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Journal articles on the topic 'Atrial fibrillation substrate'

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Author: Grafiati

Published: 11 March 2023

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1

Arentz, Thomas, Björn Müller-Edenborn, and Amir Jadidi. "Arrhythmogenic Atrial Substrate in Persistent Atrial Fibrillation." JACC: Clinical Electrophysiology 4, no. 1 (January 2018): 97–98. http://dx.doi.org/10.1016/j.jacep.2017.11.009.

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2

Kottkamp, Hans. "On the Atrial Fibrillation Substrate." Journal of the American College of Cardiology 74, no. 10 (September 2019): 1348–51. http://dx.doi.org/10.1016/j.jacc.2019.06.064.

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3

Roberts, Jason D., and Michael H. Gollob. "Atrial myopathy: A primary substrate for atrial fibrillation." Heart Rhythm 19, no. 3 (March 2022): 476–77. http://dx.doi.org/10.1016/j.hrthm.2021.12.011.

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4

Haïssaguerre, Michel, Matthew Wright, Mélèze Hocini, and Pierre Jaïs. "The Substrate Maintaining Persistent Atrial Fibrillation." Circulation: Arrhythmia and Electrophysiology 1, no. 1 (April 2008): 2–5. http://dx.doi.org/10.1161/circep.108.764233.

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5

Calkins, Hugh. "The Dynamic Substrate for Atrial Fibrillation." JACC: Clinical Electrophysiology 3, no. 4 (April 2017): 403–4. http://dx.doi.org/10.1016/j.jacep.2016.12.003.

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6

Zghaib, Tarek, Ali Keramati, Jonathan Chrispin, Dong Huang, Muhammad A. Balouch, Luisa Ciuffo, Ronald D. Berger, et al. "Multimodal Examination of Atrial Fibrillation Substrate." JACC: Clinical Electrophysiology 4, no. 1 (January 2018): 59–68. http://dx.doi.org/10.1016/j.jacep.2017.10.010.

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7

Chimenti, Cristina, Matteo A. Russo, Angelo Carpi, and Andrea Frustaci. "Histological substrate of human atrial fibrillation." Biomedicine & Pharmacotherapy 64, no. 3 (March 2010): 177–83. http://dx.doi.org/10.1016/j.biopha.2009.09.017.

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8

Kottkamp, Hans. "Atrial fibrillation substrate: The “unknown species”— From lone atrial fibrillation to fibrotic atrial cardiomyopathy." Heart Rhythm 9, no. 4 (April 2012): 481–82. http://dx.doi.org/10.1016/j.hrthm.2012.01.008.

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9

Medi, C., A. Teh, K. Roberts-Thomson, J. Morton, P. Kistler, and J. Kalman. "Advanced Right Atrial Substrate Promotes Atrial Flutter over Atrial Fibrillation." Heart, Lung and Circulation 21 (January 2012): S99. http://dx.doi.org/10.1016/j.hlc.2012.05.250.

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10

Rivner, Harold, Raul D. Mitrani, and Jeffrey J. Goldberger. "Atrial Myopathy Underlying Atrial Fibrillation." Arrhythmia & Electrophysiology Review 9, no. 2 (August 13, 2020): 61–70. http://dx.doi.org/10.15420/aer.2020.13.

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While AF most often occurs in the setting of atrial disease, current assessment and treatment of patients with AF does not focus on the extent of the atrial myopathy that serves as the substrate for this arrhythmia. Atrial myopathy, in particular atrial fibrosis, may initiate a vicious cycle in which atrial myopathy leads to AF, which in turn leads to a worsening myopathy. Various techniques, including ECG, plasma biomarkers, electroanatomical voltage mapping, echocardiography, and cardiac MRI, can help to identify and quantify aspects of the atrial myopathy. Current therapies, such as catheter ablation, do not directly address the underlying atrial myopathy. There is emerging research showing that by targeting this myopathy we can help decrease the occurrence and burden of AF.

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11

Olgin, Jeffrey E., Haris J. Sih, Steven Hanish, J. Vijay Jayachandran, Jiashin Wu, Qi Huang Zheng, Wendy Winkle, G. Keith Mulholland, Douglas P. Zipes, and Gary Hutchins. "Heterogeneous Atrial Denervation Creates Substrate for Sustained Atrial Fibrillation." Circulation 98, no. 23 (December 8, 1998): 2608–14. http://dx.doi.org/10.1161/01.cir.98.23.2608.

