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Journal articles on the topic 'Electrophysiological remodeling'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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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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4

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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6

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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7

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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8

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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9

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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10

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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11

Nigmatzyanova, A., M. Mangusheva, S. Lapshina, D. Abdulganieva, M. Afanasieva, and L. Myasoutova. "FRI0407 Electrophysiological Cardiac Remodeling in Patients with Ankylosing Spondylitis." Annals of the Rheumatic Diseases 75, Suppl 2 (June 2016): 583.1–583. http://dx.doi.org/10.1136/annrheumdis-2016-eular.4713.

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12

McDowell, Kathleen S., Sohail Zahid, Fijoy Vadakkumpadan, Joshua Blauer, Rob S. MacLeod, and Natalia A. Trayanova. "Virtual Electrophysiological Study of Atrial Fibrillation in Fibrotic Remodeling." PLOS ONE 10, no. 2 (February 18, 2015): e0117110. http://dx.doi.org/10.1371/journal.pone.0117110.

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13

Mazur, E. S., V. V. Mazur, H. A. Jaber, and Yu A. Orlov. "To the question of electrophysiological remodeling role in the genesis of ventricular ectopy in patients with postinfarction cardiosclerosis." Kazan medical journal 99, no. 2 (April 15, 2018): 207–12. http://dx.doi.org/10.17816/kmj2018-207.

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Aim. To study the character and intensity of relationship between left ventricular dilatation, severity of electrophysiological myocardium remodeling and ectopic ventricular activity in patients with postinfarction cardiosclerosis. Methods. 46 patients with postinfarction cardiosclerosis were examined (males, average age 57.9 years). All patients underwent echocardiography with detection of end diastolic volume of left ventricle and its ejection fraction, Holter monitoring with determining signal-averaged electrocardiogram and severity of ventricular ectopic activity with calculation of ventricular ectopic activity index. Based on the ejection fraction the patients were divided into two groups. Group 1 included 17 patients with ejection fraction ≥45%, and group 2 - 29 patients with ejection fraction <45%. Results. Left ventricle ejection fraction in patients from group 2 was lower, and parameters of signal-averaged electrocardiogram were worse than in patients from group 1. Ventricular ectopic activity index in patients from group 2 was 5 times higher than the average index in group 1. According to correlation analysis in the combined group, signal-averaged electrocardiogram parameters more tightly correlated with end diastolic volume than with ventricular ectopic activity index. The latter more tightly correlated with end diastolic volume (r=0.67, p <0.001), than with signal-averaged electrocardiogram parameters. After calculating partial correlation coefficient and excluding the effect of end diastolic volume, correlation coefficients of ventricular ectopic activity index and signal-averaged electrocardiogram parameters became insignificant. The received data put in question the view that electrophysiological remodeling is an independent cause of severity increase of ventricular arrhythmias. More probable is that electrophysiological remodeling and ventricular ectopic activity are related pathogenetically, and correlation between them is determined by the fact that both depend on left ventricle end diastolic volume. Conclusion. Relation between electrophysiological myocardium remodeling and ectopic ventricular activity in patients with postinfarction cardiosclerosis may depend on severity of left ventricular dilatation.

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14

Maksimova, M. S. "Electrophysiological remodeling of the heart in patients with arterial hypertension." Medical alphabet, no. 5 (April 12, 2021): 26–32. http://dx.doi.org/10.33667/2078-5631-2021-5-26-32.

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Aim. Study electrocardiographic (ECG) and vectorcardiographic (VCG) indicators for various types of structural- geometric remodeling of the left ventricle (LV) in patients with arterial hypertension (AH).Material and research methods. The analysis was performed in 336 people, including 264 patients with AH, mean age 61.02 ± 7.61 years and 72 practically healthy individuals (57.18 ± 6.47). The ECG indicators of heart rate and duration of P, QRS, RR, PQ, QT, QT corrected according to the Bazett, Friderici and Sagie formulas (QTCB, QTCF, QTCS) were assessed. Echocardiography was used to calculate myocardial mass (LVMM) and LVMM index (LVMI), relative wall thickness (RWT). In the own plane of the VCG: the area of the QRS loop (SQRS), the magnitude of the geometric vector (maxQRS) were determined.Results. Correlation analysis showed the presence of a positive relationship between LVM and LVMI with SQRS (r = 0.49 and r = 0.38), maxQRS (r = 0.28 and r=0.33) and with QRS duration (r = 0.50 and r = 0.43). The groups of patients with concentric (CG) and eccentric (EH) hypertrophy in comparison with controls and patients with AH without LVH gave significantly higher values of absolute QT, QTCF, QTCS. There was a positive correlation between QT and QTС with LVMM, LVMI and no relationship with RWT.Conclusions. In LVH, the duration of QRS and SQRS in its own plane increased. The highest SQRS values were observed in patients with CG of the left ventricle in comparison with EG. Patients with CG and EG did not differ in QRS duration. In patients with AH and LVH, the duration of absolute and corrected values of the QT interval was significantly longer than in patients without LVH. The QT interval lengthened with an increase in LVMM and LVMI. QT duration did not depend on the type of LV hypertrophy — concentric or eccentric.

