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Relevant bibliographies by topics / Electrophysiological remodeling

Academic literature on the topic 'Electrophysiological remodeling'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "Electrophysiological remodeling"

1

Wang, Yanggan, and Joseph A. Hill. "Electrophysiological remodeling in heart failure." Journal of Molecular and Cellular Cardiology 48, no. 4 (April 2010): 619–32. http://dx.doi.org/10.1016/j.yjmcc.2010.01.009.

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2

WAGONER, DAVID R. VAN. "Electrophysiological Remodeling in Human Atrial Fibrillation." Pacing and Clinical Electrophysiology 26, no. 7p2 (July 2003): 1572–75. http://dx.doi.org/10.1046/j.1460-9592.2003.t01-1-00234.x.

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3

Climent, Andreu M., María S. Guillem, Lucia Fuentes, Peter Lee, Christian Bollensdorff, María Eugenia Fernández-Santos, Susana Suárez-Sancho, et al. "Role of atrial tissue remodeling on rotor dynamics: an in vitro study." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 11 (December 1, 2015): H1964—H1973. http://dx.doi.org/10.1152/ajpheart.00055.2015.

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The objective of this article is to present an in vitro model of atrial cardiac tissue that could serve to study the mechanisms of remodeling related to atrial fibrillation (AF). We analyze the modification on gene expression and modifications on rotor dynamics following tissue remodeling. Atrial murine cells (HL-1 myocytes) were maintained in culture after the spontaneous initiation of AF and analyzed at two time points: 3.1 ± 1.3 and 9.7 ± 0.5 days after AF initiation. The degree of electrophysiological remodeling (i.e., relative gene expression of key ion channels) and structural inhomogeneity was compared between early and late cell culture times both in nonfibrillating and fibrillating cell cultures. In addition, the electrophysiological characteristics of in vitro fibrillation [e.g., density of phase singularities (PS/cm2), dominant frequency, and rotor meandering] analyzed by means of optical mapping were compared with the degree of electrophysiological remodeling. Fibrillating cell cultures showed a differential ion channel gene expression associated with atrial tissue remodeling (i.e., decreased SCN5A, CACN1C, KCND3, and GJA1 and increased KCNJ2) not present in nonfibrillating cell cultures. Also, fibrillatory complexity was increased in late- vs. early stage cultures (1.12 ± 0.14 vs. 0.43 ± 0.19 PS/cm2, P < 0.01), which was associated with changes in the electrical reentrant patterns (i.e., decrease in rotor tip meandering and increase in wavefront curvature). HL-1 cells can reproduce AF features such as electrophysiological remodeling and an increased complexity of the electrophysiological behavior associated with the fibrillation time that resembles those occurring in patients with chronic AF.

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Tomaselli, G. "Electrophysiological remodeling in hypertrophy and heart failure." Cardiovascular Research 42, no. 2 (May 1999): 270–83. http://dx.doi.org/10.1016/s0008-6363(99)00017-6.

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5

Pandit, Sandeep V., and Antony J. Workman. "Atrial Electrophysiological Remodeling and Fibrillation in Heart Failure." Clinical Medicine Insights: Cardiology 10s1 (January 2016): CMC.S39713. http://dx.doi.org/10.4137/cmc.s39713.

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Heart failure (HF) causes complex, chronic changes in atrial structure and function, which can cause substantial electrophysiological remodeling and predispose the individual to atrial fibrillation (AF). Pharmacological treatments for preventing AF in patients with HF are limited. Improved understanding of the atrial electrical and ionic/molecular mechanisms that promote AF in these patients could lead to the identification of novel therapeutic targets. Animal models of HF have identified numerous changes in atrial ion currents, intracellular calcium handling, action potential waveform and conduction, as well as expression and signaling of associated proteins. These studies have shown that the pattern of electrophysiological remodeling likely depends on the duration of HF, the underlying cardiac pathology, and the species studied. In atrial myocytes and tissues obtained from patients with HF or left ventricular systolic dysfunction, the data on changes in ion currents and action potentials are largely equivocal, probably owing mainly to difficulties in controlling for the confounding influences of multiple variables, such as patient's age, sex, disease history, and drug treatments, as well as the technical challenges in obtaining such data. In this review, we provide a summary and comparison of the main animal and human electrophysiological studies to date, with the aim of highlighting the consistencies in some of the remodeling patterns, as well as identifying areas of contention and gaps in the knowledge, which warrant further investigation.