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12

Rocken, C., B. Peters, and G. Juenemann. "Atrial amyloidosis. An arrhythmogenic substrate for persistent atrial fibrillation." ACC Current Journal Review 12, no. 2 (March 2003): 86–87. http://dx.doi.org/10.1016/s1062-1458(03)00088-6.

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13

Zhao, Yan, Lilas Dagher, Chao Huang, Peter Miller, and Nassir F. Marrouche. "Cardiac MRI to Manage Atrial Fibrillation." Arrhythmia & Electrophysiology Review 9, no. 4 (December 24, 2020): 189–94. http://dx.doi.org/10.15420/aer.2020.21.

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AF is the most common arrhythmia in clinical practice. In addition to the severe effect on quality of life, patients with AF are at higher risk of stroke and mortality. Recent studies have suggested that atrial and ventricular substrate play a major role in the development and maintenance of AF. Cardiac MRI has emerged as a viable tool for interrogating the underlying substrate in AF patients. Its advantage includes localisation and quantification of structural remodelling. Cardiac MRI of the atrial substrate is not only a tool for management and treatment of arrhythmia, but also to individualise the prevention of stroke and major cardiovascular events. This article provides an overview of atrial imaging using cardiac MRI and its clinical implications in the AF population.

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14

Tang, Ri-Bo, Chang-Sheng Ma, Jian-Zeng Dong, Rong-Hui Yu, and De-Yong Long. "PW006 Aging and atrial fibrillation substrate in patients with non-paroxysmal atrial fibrillation." Global Heart 9, no. 1 (March 2014): e265. http://dx.doi.org/10.1016/j.gheart.2014.03.2170.

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15

Stychynskyi, Oleksandr S., Alina V. Topchii, and Pavlo O. Almiz. "Substrate Modification in Catheter Treatment of Atrial Fibrillation." Ukrainian Journal of Cardiovascular Surgery, no. 3 (44) (September 21, 2021): 76–79. http://dx.doi.org/10.30702/ujcvs/21.4409/s.t.043-76-79.

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According to modern concepts, atrial fibrillation (AF) occurs when there are triggers affecting the prepared substrate (atrial myocardium) in the presence of modulating factors that contribute to the occurrence of arrhythmia. Catheter treatment of AF has been most successfully developed in the field of affecting triggers (since late 1990s, the most successful was a technique of isolation of pulmonary veins which are the main source of trigger impulses in AF). Over the past two decades, various techniques have also been proposed for influencing the fibrous substrate. The aim. To analyze the most advanced techniques for influencing the fibrous substrate during catheter treatment of AF. Materials and methods. We analyzed the experience of leading electrophysiological centers in this field. Discussion. Modern studies contain various electrophysiological criteria of fibrous myocardium. However, the signal amplitude less than 0.5 mV is considered borderline between healthy and damaged tissues by most authors. The task of the catheter action on the myocardium is to separate the fibrously altered tissue and intact tissue. This can be achieved by isolating the area of fibrosis or by transforming it into a scar tissue incapable of arrhythmogenesis. It should be noted that both methods are associated with the same frequency of the absence of AF paroxysms, which can be regarded as confirmation of the advisability of influencing the substrate. The most important is that exposure of the substrate can significantly reduce the recurrence rate of AF compared to that when the ablation procedure is limited to isolation of the pulmonary veins. Conclusions. Modern methods of influencing the areas of fibrosis in the atria can significantly improve the results of catheter treatment of AF.

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16

PAPPONE, CARLO, and VINCENZO SANTINELLI. "Substrate Ablation in Treatment of Atrial Fibrillation." Journal of Cardiovascular Electrophysiology 17, s3 (December 2006): S23—S27. http://dx.doi.org/10.1111/j.1540-8167.2006.00630.x.

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17

Parkash, Ratika. "Triggers, Substrate, and Hypertension in Atrial Fibrillation." JACC: Clinical Electrophysiology 1, no. 3 (June 2015): 174–76. http://dx.doi.org/10.1016/j.jacep.2015.05.005.

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18

Kottkamp, Hans, and Doreen Schreiber. "The Substrate in “Early Persistent” Atrial Fibrillation." JACC: Clinical Electrophysiology 2, no. 2 (April 2016): 140–42. http://dx.doi.org/10.1016/j.jacep.2016.02.010.