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15

Ruan, Hongmei, Scherise Mitchell, Monika Vainoriene, Qing Lou, Lai-Hua Xie, Shuxun Ren, Joshua I. Goldhaber, and Yibin Wang. "Giα1-Mediated Cardiac Electrophysiological Remodeling and Arrhythmia in Hypertrophic Cardiomyopathy." Circulation 116, no. 6 (August 7, 2007): 596–605. http://dx.doi.org/10.1161/circulationaha.106.682773.

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16

McDowell, Kathleen S., Sohail Zahid, Fijoy Vadakkumpadan, Joshua Blauer, Rob S. MacLeod, and Natalia A. Trayanova. "Correction: Virtual Electrophysiological Study of Atrial Fibrillation in Fibrotic Remodeling." PLOS ONE 11, no. 5 (May 19, 2016): e0156189. http://dx.doi.org/10.1371/journal.pone.0156189.

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17

Aiba, Takeshi, Ikutaro Nakajima, Takashi Noda, Hideo Okamura, Yuko Yamada, Koji Miyamoto, Kazuhiro Satomi, et al. "Cardiac Resynchronization and Electrophysiological Reverse-Remodeling in the Failing Heart." Journal of Arrhythmia 27, Supplement (2011): SY15_4. http://dx.doi.org/10.4020/jhrs.27.sy15_4.

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18

Spach, Madison S., J. Francis Heidlage, Paul C. Dolber, and Roger C. Barr. "Electrophysiological Effects of Remodeling Cardiac Gap Junctions and Cell Size." Circulation Research 86, no. 3 (February 18, 2000): 302–11. http://dx.doi.org/10.1161/01.res.86.3.302.

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19

Decker, Keith F., and Yoram Rudy. "Ionic mechanisms of electrophysiological heterogeneity and conduction block in the infarct border zone." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 5 (November 2010): H1588—H1597. http://dx.doi.org/10.1152/ajpheart.00362.2010.

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The increased incidence of arrhythmia in the healing phase after infarction has been linked to remodeling in the epicardial border zone (EBZ). Ionic models of normal zone (NZ) and EBZ myocytes were incorporated into one-dimensional models of propagation to gain mechanistic insights into how ion channel remodeling affects action potential (AP) duration (APD) and refractoriness, vulnerability to conduction block, and conduction safety postinfarction. We found that EBZ tissue exhibited abnormal APD restitution. The remodeled Na+ current ( INa) and L-type Ca2+ current ( ICa,L) promoted increased effective refractory period and prolonged APD at a short diastolic interval. While postrepolarization refractoriness due to remodeled EBZ INa was the primary determinant of the vulnerable window for conduction block at the NZ-to-EBZ transition in response to premature S2 stimuli, altered EBZ restitution also promoted APD dispersion and increased the vulnerable window at fast S1 pacing rates. Abnormal EBZ APD restitution and refractoriness also led to abnormal periodic conduction block patterns for a range of fast S1 pacing rates. In addition, we found that INa remodeling decreased conduction safety in the EBZ but that inward rectifier K+ current remodeling partially offset this decrease. EBZ conduction was characterized by a weakened AP upstroke and short intercellular delays, which prevented ICa,L and transient outward K+ current remodeling from playing a role in EBZ conduction in uncoupled tissue. Simulations of a skeletal muscle Na+ channel SkM1- INa injection into the EBZ suggested that this recently proposed antiarrhythmic therapy has several desirable effects, including normalization of EBZ effective refractory period and APD restitution, elimination of vulnerability to conduction block, and normalization of conduction in tissue with reduced intercellular coupling.

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20

Molina, Cristina E., Jordi Heijman, and Dobromir Dobrev. "Differences in Left Versus Right Ventricular Electrophysiological Properties in Cardiac Dysfunction and Arrhythmogenesis." Arrhythmia & Electrophysiology Review 5, no. 1 (2016): 14. http://dx.doi.org/10.15420/aer.2016.8.2.

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A wide range of ion channels, transporters, signaling pathways and tissue structure at a microscopic and macroscopic scale regulate the electrophysiological activity of the heart. Each region of the heart has optimised these properties based on its specific role during the cardiac cycle, leading to well-established differences in electrophysiology, Ca2+handling and tissue structure between atria and ventricles and between different layers of the ventricular wall. Similarly, the right ventricle (RV) and left ventricle (LV) have different embryological, structural, metabolic and electrophysiological features, but whether interventricular differences promote differential remodeling leading to arrhythmias is not well understood. In this article, we will summarise the available data on intrinsic differences between LV and RV electrophysiology and indicate how these differences affect cardiac function. Furthermore, we will discuss the differential remodeling of both chambers in pathological conditions and its potential impact on arrhythmogenesis.