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Wright, Peter T., Julia Gorelik, and Sian E. Harding. "Electrophysiological Remodeling: Cardiac T-Tubules and ß-Adrenoceptors." Cells 10, no. 9 (September 17, 2021): 2456. http://dx.doi.org/10.3390/cells10092456.

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Beta-adrenoceptors (βAR) are often viewed as archetypal G-protein coupled receptors. Over the past fifteen years, investigations in cardiovascular biology have provided remarkable insights into this receptor family. These studies have shifted pharmacological dogma, from one which centralized the receptor to a new focus on structural micro-domains such as caveolae and t-tubules. Important studies have examined, separately, the structural compartmentation of ion channels and βAR. Despite links being assumed, relatively few studies have specifically examined the direct link between structural remodeling and electrical remodeling with a focus on βAR. In this review, we will examine the nature of receptor and ion channel dysfunction on a substrate of cardiomyocyte microdomain remodeling, as well as the likely ramifications for cardiac electrophysiology. We will then discuss the advances in methodologies in this area with a specific focus on super-resolution microscopy, fluorescent imaging, and new approaches involving microdomain specific, polymer-based agonists. The advent of powerful computational modelling approaches has allowed the science to shift from purely empirical work, and may allow future investigations based on prediction. Issues such as the cross-reactivity of receptors and cellular heterogeneity will also be discussed. Finally, we will speculate as to the potential developments within this field over the next ten years.

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Patel, Kiran Haresh Kumar, Timothy Nicholas Jones, Susanne Sattler, Justin C. Mason, and Fu Siong Ng. "Proarrhythmic electrophysiological and structural remodeling in rheumatoid arthritis." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 5 (November 1, 2020): H1008—H1020. http://dx.doi.org/10.1152/ajpheart.00401.2020.

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Chronic inflammatory disorders, including rheumatoid arthritis (RA), are associated with a twofold increase in the incidence of sudden cardiac death (SCD) compared with the healthy population. Although this is partly explained by an increased prevalence of coronary artery disease, growing evidence suggests that ischemia alone cannot completely account for the increased risk. The present review explores the mechanisms of cardiac electrophysiological remodeling in response to chronic inflammation in RA. In particular, it focuses on the roles of nonischemic structural remodeling, altered cardiac ionic currents, and autonomic nervous system dysfunction in ventricular arrhythmogenesis and SCD. It also explores whether common genetic elements predispose to both RA and SCD. Finally, it evaluates the potential dual effects of disease-modifying therapy in both diminishing and promoting the risk of ventricular arrhythmias and SCD.

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Zipes, Douglas P. "Electrophysiological Remodeling of the Heart Owing to Rate." Circulation 95, no. 7 (April 1997): 1745–48. http://dx.doi.org/10.1161/01.cir.95.7.1745.

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Hegyi, Bence, Julie Bossuyt, Leigh G. Griffiths, Rafael Shimkunas, Zana Coulibaly, Zhong Jian, Kristin N. Grimsrud, et al. "Complex electrophysiological remodeling in postinfarction ischemic heart failure." Proceedings of the National Academy of Sciences 115, no. 13 (March 12, 2018): E3036—E3044. http://dx.doi.org/10.1073/pnas.1718211115.