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19

Nademanee, Koonlawee, Evan Lockwood, Naoya Oketani, and Brett Gidney. "Catheter ablation of atrial fibrillation guided by complex fractionated atrial electrogram mapping of atrial fibrillation substrate." Journal of Cardiology 55, no. 1 (January 2010): 1–12. http://dx.doi.org/10.1016/j.jjcc.2009.11.002.

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20

Burgon, Nathan, Troy J. Badger, Nazem W. Akoum, Gaston Vergara, Lori McMullan, Yaw A. Adjei-Poku, Thomas S. Haslam, et al. "ASSESSMENT OF THE LEFT ATRIAL SUBSTRATE IN LONE ATRIAL FIBRILLATION: IMPLICATIONS FOR STAGING OF ATRIAL FIBRILLATION." Journal of the American College of Cardiology 55, no. 10 (March 2010): A83.E780. http://dx.doi.org/10.1016/s0735-1097(10)60781-4.

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21

Sepehri Shamloo, Alireza, Daniela Husser, Petra Buettner, Karin Klingel, Gerhard Hindricks, and Andreas Bollmann. "Atrial septum biopsy for direct substrate characterization in atrial fibrillation." Journal of Cardiovascular Electrophysiology 31, no. 1 (December 15, 2019): 308–12. http://dx.doi.org/10.1111/jce.14308.

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22

Robinson, M. Clive, Murali Chiravuri, Robert Winslow, Craig McPherson, and Murthy Chamarthy. "Extended Posterior Left Atrial Substrate Ablation for Advanced Atrial Fibrillation." Chest 144, no. 4 (October 2013): 162A. http://dx.doi.org/10.1378/chest.1704612.

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23

Kottkamp, Hans. "Human atrial fibrillation substrate: towards a specific fibrotic atrial cardiomyopathy." European Heart Journal 34, no. 35 (June 11, 2013): 2731–38. http://dx.doi.org/10.1093/eurheartj/eht194.

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24

Rangnekar, G., A. Brooks, and P. Sanders. "Presence of Abnormal Atrial Substrate in New Onset Atrial Fibrillation." Heart, Lung and Circulation 20 (January 2011): S105. http://dx.doi.org/10.1016/j.hlc.2011.05.261.

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25

Mao, Jun, Benjamin J. Scherlag, Yu Liu, Youqi Fan, Vandana Varma, Stavros Stavrakis, and Sunny S. Po. "The atrial neural network as a substrate for atrial fibrillation." Journal of Interventional Cardiac Electrophysiology 35, no. 1 (June 14, 2012): 3–9. http://dx.doi.org/10.1007/s10840-012-9692-3.

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26

GOETTE, A. "Atrial amyloidosis and atrial fibrillation: a gender-dependent ?arrhythmogenic substrate??" European Heart Journal 25, no. 14 (July 2004): 1185–86. http://dx.doi.org/10.1016/j.ehj.2004.04.014.

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27

Kim, Albert M., Jeffrey E. Olgin, and Thomas H. Everett. "Role of atrial substrate and spatiotemporal organization in atrial fibrillation." Heart Rhythm 6, no. 8 (August 2009): S1—S7. http://dx.doi.org/10.1016/j.hrthm.2009.02.010.

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28

Mitchell, Russell, and Cesar Augusto Bonilla Isaza. "Long-standing Persistent Atrial Fibrillation Ablation: the Role of the Inter- and Intra-atrial Bundles." Journal of Cardiac Arrhythmias 33, no. 2 (September 25, 2020): 73–81. http://dx.doi.org/10.24207/jca.v33i2.3368.

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Catheter ablation has become the mainstream treatment of atrial fibrillation, but still remains a challenge in those patient with persistent and long standing persistent atrial fibrillation. In addition of isolation of the pulmonary veins, any other areas that can trigger or perpetuate atrial fibrillation need to be isolated. Current technologies may allow to effectively deliver permanently lasting lesions, and therefore improve clinical outcomes after ablation. The specialized conduction system including the Bachmann and septopulmonary bundles, are important substrate targets for the management of atrial fibrillation. The anatomical location of these fibers, and the corresponding approach for ablation are described in this case.

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29

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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30

Luca, Adrian, Todd Kallmyer, and Nathalie Virag. "Atrial fibrillation septal pacing: translation of modelling results." EP Europace 18, suppl_4 (December 1, 2016): iv53—iv59. http://dx.doi.org/10.1093/europace/euw360.