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21

Han, Bo, Mark L. Trew, and Callum M. Zgierski-Johnston. "Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis." Cells 10, no. 11 (October 28, 2021): 2923. http://dx.doi.org/10.3390/cells10112923.

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Cardiac electrophysiological disorders, in particular arrhythmias, are a key cause of morbidity and mortality throughout the world. There are two basic requirements for arrhythmogenesis: an underlying substrate and a trigger. Altered conduction velocity (CV) provides a key substrate for arrhythmogenesis, with slowed CV increasing the probability of re-entrant arrhythmias by reducing the length scale over which re-entry can occur. In this review, we examine methods to measure cardiac CV in vivo and ex vivo, discuss underlying determinants of CV, and address how pathological variations alter CV, potentially increasing arrhythmogenic risk. Finally, we will highlight future directions both for methodologies to measure CV and for possible treatments to restore normal CV.

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22

Strelnikov, A. G., A. B. Romanov, S. N. Artemenko, D. V. Losik, I. O. Grazhdankin, R. T. Kamiev, A. N. Turov, and Ye A. Pokushalov. "Correction of the effects of myocardial infarction by intramyocardial injection of autologous bone marrow mononuclear cells." Patologiya krovoobrashcheniya i kardiokhirurgiya 17, no. 2 (October 10, 2015): 37. http://dx.doi.org/10.21688/1681-3472-2013-4-37-39.

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To assess the functional recovery and remodeling of postinfarction myocardium, a combined technology of single-photon emission computed tomography (SPECT) and endocardial electrophysiological 3D reconstruction of the heart in patients with left ventricular dysfunction after myocardial infarction was used.

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23

Kang, Yiyuan, Jia Liu, Bin Song, Xiaoli Feng, Lingling Ou, Limin Wei, Xuan Lai, and Longquan Shao. "Potential Links between Cytoskeletal Disturbances and Electroneurophysiological Dysfunctions Induced in the Central Nervous System by Inorganic Nanoparticles." Cellular Physiology and Biochemistry 40, no. 6 (2016): 1487–505. http://dx.doi.org/10.1159/000453200.

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Inorganic nanomaterials have been widely applied in biomedicine. However, several studies have noted that inorganic nanoparticles can enter the brain and induce cytoskeletal remodeling, as well as electrophysiological alterations, which are related to neurodevelopmental disorders and neurodegenerative diseases. The toxic effects of inorganic nanomaterials on the cytoskeleton and electrophysiology are summarized in this review. The relationships between inorganic NPs-induced cytoskeletal and electrophysiological alterations in the central nervous system remain obscure. We propose several potential relationships, including those involving N-methyl-D-aspartate receptor function, ion channels, transient receptor potential channels, and the Rho pathway.

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Mazur, E. S., V. V. Mazur, Kh A. Djaber, and Yu A. Orlov. "Structural and electrophysiological remodeling interrelation in postinfarction cardiosclerosis and dilated cardiomyopathy." Kazanskiy meditsinskiy zhurnal 97, no. 2 (2016): 173–77. http://dx.doi.org/10.17750/kmj2015-173.

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Mazur, E. S., V. V. Mazur, Kh A. Djaber, and Yu A. Orlov. "Structural and electrophysiological remodeling interrelation in postinfarction cardiosclerosis and dilated cardiomyopathy." Kazan medical journal 97, no. 2 (April 15, 2016): 173–77. http://dx.doi.org/10.17750/kmj2016-173.

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Aim. To study the interrelation of ventricles echocardiographic parameters and signal-averaged electrocardiogram indicators in patients with postinfarction cardiosclerosis and dilated cardiomyopathy.Methods. 28 patients with postinfarction cardiosclerosis (men aged 49 to 71 years) and 29 patients with dilated cardiomyopathy (men aged 24 to 61 years) were examined. All patients underwent echocardiography, by which left ventricle final diastolic and systolic volumes with ejection fraction calculation, right ventricle end diastolic and systolic volumes were determined. According to the signal-averaged electrocardiogram, filtered ventricular complex duration, the ventricular complex with an amplitude of less than 40 mV terminal part duration and signal root-mean-square (rms) amplitude of the ventricular complex last 40 ms were evaluated.Results.. According to the correlation analysis, increase in left ventricle end-diastolic and systolic volumes and decrease in its ejection fraction, as well as an increase in right ventricle end-diastolic and systolic volumes were associated with an increase in the filtered ventricular complex duration and the ventricular complex with an amplitude of less than 40 mV terminal part duration in patients with postinfarction cardiosclerosis. The left ventricle volumes increase and ejection fraction reduction were also associated with the signal rms amplitude of the ventricular complex last 40 ms reduction in patients with postinfarction cardiosclerosis. Similar interrelation was not found in patients with dilated cardiomyopathy.Conclusion. In patients with postinfarction cardiosclerosis cavities dilation and reduced systolic ventricular function are accompanied by the myocardium electrophysiological properties deterioration; in patients with dilated cardiomyopathy interrelation between structural and electrophysiological indicators of myocardial remodeling was not found.

