play roles in the predisposition to left atrial myopathy. Functional studies are needed to confirm their pathogenicity.

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Aonuma, Kazuhiro, DongZhu Xu, Nobuyuki Murakoshi, Kazuko Tajiri, Yuta Okabe, Zixun Yuan, Siqi Li, et al. "Novel preventive effect of isorhamnetin on electrical and structural remodeling in atrial fibrillation." Clinical Science 136, no. 24 (December 2022): 1831–49. http://dx.doi.org/10.1042/cs20220319.

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Abstract Isorhamnetin, a natural flavonoid, has strong antioxidant and antifibrotic effects, and a regulatory effect against Ca2+-handling. Atrial remodeling due to fibrosis and abnormal intracellular Ca2+ activities contributes to initiation and persistence of atrial fibrillation (AF). The present study investigated the effect of isorhamnetin on angiotensin II (AngII)-induced AF in mice. Wild-type male mice (C57BL/6J, 8 weeks old) were assigned to three groups: (1) control group, (2) AngII-treated group, and (3) AngII- and isorhamnetin-treated group. AngII (1000 ng/kg/min) and isorhamnetin (5 mg/kg) were administered continuously via an implantable osmotic pump for two weeks and intraperitoneally one week before initiating AngII administration, respectively. AF induction and electrophysiological studies, Ca2+ imaging with isolated atrial myocytes and HL-1 cells, and action potential duration (APD) measurements using atrial tissue and HL-1 cells were performed. AF-related molecule expression was assessed and histopathological examination was performed. Isorhamnetin decreased AF inducibility compared with the AngII group and restored AngII-induced atrial effective refractory period prolongation. Isorhamnetin eliminated abnormal diastolic intracellular Ca2+ activities induced by AngII. Isorhamnetin also abrogated AngII-induced APD prolongation and abnormal Ca2+ loading in HL-1 cells. Furthermore, isorhamnetin strongly attenuated AngII-induced left atrial enlargement and atrial fibrosis. AngII-induced elevated expression of AF-associated molecules, such as ox-CaMKII, p-RyR2, p-JNK, p-ERK, and TRPC3/6, was improved by isorhamnetin treatment. The findings of the present study suggest that isorhamnetin prevents AngII-induced AF vulnerability and arrhythmogenic atrial remodeling, highlighting its therapeutic potential as an anti-arrhythmogenic pharmaceutical or dietary supplement.

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Wałek, Paweł, Joanna Roskal-Wałek, Patryk Dłubis, Justyna Tracz, and Beata Wożakowska-Kapłon. "Left Atrial Wall Motion Velocity Assessed during Atrial Fibrillation Predicts Sinus Rhythm Maintenance after Electrical Cardioversion in Patients with Persistent Atrial Fibrillation." International Journal of Environmental Research and Public Health 19, no. 23 (November 23, 2022): 15508. http://dx.doi.org/10.3390/ijerph192315508.

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Reduced left atrial wall motion velocity measured during AF (LAWMV) indicates left atrial remodeling. The aim of this study was to investigate whether LAWMV assessed with tissue Doppler imaging during atrial fibrillation (AF) predicts sinus rhythm (SR) maintenance after direct current cardioversion (DCCV) for persistent AF. The study included 126 patients who underwent DCCV and were followed for 12 months. At 12 months, maintained SR was reported in 55 patients (43.7%). We noted that LAWMV was higher in patients with maintained SR at 12 months than in those with recurrent AF (3.69 ± 0.84 vs. 2.86 ± 1.09; p < 0.001). In the multivariable regression model containing echocardiographic variables, LAWMV was an independent predictor of SR maintenance at 12 months (odds ratio [OR] 1.72, 95% confidence interval [CI] 1.1–2.69; p = 0.017). Similarly, LAWMW was an independent predictor of SR maintenance at 12 months (OR 1.81, 95% CI 1.19–2.77; p = 0.006) in the multivariate regression model containing both echocardiographic and clinical variables. LAWMV predicts SR maintenance after DCCV for persistent AF. Echocardiographic markers of left atrial mechanical remodeling are better at predicting SR maintenance than markers of structural remodeling.

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