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Aims Atrial fibrillation (AF) septal pacing consists of rapid pacing from a ring of electrodes around the atrial septum, leading to local capture of both atria during AF. The present model-based study evaluated the impact of the number of stimulation electrodes in the septal ring on AF capture for different types of sustained AF dynamics. Methods and results Using a biophysical model of AF based on CT scans from an AF patient, models with different AF substrates (Cholinergic AF and Meandering Wavelets) were created by varying the atrial membrane kinetics. Rapid pacing was applied from the septum area with a ring of 1, 2, 3, 4, 6, 8, or 12 electrodes during 20 seconds at a pacing cycle lengths (PCLs) in the range 60–100% of AF cycle length (AFCL), in 4% steps. Percentage of captured tissue during rapid pacing was determined using 24 sensing electrode pairs evenly distributed on the atrial surface. Results were averaged over 10 AF simulations. For Cholinergic AF, the number of stimulation electrodes on the septal ring had no significant impact on AF capture independently of AF dynamics. For Meandering Wavelets, more electrodes were needed to achieve AF capture in the presence of complex AF. Conclusion Changes in AF substrate significantly impacted septal pacing outcomes and response to rapid AF pacing may similarly vary patient-to-patient. The number of stimulation electrodes had a lesser impact, suggesting that the design of a ring with 3–4 electrodes around the septum would be sufficient for most AF dynamics.

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31

Mahnkopf, Christian, Younghoon Kwon, and Nazem Akoum. "Atrial Fibrosis, Ischaemic Stroke and Atrial Fibrillation." Arrhythmia & Electrophysiology Review 10, no. 4 (December 15, 2021): 225–29. http://dx.doi.org/10.15420/aer.2021.51.

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Atrial fibrosis is an important component of the arrhythmic substrate in AF. Evidence suggests that atrial fibrosis also plays a role in increasing the risk of stroke in patients with the arrhythmia. Patients with embolic stroke of undetermined source (ESUS), who are suspected to have AF but are rarely shown to have it, frequently demonstrate evidence of atrial fibrosis; measured using late-gadolinium enhancement MRI, this manifests as atrial remodelling encompassing structural, functional and electrical properties. In this review, the authors discuss the available evidence linking atrial disease, including fibrosis, with the risk of ischaemic stroke in AF, as well as in the ESUS population, in whom it has been linked to recurrent stroke and new-onset AF. They also discuss the implications of this association on future research that may elucidate the mechanism of stroke and stroke prevention strategies in the AF and ESUS populations.

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32

CHANG, SHIH-LIN, CHING-TAI TAI, YENN-JIANG LIN, WANWARANG WONGCHAROEN, LI-WEI LO, TA-CHUAN TUAN, AMEYA R. UDYAVAR, et al. "Biatrial Substrate Properties in Patients with Atrial Fibrillation." Journal of Cardiovascular Electrophysiology 18, no. 11 (November 2007): 1134–39. http://dx.doi.org/10.1111/j.1540-8167.2007.00941.x.

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33

Haïssaguerre, Michel, Prashanthan Sanders, Mélèze Hocini, Pierre Jaïs, and Jacques Clémenty. "Pulmonary veins in the substrate for atrial fibrillation." Journal of the American College of Cardiology 43, no. 12 (June 2004): 2290–92. http://dx.doi.org/10.1016/j.jacc.2004.03.036.

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34

Zemlin, C., and R. D. Veenstra. "What Is the Structural Substrate for Atrial Fibrillation?" Cardiology 114, no. 1 (2009): 19–21. http://dx.doi.org/10.1159/000210397.

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35

Sitges, Marta. "Reversing the Substrate for Atrial Fibrillation With CRT?" JACC: Cardiovascular Imaging 9, no. 2 (February 2016): 112–13. http://dx.doi.org/10.1016/j.jcmg.2015.06.021.

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36

Nguyen, Bich Lien, Michael C. Fishbein, Lan S. Chen, Peng-Sheng Chen, and Saqib Masroor. "Histopathological substrate for chronic atrial fibrillation in humans." Heart Rhythm 6, no. 4 (April 2009): 454–60. http://dx.doi.org/10.1016/j.hrthm.2009.01.010.