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Jeyaraj, Darwin D., Lance D. Wilson, Steven Poelzing, Xiaoping Wan, and David S. Rosenbaum. "Segmental versus transmural remodeling as electrophysiological basis for T-wave memory." Heart Rhythm 2, no. 5 (May 2005): S217. http://dx.doi.org/10.1016/j.hrthm.2005.02.678.

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Wu, Jinjin, Wanping Zhou, Lanping Wu, Yijiao Qian, Yanan Lu, and Fen Li. "Ionic mechanisms underlying atrial electrical remodeling after a fontan-style operation in a canine model." Heart and Vessels 35, no. 5 (January 7, 2020): 731–41. http://dx.doi.org/10.1007/s00380-019-01544-5.

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AbstractAtrial arrhythmia is an important cause of late death in patients after the Fontan-Style operation. However, the detailed electrophysiological characteristics of the post-Fontan atrium and its underlying mechanisms are largely unknown. In this study, we investigated electrophysiological characteristics and the ionic remodeling in the right atrium (RA) of a canine model after the Fontan operation. We performed the operation of RA to pulmonary artery connection to mimic the Fontan operation. We undertook hemodynamic measurements, cardiac electrophysiological studies, and ion current measurements. The expression of ionic channels was analyzed by PCR and western-blotting. Our Fontan model induced RA hypertension, enlarged the size of RA, and increased atrial fibrosis, representing the classic characteristic of Fontan patients. In the Fontan group, the atrial effective refractory period and the active potential duration were reduced, and the atrial tachycardia has been more often to be induced. The electrical conduction mapping showed that the Fontan group reduced the conduction velocity. The Fontan operation significantly down-regulated the expression of KCND3/Kv4.3, CACNA1C/Cav1.2 and SCN5A, but up-regulated the expression of KCNJ2/Kir2.1. Correspondingly, The Fontan operation reduced transient-outward (Ito) and L-type Ca2 (ICa,L) and INa currents, while increasing the inward-rectifier current (IK1). Thus, the net shortening of the action potential in the post-Fontan atrium is associated with the altered expression of ionic channels which disturbed the balance between inward and outward currents. Taken together, the Fontan operation induces the ionic remodeling, and thus altered electrophysiological characteristics of the right atrium, improving our understanding on the pathophysiology of atrial arrhythmias in Fontan patients.

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

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

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Kontogeorgis, Andrianos, Xiaodong Li, Eunice Y. Kang, Jonathan E. Feig, Marc Ponzio, Guoxin Kang, Riyaz A. Kaba, et al. "Decreased connexin43 expression in the mouse heart potentiates pacing-induced remodeling of repolarizing currents." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (November 2008): H1905—H1916. http://dx.doi.org/10.1152/ajpheart.590.2008.

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Gap junction redistribution and reduced expression, a phenomenon termed gap junction remodeling (GJR), is often seen in diseased hearts and may predispose toward arrhythmias. We have recently shown that short-term pacing in the mouse is associated with changes in connexin43 (Cx43) expression and localization but not with increased inducibility into sustained arrhythmias. We hypothesized that short-term pacing, if imposed on murine hearts with decreased Cx43 abundance, could serve as a model for evaluating the electrophysiological effects of GJR. We paced wild-type (normal Cx43 abundance) and heterozygous Cx43 knockout (Cx43+/−; 66% mean reduction in Cx43) mice for 6 h at 10–15% above their average sinus rate. We investigated the electrophysiological effects of pacing on the whole animal using programmed electrical stimulation and in isolated ventricular myocytes with patch-clamp studies. Cx43+/− myocytes had significantly shorter action potential durations (APD) and increased steady-state ( Iss) and inward rectifier ( IK1) potassium currents compared with those of wild-type littermate cells. In Cx43+/− hearts, pacing resulted in a significant prolongation of ventricular effective refractory period and APD and significant diminution of Iss compared with unpaced Cx43+/− hearts. However, these changes were not seen in paced wild-type mice. These data suggest that Cx43 abundance plays a critical role in regulating currents involved in myocardial repolarization and their response to pacing. Our study may aid in understanding how dyssynchronous activation of diseased, Cx43-deficient myocardial tissue can lead to electrophysiological changes, which may contribute to the worsened prognosis often associated with pacing in the failing heart.

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Ueta, Yoshifumi, and Mariko Miyata. "Electrophysiological and anatomical characterization of synaptic remodeling in the mouse whisker thalamus." STAR Protocols 2, no. 3 (September 2021): 100743. http://dx.doi.org/10.1016/j.xpro.2021.100743.

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NOWINSKI, KAROLINA, LILIANE WECKE, FREDRIK GADLER, CECILIA LINDE, and LENNART BERGFELDT. "Pacing-Induced Electrophysiological Remodeling in Hypertrophic Obstructive Cardiomyopathy-Observations on Cardiac Memory." Pacing and Clinical Electrophysiology 28, no. 6 (June 2005): 561–67. http://dx.doi.org/10.1111/j.1540-8159.2005.09469.x.