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Heart failure (HF) following myocardial infarction (MI) is associated with high incidence of cardiac arrhythmias. Development of therapeutic strategy requires detailed understanding of electrophysiological remodeling. However, changes of ionic currents in ischemic HF remain incompletely understood, especially in translational large-animal models. Here, we systematically measure the major ionic currents in ventricular myocytes from the infarct border and remote zones in a porcine model of post-MI HF. We recorded eight ionic currents during the cell’s action potential (AP) under physiologically relevant conditions using selfAP-clamp sequential dissection. Compared with healthy controls, HF-remote zone myocytes exhibited increased late Na+ current, Ca2+-activated K+ current, Ca2+-activated Cl− current, decreased rapid delayed rectifier K+ current, and altered Na+/Ca2+ exchange current profile. In HF-border zone myocytes, the above changes also occurred but with additional decrease of L-type Ca2+ current, decrease of inward rectifier K+ current, and Ca2+ release-dependent delayed after-depolarizations. Our data reveal that the changes in any individual current are relatively small, but the integrated impacts shift the balance between the inward and outward currents to shorten AP in the border zone but prolong AP in the remote zone. This differential remodeling in post-MI HF increases the inhomogeneity of AP repolarization, which may enhance the arrhythmogenic substrate. Our comprehensive findings provide a mechanistic framework for understanding why single-channel blockers may fail to suppress arrhythmias, and highlight the need to consider the rich tableau and integration of many ionic currents in designing therapeutic strategies for treating arrhythmias in HF.

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Aiba, Takeshi, Gordon F. Tomaselli, and Wataru Shimizu. "Electrophysiological Remodeling in Heart Failure Dyssynchrony vs. Resynchronization." Journal of Arrhythmia 26, no. 2 (2010): 79–90. http://dx.doi.org/10.1016/s1880-4276(10)80011-0.

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Dissertations / Theses on the topic "Electrophysiological remodeling"

1

Bonilla, Ingrid Marie. "Acquired Electrophysiological Remodeling and Cardiac Arrhythmias." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396024058.

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Li, Li. "Electrophysiological, structural and molecular remodeling of chronically infarcted rabbit heart." online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1130882699.

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Kanagaratnam, Prapakaran. "The role of connexins in the electrophysiological remodelling of human atrial fibrillation." Thesis, Imperial College London, 2002. http://hdl.handle.net/10044/1/7530.

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Alayoubi, Samha. "Load-dependent electrophysiological and structural cardiac remodelling studied in ultrathin myocardial slices." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/44552.

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Introduction: Myocardial slices are becoming an established system to study cardiac electrophysiology and pharmacological research and development. Unlike other preparations, cardiac slices are a multicellular preparation that has an intermediate, adequate complexity required for this research. Previous studies have successfully obtained slices from human biopsies and animal models, where the electrical and structural parameters could be maintained for several hours - a process which is comparable to other preparation types. Therefore, we aimed to use left ventricular myocardial slices obtained from rat models of mechanical unloading (HAHLT) and from two models of overload (TAC and SHR), to investigate electrophysiological and structural alterations in these models. Methods: Mechanical unloading was achieved by heterotopic abdominal heart and lung transplantation (HAHLT, 8 weeks) and overload was induced by thoracic aortic constriction (TAC, 10 and 20 weeks) in male Lewis rats. Spontaneous hypertensive rats (SHR) were also used as a second model of overload and were primarily induced by hypertension (3, 12 and 20 months). Brown Norway and Wistar Kyoto rats were used as the control groups for SHR. Myocardial slices from the left ventricle (LV) free wall were cut (300-350 μm thick) tangentially to the epicardial surface using a high-precision slow-advancing Vibratome and were point-stimulated using a multi-electrode array system (MEA), therefore, acquiring field potentials (FPs). Field potential duration (FPD) and conduction velocity (CV) were analysed locally and transmurally across the LV free wall. In addition, FPD heterogeneity within each slice was calculated. For the SHR group, the same slices used for the MEA recording were preserved and used subsequently to measure Cx43, Nav1.5 protein levels and fibrosis. Results: Slices obtained from normal rat hearts that are chronically unloaded were found to develop atrophy at a whole heart level. They showed an increase in FPD and its heterogeneity with preserved conduction properties when compared to controls. In TACs, an in vivo whole heart function assessment confirmed hypertrophy with no signs of cardiac dysfunction. Slices from TAC rats showed an increase in FPD at both 10 and 20 weeks after banding. FPD heterogeneity was increased at 10 weeks but normalised at 20 weeks. Changes in CV properties were observed in this group, showing a faster CV and longitudinal conduction velocity (CVL) at 10 weeks and no change at 20 weeks. Transverse conduction velocity (CVT) was unchanged in the TAC group. In SHRs, however, hypertrophy was confirmed and signs of dysfunction in the aged group (20 months) were observed due to the decrease in EF by 18%, especially when compared to the 12 months group. FPD and its heterogeneity was unchanged in SHR when compared to controls. Disease and age-related abnormalities in CV properties were observed in SHR and these were associated with changes in Cx43, Nav1.5 protein level and fibrosis. Conclusion: Myocardial slices are a suitable multicellular preparation to study electrophysiological remodelling obtained from different rat models of cardiovascular disease. In addition, it was possible to investigate the changes in CV and FPD transmurally in rats using this type of preparation method. Thus, this study supports the use of this multicellular preparation in understanding the mechanisms of cardiac disease and the testing of new treatments and therapeutic targets.