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37

Frustaci, Andrea, Cristina Chimenti, Fulvio Bellocci, Emanuela Morgante, Matteo A. Russo, and Attilio Maseri. "Histological Substrate of Atrial Biopsies in Patients With Lone Atrial Fibrillation." Circulation 96, no. 4 (August 19, 1997): 1180–84. http://dx.doi.org/10.1161/01.cir.96.4.1180.

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38

Sim, Iain, Martin Bishop, Mark O’Neill, and Steven E. Williams. "Left atrial voltage mapping: defining and targeting the atrial fibrillation substrate." Journal of Interventional Cardiac Electrophysiology 56, no. 3 (May 10, 2019): 213–27. http://dx.doi.org/10.1007/s10840-019-00537-8.

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39

Stiles, Martin K., Bobby John, Christopher X. Wong, Pawel Kuklik, Anthony G. Brooks, Dennis H. Lau, Hany Dimitri, et al. "Paroxysmal Lone Atrial Fibrillation Is Associated With an Abnormal Atrial Substrate." Journal of the American College of Cardiology 53, no. 14 (April 2009): 1182–91. http://dx.doi.org/10.1016/j.jacc.2008.11.054.

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40

Rangnekar, G., A. Brooks, S. Willoughby, M. Middeldorp, J. Kim, S. Thanigaimani, E. Rasheed, et al. "Newly Diagnosed Atrial Fibrillation Patients Show Evidence of Abnormal Atrial Substrate." Heart, Lung and Circulation 21 (January 2012): S104—S105. http://dx.doi.org/10.1016/j.hlc.2012.05.262.

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41

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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42

Wong, G., C. Nalliah, A. Voskoboinik, B. Pathik, S. Prabhu, L. Ling, G. Lee, J. Morton, P. Kistler, and J. Kalman. "High Density Mapping of Atrial Fibrillation: Regional Atrial Substrate Abnormalities and Implications for Substrate Ablation." Heart, Lung and Circulation 26 (2017): S183. http://dx.doi.org/10.1016/j.hlc.2017.06.320.

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43

Heijman, Jordi, Azinwi Phina Muna, Tina Veleva, Cristina E. Molina, Henry Sutanto, Marcel Tekook, Qiongling Wang, et al. "Atrial Myocyte NLRP3/CaMKII Nexus Forms a Substrate for Postoperative Atrial Fibrillation." Circulation Research 127, no. 8 (September 25, 2020): 1036–55. http://dx.doi.org/10.1161/circresaha.120.316710.

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Rationale: Postoperative atrial fibrillation (POAF) is a common and troublesome complication of cardiac surgery. POAF is generally believed to occur when postoperative triggers act on a preexisting vulnerable substrate, but the underlying cellular and molecular mechanisms are largely unknown. Objective: To identify cellular POAF mechanisms in right atrial samples from patients without a history of atrial fibrillation undergoing open-heart surgery. Methods and Results: Multicellular action potentials, membrane ion-currents (perforated patch-clamp), or simultaneous membrane-current (ruptured patch-clamp) and [Ca 2+ ] i -recordings in atrial cardiomyocytes, along with protein-expression levels in tissue homogenates or cardiomyocytes, were assessed in 265 atrial samples from patients without or with POAF. No indices of electrical, profibrotic, or connexin remodeling were noted in POAF, but Ca 2+ -transient amplitude was smaller, although spontaneous sarcoplasmic reticulum (SR) Ca 2+ -release events and L-type Ca 2+ -current alternans occurred more frequently. CaMKII (Ca 2+ /calmodulin-dependent protein kinase-II) protein-expression, CaMKII-dependent phosphorylation of the cardiac RyR2 (ryanodine-receptor channel type-2), and RyR2 single-channel open-probability were significantly increased in POAF. SR Ca 2+ -content was unchanged in POAF despite greater SR Ca 2+ -leak, with a trend towards increased SR Ca 2+ -ATPase activity. Patients with POAF also showed stronger expression of activated components of the NLRP3 (NACHT, LRR, and PYD domains-containing protein-3)-inflammasome system in atrial whole-tissue homogenates and cardiomyocytes. Acute application of interleukin-1β caused NLRP3-signaling activation and CaMKII-dependent RyR2/phospholamban hyperphosphorylation in an immortalized mouse atrial cardiomyocyte cell-line (HL-1-cardiomyocytes) and enhanced spontaneous SR Ca 2+ -release events in both POAF cardiomyocytes and HL-1-cardiomyocytes. Computational modeling showed that RyR2 dysfunction and increased SR Ca 2+ -uptake are sufficient to reproduce the Ca 2+ -handling phenotype and indicated an increased risk of proarrhythmic delayed afterdepolarizations in POAF subjects in response to interleukin-1β. Conclusions: Preexisting Ca 2+ -handling abnormalities and activation of NLRP3-inflammasome/CaMKII signaling are evident in atrial cardiomyocytes from patients who subsequently develop POAF. These molecular substrates sensitize cardiomyocytes to spontaneous Ca 2+ -releases and arrhythmogenic afterdepolarizations, particularly upon exposure to inflammatory mediators. Our data reveal a potential cellular and molecular substrate for this important clinical problem.