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da Cunha, D. N. Q., R. L. Hamlin, G. E. Billman, and C. A. Carnes. "n-3 (omega-3) polyunsaturated fatty acids prevent acute atrial electrophysiological remodeling." British Journal of Pharmacology 150, no. 3 (February 2007): 281–85. http://dx.doi.org/10.1038/sj.bjp.0706977.

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Jayachandran, J. Vijay, Douglas P. Zipes, Juan Weksler, and Jeffrey E. Olgin. "Role of the Na + /H + Exchanger in Short-Term Atrial Electrophysiological Remodeling." Circulation 101, no. 15 (April 18, 2000): 1861–66. http://dx.doi.org/10.1161/01.cir.101.15.1861.

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Gomez, Juan F., Karen Cardona, Laura Martinez, Javier Saiz, and Beatriz Trenor. "Electrophysiological and Structural Remodeling in Heart Failure Modulate Arrhythmogenesis. 2D Simulation Study." PLoS ONE 9, no. 7 (July 23, 2014): e103273. http://dx.doi.org/10.1371/journal.pone.0103273.

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Nattel, S. "A spotlight on electrophysiological remodeling and the molecular biology of ion channels." Cardiovascular Research 42, no. 2 (May 1999): 267–69. http://dx.doi.org/10.1016/s0008-6363(99)00072-3.

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HARDZIYENKA, M., M. CAMPIAN, and H. TAN. "376 Right ventricular failure: electrophysiological remodeling in right ventricle precedes clinical signs." European Journal of Heart Failure Supplements 6, no. 1 (June 2007): 87. http://dx.doi.org/10.1016/s1567-4215(07)60244-6.

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Gomez, Juan F., Karen Cardona, Lucia Romero, Jose M. Ferrero, and Beatriz Trenor. "Electrophysiological and Structural Remodeling in Heart Failure Modulate Arrhythmogenesis. 1D Simulation Study." PLoS ONE 9, no. 9 (September 5, 2014): e106602. http://dx.doi.org/10.1371/journal.pone.0106602.

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Acimovic, Ivana, Marwan Refaat, Adrien Moreau, Anton Salykin, Steve Reiken, Yvonne Sleiman, Monia Souidi, et al. "Post-Translational Modifications and Diastolic Calcium Leak Associated to the Novel RyR2-D3638A Mutation Lead to CPVT in Patient-Specific hiPSC-Derived Cardiomyocytes." Journal of Clinical Medicine 7, no. 11 (November 8, 2018): 423. http://dx.doi.org/10.3390/jcm7110423.

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Background: Sarcoplasmic reticulum Ca2+ leak and post-translational modifications under stress have been implicated in catecholaminergic polymorphic ventricular tachycardia (CPVT), a highly lethal inherited arrhythmogenic disorder. Human induced pluripotent stem cells (hiPSCs) offer a unique opportunity for disease modeling. Objective: The aims were to obtain functional hiPSC-derived cardiomyocytes from a CPVT patient harboring a novel ryanodine receptor (RyR2) mutation and model the syndrome, drug responses and investigate the molecular mechanisms associated to the CPVT syndrome. Methods: Patient-specific cardiomyocytes were generated from a young athletic female diagnosed with CPVT. The contractile, intracellular Ca2+ handling and electrophysiological properties as well as the RyR2 macromolecular remodeling were studied. Results: Exercise stress electrocardiography revealed polymorphic ventricular tachycardia when treated with metoprolol and marked improvement with flecainide alone. We found abnormal stress-induced contractile and electrophysiological properties associated with sarcoplasmic reticulum Ca2+ leak in CPVT hiPSC-derived cardiomyocytes. We found inadequate response to metoprolol and a potent response of flecainide. Stabilizing RyR2 with a Rycal compound prevents those abnormalities specifically in CPVT hiPSC-derived cardiomyocytes. The RyR2-D3638A mutation is located in the conformational change inducing-central core domain and leads to RyR2 macromolecular remodeling including depletion of PP2A and Calstabin2. Conclusion: We identified a novel RyR2-D3638A mutation causing 3D conformational defects and aberrant biophysical properties associated to RyR2 macromolecular complex post-translational remodeling. The molecular remodeling is for the first time revealed using patient-specific hiPSC-derived cardiomyocytes which may explain the CPVT proband’s resistance. Our study promotes hiPSC-derived cardiomyocytes as a suitable model for disease modeling, testing new therapeutic compounds, personalized medicine and deciphering underlying molecular mechanisms.

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Patel, Kiran Haresh Kumar, Taesoon Hwang, Curtis Se Liebers, and Fu Siong Ng. "Epicardial adipose tissue as a mediator of cardiac arrhythmias." American Journal of Physiology-Heart and Circulatory Physiology 322, no. 2 (February 1, 2022): H129—H144. http://dx.doi.org/10.1152/ajpheart.00565.2021.