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Schwarzwald, Colin C. "Atrial and AV-nodal physiology in horses electrophysiologic and echocardiographic characterization and pharmacologic effects of diltiazem /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1158079213.

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6

Neo, Melissa. "Atrial electrophysiological and structural changes in obesity and diabetes mellitus." Thesis, 2017. http://hdl.handle.net/2440/111992.

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Atrial fibrillation (AF) is the most commonly presented arrhythmia in the clinical setting, and its prevalence contributes significantly towards morbidity and mortality rates in the general population. Obesity and diabetes mellitus (DM, type I and type II DM) are recognised, well established independent risk factors of AF which can occur and contribute towards the development of AF both individually and in a concomitant fashion. The pathophysiological processes by which a proarrhythmic atrial substrate is produced in obesity and DM have not been fully elucidated. Further characterisation of the atrial substrate in obesity and DM induced AF is required. Chapter one addresses the mechanistic components which may contribute towards establishing AF, and discusses the early and current insights underlying the pathogenesis of AF; This chapter describes the current literature available on the electrophysiological and structural components which may lead to the development of a vulnerable atrial substrate; these include the role of the action potential (AP), the relationship between the AP and the effective refractory period (ERP), and the contribution of inflammation and fibrosis towards AF development. Chapter two investigates the feasibility and result of combined application of simultaneous high density conduction mapping with intracellular membrane potential recording to better understand the genesis and maintenance of arrhythmias in the isolated atria. Described are the ability to observe changes in action potential (AP) morphology at a given recording region, regional differences in AP restitution, lack of correlation between AP duration (APD) and the atrial effective refractory period (ERP), and AP alternans in amplitude, and, duration. Chapter three assesses electrophysiological and structural changes in a rat model of type I DM (T1DM) using streptozotocin (STZ), which preferentially exerts toxicity to the insulin-producing beta cells of the pancreas to elicit the T1DM phenotype. This chapter demonstrates the impact of untreated T1DM on the atrial myocardium. At the structural level, T1DM animals demonstrated atrial cardiomyocyte hypertrophy with increased fibrosis. At the electrophysiological level, there was an abbreviation of the ERP with increased heterogeneity in conduction, as well as prolongation of the AP. Chapter four describes the impact of obesity, type II DM (T2DM) and age on the electrical and structural properties of the atria using the Zucker (fa/fa) rat model. This chapter reports cardiomyocyte hypertrophy, increased fibrosis, prolongation of the APD, increased heterogeneity and slowed conduction, with differences in ERP between the left and right atrium of the DM animals. These results highlight the potential difference between the pathogenesis of T2DM from T1DM on the atrial myocardium in the predisposition towards development of AF. Chapter five summarises the observations made in the T1DM and T2DM studies of chapters three and four respectively; this chapter discusses the similarities and differences shared in the data obtained from the studies, with a brief description of the potential mechanisms involved in DM-induced pathogenesis of AF, Additionally, the potential importance of segregating the diabetic states as having individual and differential influences on the atrial myocardium is highlighted. Future directions and areas of further research conclude this chapter.
Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, Adelaide Medical School, 2017.