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44

Qin, Xinghua, Yudi Zhang, and Qiangsun Zheng. "Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation." International Journal of Molecular Sciences 23, no. 15 (July 27, 2022): 8291. http://dx.doi.org/10.3390/ijms23158291.

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Atrial fibrillation (AF), the most common sustained arrhythmia, is closely intertwined with metabolic abnormalities. Recently, a metabolic paradox in AF pathogenesis has been suggested: under different forms of pathogenesis, the metabolic balance shifts either towards (e.g., obesity and diabetes) or away from (e.g., aging, heart failure, and hypertension) fatty acid oxidation, yet they all increase the risk of AF. This has raised the urgent need for a general consensus regarding the metabolic changes that predispose patients to AF. “Metabolic flexibility” aptly describes switches between substrates (fatty acids, glucose, amino acids, and ketones) in response to various energy stresses depending on availability and requirements. AF, characterized by irregular high-frequency excitation and the contraction of the atria, is an energy challenge and triggers a metabolic switch from preferential fatty acid utilization to glucose metabolism to increase the efficiency of ATP produced in relation to oxygen consumed. Therefore, the heart needs metabolic flexibility. In this review, we will briefly discuss (1) the current understanding of cardiac metabolic flexibility with an emphasis on the specificity of atrial metabolic characteristics; (2) metabolic heterogeneity among AF pathogenesis and metabolic inflexibility as a common pathological basis for AF; and (3) the substrate-metabolism mechanism underlying metabolic inflexibility in AF pathogenesis.

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45

Ali, Rheeda L., Joe B. Hakim, Patrick M. Boyle, Sohail Zahid, Bhradeev Sivasambu, Joseph E. Marine, Hugh Calkins, Natalia A. Trayanova, and David D. Spragg. "Arrhythmogenic propensity of the fibrotic substrate after atrial fibrillation ablation: a longitudinal study using magnetic resonance imaging-based atrial models." Cardiovascular Research 115, no. 12 (April 12, 2019): 1757–65. http://dx.doi.org/10.1093/cvr/cvz083.

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Abstract Aims Inadequate modification of the atrial fibrotic substrate necessary to sustain re-entrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-magnetic resonance imaging (MRI) can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. Methods and results Pre- and post-ablation individualized left atrial models were constructed from 12 AF patients who underwent pre- and post-PVI LGE-MRI, in six of whom PVI failed. Pre-ablation AF sustained by RDs was induced in 10 models. RDs in the post-ablation models were classified as either preserved or emergent. Pre-ablation models derived from patients for whom the procedure failed exhibited a higher number of RDs and larger areas defined as promoting RD formation when compared with atrial models from patients who had successful ablation, 2.6 ± 0.9 vs. 1.8 ± 0.2 and 18.9 ± 1.6% vs. 13.8 ± 1.5%, respectively. In cases of successful ablation, PVI eliminated completely the RDs sustaining AF. Preserved RDs unaffected by ablation were documented only in post-ablation models of patients who experienced recurrent AF (2/5 models); all of these models had also one or more emergent RDs at locations distinct from those of pre-ablation RDs. Emergent RDs occurred in regions that had the same characteristics of the fibrosis spatial distribution (entropy and density) as regions that harboured RDs in pre-ablation models. Conclusion Recurrent AF after PVI in the fibrotic atria may be attributable to both preserved RDs that sustain AF pre- and post-ablation, and the emergence of new RDs following ablation. The same levels of fibrosis entropy and density underlie the pro-RD propensity in both pre- and post-ablation substrates.

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Nemirovsky, Dmitry, and Joseph A. Gomes. "Is the electrical substrate of vagal atrial fibrillation different from that of non-vagal atrial fibrillation?" Heart Rhythm 2, no. 5 (May 2005): S183—S184. http://dx.doi.org/10.1016/j.hrthm.2005.02.573.