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Obesity is associated with higher risks of cardiac arrhythmias. Although this may be partly explained by concurrent cardiometabolic ill-health, growing evidence suggests that increasing adiposity independently confers risk for arrhythmias. Among fat depots, epicardial adipose tissue (EAT) exhibits a proinflammatory secretome and, given the lack of fascial separation, has been implicated as a transducer of inflammation to the underlying myocardium. The present review explores the mechanisms underpinning adverse electrophysiological remodeling as a consequence of EAT accumulation and the consequent inflammation. We first describe the physiological and pathophysiological function of EAT and its unique secretome and subsequently discuss the evidence for ionic channel and connexin expression modulation as well as fibrotic remodeling induced by cytokines and free fatty acids that are secreted by EAT. Finally, we highlight how weight reduction and regression of EAT volume may cause reverse remodeling to ameliorate arrhythmic risk.

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Aabedi, Alexander, Benjamin Lipkin, Jacob S. Young, Leighton Hinkley, Anne Findlay, Andy Daniel, Saritha Krishna, et al. "CNSC-05. ELECTROPHYSIOLOGICAL PATTERNS OF GLIOMA-INDUCED NEURONAL NETWORK REMODELING ARE CONSERVED ACROSS TUMOR SUBTYPE." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii22. http://dx.doi.org/10.1093/neuonc/noac209.086.

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Abstract Recent evidence indicates that diffuse gliomas engage with neurons at the single-unit and circuit level through differing mechanisms. Certain malignant gliomas form glioma-neuron excitatory glutamatergic synapses and modulate neuron-neuron synapses through activity-dependent paracrine signaling, while others establish glioma-glioma connections via tumor microtubes. It is therefore possible that diffuse gliomas remodel neuronal circuits in a defined and predictable manner and demonstrate distinct electrophysiological profiles with prognostic and therapeutic significance. Here we apply machine learning principles in 140 patients across glioma subtypes to uncover unique electrophysiological features non-invasively via magnetoencephalography (discovery dataset) followed by feature validation using subdural electrocorticography (validation dataset). Following spatial-temporal registration, we fit an elastic net logistic regression classifier to distinguish between power spectra arising from glioma-remodeled cortex and within-subject control conditions. Model significance was determined non-parametrically by re-training each model 1,000 times with randomly permuted class labels and testing the true phi coefficient against the null distribution. In the discovery dataset, we were able to classify glioma infiltration based on tumor intrinsic neuronal activity (p < 0.05) in 127 patients (90.7%). We identified 30 electrophysiological features which revealed increased power in the delta range (1-4 Hz) and decreased power in the beta range (12-20 Hz) as a unique signature of glioma remodeling (p < 0.05) which was preserved in the validation dataset as well as across WHO 2021 diffuse glioma subtypes. In order to identify gene expression programs and signaling mechanisms that may contribute to glioma-induced remodeling but are potentially not identified in the current clinical classification scheme, we assessed targeted, next generation sequencing and DNA mutations as covariates, which again demonstrated the significance of the delta-beta spectral features. These data support converging mechanisms of glioma-induced neuronal network remodeling across tumor subtypes, setting the stage for novel therapies such as neuromodulation.

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Wei, Ning, and Elena G. Tolkacheva. "Mechanisms of arrhythmia termination during acute myocardial ischemia: Role of ephaptic coupling and complex geometry of border zone." PLOS ONE 17, no. 3 (March 15, 2022): e0264570. http://dx.doi.org/10.1371/journal.pone.0264570.

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Myocardial ischemia occurs when blood flow to the heart is reduced, preventing the heart muscle from receiving enough oxygen required for survival. Several anatomical and electrophysiological changes occur at the ischemic core (IC) and border zone (BZ) during myocardial ischemia, for example, gap junctional remodeling, changes in ionic channel kinetics and electrophysiologic changes in cell excitability, which promote the development of cardiac arrhythmia. Ephaptic coupling (EpC), which is an electrical field effect developed in the shared cleft space between adjacent cells, has been suggested to rescue the conduction when gap junctions are impaired, such as myocardial ischemia. In this manuscript, we explored the impact of EpC, electrophysiological and anatomical components of myocardial ischemia on reentry termination during non-ischemic and ischemic condition. Our results indicated that EpC and BZ with complex geometry have opposite effects on the reentry termination. In particular, the presence of homogeneous EpC terminates reentry, whereas BZ with complex geometry alone facilitates reentry by producing wave break-up and alternating conduction block. The reentry is terminated in the presence of homogeneous or heterogeneous EpC despite the presence of complex geometry of the BZ, independent of the location of BZ. The inhibition of reentry can be attributed to a current-to-load mismatch. Our results points to an antiarrhythmic role of EpC and a pro-arrhythmic role of BZ with complex geometry.

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Schotten, Ulrich, Sander Verheule, Paulus Kirchhof, and Andreas Goette. "Pathophysiological Mechanisms of Atrial Fibrillation: A Translational Appraisal." Physiological Reviews 91, no. 1 (January 2011): 265–325. http://dx.doi.org/10.1152/physrev.00031.2009.