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Books on the topic "Electrophysiological remodeling"

1

Zhong, Guoqiang. Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling. INTECH Open Access Publisher, 2012.

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Book chapters on the topic "Electrophysiological remodeling"

1

Akar, Fadi G., and Gordon F. Tomaselli. "Electrophysiological Remodeling in Heart Failure." In Electrical Diseases of the Heart, 369–86. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4881-4_22.

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DeMello, Walmor C. "Structural and Electrophysiological Remodeling of the Failing Heart." In Renin Angiotensin System and Cardiovascular Disease, 81–91. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-186-8_7.

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El-Sherif, Nabil. "Post-infarction Remodeling and Arrhythmogenesis: Molecular, Ionic, and Electrophysiological Substrates." In Heart Rate and Rhythm, 283–304. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17575-6_15.

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Zhong, Guoqiang, Jinyi Li, Honghong Ke, Yan He, Weiyan Xu, and Yanmei Zhao. "Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling." In Advances in Electrocardiograms - Clinical Applications. InTech, 2012. http://dx.doi.org/10.5772/22801.

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5

Kurotobi, Toshiya. "Novel Index for Determining the Development of Electrophysiological and Structural Atrial Remodeling in Patient with Atrial Fibrillation." In Atrial Fibrillation - Basic Research and Clinical Applications. InTech, 2012. http://dx.doi.org/10.5772/25755.

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Papadakis, Michael, and Sanjay Sharma. "Cardiovascular adaptation to exercise and sport: (according to type of sport, gender, and ethnicity)." In The ESC Textbook of Cardiovascular Medicine, edited by Antonio Pelliccia, 2913–16. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0705.

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‘Athlete’s heart’ is associated with several structural and electrophysiological adaptations, which are reflected on the 12-lead electrocardiogram (ECG) and imaging studies. Most studies investigating cardiac remodelling in athletes are based on cohorts of white, adult, male athletes competing in the most popular sports. Evidence suggests, however, that sporting discipline and the athlete’s gender and ethnicity are important determinants of cardiovascular adaptation to exercise. Athletes competing in endurance sports demonstrate more pronounced adaptations in comparison to athletes performing static or resistance training. The ECG of endurance athletes is more likely to demonstrate repolarization anomalies in the anterior leads and ventricular dilatation on imaging studies, causing considerable overlap with arrhythmogenic right ventricular cardiomyopathy and dilated cardiomyopathy. Female athletes exhibit less pronounced adaptations compared to males, in terms of the prevalence of ECG changes and absolute cardiac dimensions. Importantly, female endurance athletes are more likely to demonstrate eccentric hypertrophy compared to males, suggesting that concentric remodelling or hypertrophy in female endurance athletes is unlikely to be the consequence of physiological adaptation to training. The most pronounced paradigm of ethnically distinct cardiovascular adaptation to exercise stems from black athletes, who exhibit a significantly higher prevalence of repolarization anomalies and left ventricular hypertrophy compared to white athletes, making the differentiation between athlete’s heart and hypertrophic cardiomyopathy challenging in this ethnic group.

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Papadakis, Michael, and Sanjay Sharma. "Cardiovascular adaptation to exercise and sport: (according to type of sport, gender, and ethnicity)." In ESC CardioMed, edited by Antonio Pelliccia, 2913–16. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0705_update_001.