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Squara, Fabien, Didier Scarlatti, Sok-Sithikun Bun, Pamela Moceri, Emile Ferrari, Olivier Meste, and Vicente Zarzoso. "Fibrillatory Wave Amplitude Evolution during Persistent Atrial Fibrillation Ablation: Implications for Atrial Substrate and Fibrillation Complexity Assessment." Journal of Clinical Medicine 11, no. 15 (August 3, 2022): 4519. http://dx.doi.org/10.3390/jcm11154519.

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Background. Fibrillatory Wave Amplitude (FWA) has been described as a non-invasive marker of atrial fibrillation (AF) complexity, and it predicts catheter ablation outcome. However, the actual determinants of FWA remain incompletely understood. Objective. To assess the respective implications of anatomical atrial substrate and AF spectral characteristics for FWA. Methods. Persistent AF patients undergoing radiofrequency catheter ablation were included. FWA was measured on 1-min ECG by TQ concatenation in Lead I, V1, V2, and V5 at baseline and immediately before AF termination. FWA evolution during ablation was compared to that of AF dominant frequency (DF) measured by Independent Component Analysis on 12-lead ECG. FWA was compared to the extent of endocardial low-voltage areas (LVA I < 10%; II 10–20%; III 20–30%; IV > 30%), to the surface of healthy left atrial tissue, and to P-wave amplitude in sinus rhythm. The predictive value of FWA for AF recurrence during follow-up was assessed. Results. We included 29 patients. FWA remained stable along ablation procedure with comparable values at baseline and before AF termination (Lead I p = 0.54; V1 p = 0.858; V2 p = 0.215; V5 p = 0.14), whereas DF significantly decreased (5.67 ± 0.68 vs. 4.95 ± 0.58 Hz, p < 0.001). FWA was higher in LVA-I than in LVA-II, -III, and -IV in Lead I and V5 (p = 0.02 and p = 0.01). FWA in V5 was strongly correlated with the surface of healthy left atrial tissue (R = 0.786; p < 0.001). FWA showed moderate to strong correlation to P-wave amplitude in all leads. Finally, FWA did not predict AF recurrence after a follow-up of 23.3 ± 9.8 months. Conclusions. These findings suggest that FWA is unrelated to AF complexity but is mainly determined by the amount of viable atrial myocytes. Therefore, FWA should only be referred as a marker of atrial tissue pathology.

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Spragg, David D., Irfan Khurram, and Saman Nazarian. "Role of Magnetic Resonance Imaging of Atrial Fibrosis in Atrial Fibrillation Ablation." Arrhythmia & Electrophysiology Review 2, no. 2 (2013): 124. http://dx.doi.org/10.15420/aer.2013.2.2.124.

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Atrial fibrillation (AF) likely involves a complex interplay between triggering activity, usually from pulmonary vein foci, and maintenance of the arrhythmia by an arrhythmogenic substrate. Both components of AF, triggers and substrate have been linked to atrial fibrosis and attendant changes in atrial electrophysiology. Recently, there has been a growing use of imaging modalities, particularly cardiac magnetic resonance (CMR), to quantify the burden of atrial fibrosis and scar in patients either undergoing AF ablation, or who have recently had the procedure. How to use the CMR derived data is still an open area of investigation. The aim of this article is to summarise what is known as atrial fibrosis, as assessed by traditional catheter-based techniques and newer imaging approaches, and to report on novel efforts from our group to advance the use of CMR in AF ablation patients.

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Lee, Kun-Tai, and Wen-Ter Lai. "CHARACTERISTICS OF ATRIAL SUBSTRATE AND INDUCIBILITY FOR ATRIAL FIBRILLATION IN HYPERCHOLESTEROLEMIA RABBITS." Journal of the American College of Cardiology 55, no. 10 (March 2010): A15.E143. http://dx.doi.org/10.1016/s0735-1097(10)60144-1.

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Mahajan, R., A. Brooks, J. Manavis, J. Wood, J. Finnie, C. Sameul, D. Lau, J. Selvanayagam, K. Roberts-Thomson, and P. Sanders. "Atrial Fibrillation and Obesity: Impact of Weight Reduction on the Atrial Substrate." Heart, Lung and Circulation 22 (January 2013): S1—S2. http://dx.doi.org/10.1016/j.hlc.2013.05.002.

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