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Atrial fibrillation (AF) is an arrhythmia that can occur as the result of numerous different pathophysiological processes in the atria. Some aspects of the morphological and electrophysiological alterations promoting AF have been studied extensively in animal models. Atrial tachycardia or AF itself shortens atrial refractoriness and causes loss of atrial contractility. Aging, neurohumoral activation, and chronic atrial stretch due to structural heart disease activate a variety of signaling pathways leading to histological changes in the atria including myocyte hypertrophy, fibroblast proliferation, and complex alterations of the extracellular matrix including tissue fibrosis. These changes in electrical, contractile, and structural properties of the atria have been called “atrial remodeling.” The resulting electrophysiological substrate is characterized by shortening of atrial refractoriness and reentrant wavelength or by local conduction heterogeneities caused by disruption of electrical interconnections between muscle bundles. Under these conditions, ectopic activity originating from the pulmonary veins or other sites is more likely to occur and to trigger longer episodes of AF. Many of these alterations also occur in patients with or at risk for AF, although the direct demonstration of these mechanisms is sometimes challenging. The diversity of etiological factors and electrophysiological mechanisms promoting AF in humans hampers the development of more effective therapy of AF. This review aims to give a translational overview on the biological basis of atrial remodeling and the proarrhythmic mechanisms involved in the fibrillation process. We pay attention to translation of pathophysiological insights gained from in vitro experiments and animal models to patients. Also, suggestions for future research objectives and therapeutical implications are discussed.

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Poudel, Pradeep, Yanmin Xu, Zhanqian Cui, Deepak Sharma, Bing Tian, and Sudarshan Paudel. "Atrial Fibrillation: Recent Advances in Understanding the Role of MicroRNAs in Atrial Remodeling with an Electrophysiological Overview." Cardiology 131, no. 1 (2015): 58–67. http://dx.doi.org/10.1159/000375403.

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Atrial fibrillation (AF) is a highly prevalent condition associated with pronounced cardiovascular-related morbidity, mortality and socioeconomic burden. It accounts for more hospitalization days than does any other arrhythmia. This article reviews the basic electrophysiology of AF, electrical and structural remodeling in AF and recent advances in understanding the molecular mechanisms of AF in relation to specific microRNAs. This paper also reviews the potential role of microRNAs as novel therapeutic targets as well as biomarkers in the management of AF. AF shows characteristics typical of altered electrophysiology that promote ectopic activity and facilitate reentry, thereby contributing to the progression from short paroxysmal AF to a persistent, permanent form via atrial remodeling, even in the absence of progressive underlying heart disease. MicroRNAs have been suggested to influence the development of AF by regulating gene expression at the post-transcriptional level. Increasing evidence has identified various microRNA modifications and their impacts on AF initiation and maintenance through electrical and structural remodeling. The discovery of specific microRNAs as novel therapeutic targets and some experimental evidence implicating microRNAs as potential molecular diagnostic markers have had a significant impact on the diagnosis and management of AF and demand further research.

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Climent, Andreu M., Maria S. Guillem, Felipe Atienza, and Francisco Fernández-Avilés. "Electrophysiological characteristics of permanent atrial fibrillation: insights from research models of cardiac remodeling." Expert Review of Cardiovascular Therapy 13, no. 1 (November 29, 2014): 1–3. http://dx.doi.org/10.1586/14779072.2015.986465.

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Tsvetkova, A. S., V. V. Krandycheva, and S. N. Kharin. "Electrophysiological remodeling of the right ventricle in experimental heart failure of different etiologies." Bulletin of Siberian Medicine 18, no. 2 (August 11, 2019): 165–74. http://dx.doi.org/10.20538/1682-0363-2019-2-165-174.

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The aim of the study was to evaluate electrophysiological remodeling of the right ventricle in rats in experimental heart failure of different etiologies. Materials and methods. Isadrin-, doxorubicin- and monocrotaline-induced heart failure models were developed. Unipolar epicardial electrograms of the ventricles (256 recording sites) were recorded using a 144-channel system. The cardiac output and pressure in both ventricles of the heart were measured. Activation-recovery intervals were used as an index of duration of local repolarization, and the general and local dispersions of activation-recovery intervals were used as an index of heterogeneity of ventricular repolarization. Results. In all models of heart failure, the following were identified: 1) non-uniform prolongation of repolarization with the greatest elongation at the apex of the right ventricle; 2) an increase in apicobasal differences of repolarization with the greatest change in the right ventricle; 3) an increase in the heterogeneity of the repolarization of the epicardial layer of the ventricles with heterogeneous changes in the local heterogeneity of repolarization and a decrease in the interregional differences in the heterogeneity of the electrophysiological properties of the myocardium; 4) more pronounced changes in the repolarization of the right ventricle than in the repolarization of the left ventricle. Conclusion. Thus, irrespective of the cause of the heart failure, the following changes occur: 1) prolongation of the right ventricular repolarization occurs non-uniformly (mostly due to the apical area), which results in an increase in the right ventricular repolarization heterogeneity; 2) an increase in the heterogeneity of right ventricular repolarization is observed, which causes an increase in the overall heterogeneity of the ventricular epicardial surface.