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Abstract:

‘Athlete’s heart’ is associated with several structural and electrophysiological adaptations, which are reflected on the 12-lead electrocardiogram (ECG) and imaging studies. Most studies investigating cardiac remodelling in athletes are based on cohorts of white, adult, male athletes competing in the most popular sports. Evidence suggests, however, that sporting discipline and the athlete’s gender and ethnicity are important determinants of cardiovascular adaptation to exercise. Athletes competing in endurance sports demonstrate more pronounced adaptations in comparison to athletes performing static or resistance training. The ECG of endurance athletes is more likely to demonstrate repolarization anomalies in the anterior leads and ventricular dilatation on imaging studies, causing considerable overlap with arrhythmogenic right ventricular cardiomyopathy and dilated cardiomyopathy. Female athletes exhibit less pronounced adaptations compared to males, in terms of the prevalence of ECG changes and absolute cardiac dimensions. Importantly, female endurance athletes are more likely to demonstrate eccentric hypertrophy compared to males, suggesting that concentric remodelling or hypertrophy in female endurance athletes is unlikely to be the consequence of physiological adaptation to training. The most pronounced paradigm of ethnically distinct cardiovascular adaptation to exercise stems from black athletes, who exhibit a significantly higher prevalence of repolarization anomalies and left ventricular hypertrophy compared to white athletes, making the differentiation between athlete’s heart and hypertrophic cardiomyopathy challenging in this ethnic group.

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Papadakis, Michael, and Sanjay Sharma. "Cardiovascular adaptation to exercise and sport (according to type of sport, sex, and ethnicity)." In ESC CardioMed, edited by Antonio Pelliccia, 2913–16. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0705_update_002.

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Abstract:

‘Athlete’s heart’ is associated with several structural and electrophysiological adaptations, which are reflected on the 12-lead electrocardiogram (ECG) and imaging studies. Most studies investigating cardiac remodelling in athletes are based on cohorts of white, adult, male athletes competing in the most popular sports. Evidence suggests, however, that sporting discipline and the athlete’s sex and ethnicity are important determinants of cardiovascular adaptation to exercise. Athletes competing in endurance sports demonstrate more pronounced adaptations in comparison to athletes performing static or resistance training. The ECG of endurance athletes is more likely to demonstrate repolarization anomalies in the anterior leads and ventricular dilatation on imaging studies, causing considerable overlap with arrhythmogenic right ventricular cardiomyopathy and dilated cardiomyopathy. Female athletes exhibit less pronounced adaptations compared to males, in terms of the prevalence of ECG changes and absolute cardiac dimensions. Importantly, female endurance athletes are more likely to demonstrate eccentric hypertrophy compared to males, suggesting that concentric remodelling or hypertrophy in female endurance athletes is unlikely to be the consequence of physiological adaptation to training. The most pronounced paradigm of ethnically distinct cardiovascular adaptation to exercise stems from Black athletes, who exhibit a significantly higher prevalence of repolarization anomalies and left ventricular hypertrophy compared to white athletes, making the differentiation between athlete’s heart and hypertrophic cardiomyopathy challenging in this ethnic group.

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Conference papers on the topic "Electrophysiological remodeling"

1

Westhofen, S., L. Dreher, A. El-Armouche, H. Vitzhum, H. Reichenspurner, H. Ehmke, and P. Schwoerer. "Altered Electrophysiological Remodeling Induced by Mechanical Unloading in Phospholamban Deficient Mice." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678819.

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Seemann, G., H. Ying, D. L. Weiss, F. B. Sachse, and O. Dossel. "Effects of electrophysiological remodeling in human right atrium: a simulation study." In Computers in Cardiology, 2005. IEEE, 2005. http://dx.doi.org/10.1109/cic.2005.1588036.

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

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

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Zhou, Xin, Jakub Tomek, and Blanca Rodriguez. "Investigation of the Electrophysiological Remodelling in Acute and Chronic Post-Myocardial Infarction." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.338.

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