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Palandri, Chiara, Lorenzo Santini, Lucrezia Giammarino, Monica Musumeci, Jose Manuel Pioner, Cecilia Ferrantini, and Raffaele Coppini. "Electrophysiological remodeling in primary versus secondary cardiac hypertrophy: A study in human cardiomyocytes." Vascular Pharmacology 146 (October 2022): 107064. http://dx.doi.org/10.1016/j.vph.2022.107064.

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Mahajan, Rajiv, Dennis H. Lau, Anthony G. Brooks, Nicholas J. Shipp, Jim Manavis, John P. M. Wood, John W. Finnie, et al. "Electrophysiological, Electroanatomical, and Structural Remodeling of the Atria as Consequences of Sustained Obesity." Journal of the American College of Cardiology 66, no. 1 (July 2015): 1–11. http://dx.doi.org/10.1016/j.jacc.2015.04.058.

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Nesterova, Tatyana, Konstantin Ushenin, Dmitry Shmarko, and Olga Solovyova. "Electrophysiological Biomarkers for Age-Related Changes in Human Atrial Cardiomyocytes: In Silico Study." ITM Web of Conferences 31 (2020): 01004. http://dx.doi.org/10.1051/itmconf/20203101004.

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Age-related changes in human cardiomyocytes are closely related to cardiac diseases, especially atrial fibrillation. Restricted availability of biological preparations from the human atrial myocardium complicates experimental studies on the aging processes in cardiomyocytes. In this preliminary study, we used available experimental data on the age-related changes in ionic conductances in canine atrial cardiomyocytes to predict possible consequences of similar remodeling in humans using two mathematical models (Courtemanche98 and Maleckar09) of human atrial cardiomyocytes. The study was performed using the model population approach, allowing one to assess variability in the cellular response to different interventions affecting model parameters. Here, this approach was used to evaluate the effects of age-related parameter modulation on action potential biomarkers in the two models. Simulation results show a significant decrease in the action potential duration and membrane potential at 20% of the action potential duration in aging. These model predictions are consistent with experimental data from mammalians. The action potential characteristics are shown to serve as notable biomarkers of age-related electrophysiological remodeling in human atrial cardiomyocytes. A comparison of the two models shows different behavior in the prediction of repolarization abnormalities.

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Ryabov, I. A., T. Yu Chichkova, S. E. Mamchur, and E. A. Khomenko. "CARDIAC CONTRACTILITY MODULATION IN HEART FAILURE PATIENTS. FUNDAMENTAL MECHANISMS AND CLINICAL RESULTS." Siberian Medical Journal 34, no. 2 (July 11, 2019): 26–32. http://dx.doi.org/10.29001/2073-8552-2019-34-2-26-32.

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This review highlights the preclinical and clinical data about a relatively new electrophysiological method for chronic heart failure (CHF) treatment, cardiac contractility modulation (CCM). The review presents efficacy and safety data. An updated information about the capability of CCM to influence the molecular genetic apparatus of the cardiomyocytes is proposed. In addition, the review assesses prospects for application of CCM as a tool for reverse cardiac remodeling in patients with CHF.

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S. Ramos, Kennedy, Lisa Pool, Mathijs S. van Schie, Leonoor F. J. M. Wijdeveld, Willemijn F. B. van der Does, Luciënne Baks, H. M. Danish Sultan, et al. "Degree of Fibrosis in Human Atrial Tissue Is Not the Hallmark Driving AF." Cells 11, no. 3 (January 26, 2022): 427. http://dx.doi.org/10.3390/cells11030427.

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Background: The current paradigm is that fibrosis promotes electrophysiological disorders and drives atrial fibrillation (AF). In this current study, we investigated the relation between the degree of fibrosis in human atrial tissue samples of controls and patients in various stages of AF and the degree of electrophysiological abnormalities. Methods: The degree of fibrosis was measured in the atrial tissue and serum of patients in various stages of AF and the controls. Hereto, picrosirius and H&E staining were performed to quantify degree of total, endo-perimysial fibrosis, and cardiomyocyte diameter. Western blot quantified fibrosis markers: neural cell adhesion molecule, tissue inhibitor of metalloproteinase, lysyl oxidase, and α-smooth muscle actin. In serum, the ratio carboxyl-terminal telopeptide of collagen/matrix-metalloproteinase1 was determined. High-resolution epicardial mapping evaluated low-voltage areas and conduction abnormalities. Results: No significant differences were observed in the degree of fibrosis between the groups. Finally, no significant correlation—absolute nor spatial—was observed between all electrophysiological parameters and histological fibrosis markers. Conclusions: No differences in the degree of fibrosis were observed in patients from various stages of AF compared to the controls. Moreover, electrophysiological abnormalities did not correlate with any of the fibrosis markers. The findings indicate that fibrosis is not the hallmark of structural remodeling in AF.

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