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1
Gibson, Sarah E., Carol F. Farver, and Richard A. Prayson. "Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy: An Autopsy Case and Review of the Literature." Archives of Pathology & Laboratory Medicine 130, no. 2 (February 1, 2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.
Повний текст джерелаАнотація:
Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.
2
De Sensi, Francesco, Diego Penela, David Soto-Iglesias, Antonio Berruezo, and Ugo Limbruno. "Imaging Techniques for the Study of Fibrosis in Atrial Fibrillation Ablation: From Molecular Mechanisms to Therapeutical Perspectives." Journal of Clinical Medicine 10, no. 11 (May 24, 2021): 2277. http://dx.doi.org/10.3390/jcm10112277.
Повний текст джерелаАнотація:
Atrial fibrillation (AF) is the most prevalent form of cardiac arrhythmia. It is often related to diverse pathological conditions affecting the atria and leading to remodeling processes including collagen accumulation, fatty infiltration, and amyloid deposition. All these events generate atrial fibrosis, which contribute to beget AF. In this scenario, cardiac imaging appears as a promising noninvasive tool for monitoring the presence and degree of LA fibrosis and remodeling. The aim of this review is to comprehensively examine the bench mechanisms of atrial fibrosis moving, then to describe the principal imaging techniques that characterize it, such as cardiac magnetic resonance (CMR) and multidetector cardiac computed tomography (MDCT), in order to tailor atrial fibrillation ablation to each individual.
3
Villarroel-Ábrego, Hugo, Martha Reyes-Villatoro, and Camila Flores-Ventura. "Fibrosis atrial derecha y síndrome del nodo enfermo." Revista de Ecocardiografía Práctica y Otras Técnicas de Imagen Cardíaca 2, no. 1 (December 31, 2019): 30–33. http://dx.doi.org/10.37615/retic.v2n1a8.
Повний текст джерелаАнотація:
Varón de 57 años hipertenso y obeso consultó para valoración por disnea de esfuerzos. Se detectó leve hipertensión pulmonar por disfunción diastólica sin hipertrofia ventricular, incompetencia cronotrópica y fibrosis atrial derecha aislada por resonancia magnética. No había deterioro del strain del ventrículo dere-cho, pero sí de la aurícula derecha. Se implantó un marcapaso permanente. Se discute cómo, subyacente a la aparición de trastornos del automatismo y arritmias atriales, puede haber un sustrato de fibrosis no isquémica
4
Aronis, Konstantinos N., Rheeda L. Ali, Jialiu A. Liang, Shijie Zhou, and Natalia A. Trayanova. "Understanding AF Mechanisms Through Computational Modelling and Simulations." Arrhythmia & Electrophysiology Review 8, no. 3 (August 9, 2019): 210–19. http://dx.doi.org/10.15420/aer.2019.28.2.
Повний текст джерелаАнотація:
AF is a progressive disease of the atria, involving complex mechanisms related to its initiation, maintenance and progression. Computational modelling provides a framework for integration of experimental and clinical findings, and has emerged as an essential part of mechanistic research in AF. The authors summarise recent advancements in development of multi-scale AF models and focus on the mechanistic links between alternations in atrial structure and electrophysiology with AF. Key AF mechanisms that have been explored using atrial modelling are pulmonary vein ectopy; atrial fibrosis and fibrosis distribution; atrial wall thickness heterogeneity; atrial adipose tissue infiltration; development of repolarisation alternans; cardiac ion channel mutations; and atrial stretch with mechano-electrical feedback. They review modelling approaches that capture variability at the cohort level and provide cohort-specific mechanistic insights. The authors conclude with a summary of future perspectives, as envisioned for the contributions of atrial modelling in the mechanistic understanding of AF.
5
Pong, Terrence, Joy Aparicio-Valenzuela, Oluwatomisin Obafemi, Kevin Cyr, Cody Carlton, Calvin Taylor, and Anson Lee. "High-resolution spatiotemporal changes in dominant frequency and structural organization during persistent atrial fibrillation." PLOS ONE 18, no. 2 (February 14, 2023): e0271846. http://dx.doi.org/10.1371/journal.pone.0271846.
Повний текст джерелаАнотація:
Objective Analyze changes in frequency activity and structural organization that occur over time with persistent atrial fibrillation (AF) Background Little is known about the frequency characteristics of the epicardium during transition from paroxysmal to persistent AF. Accurate identification of areas of high dominant frequency (DF) is often hampered by limited spatial resolution. Improvements in electrode arrays provide high spatiotemporal resolution, allowing for characterization of the changes that occur during this transition. Methods AF was induced in adult Yorkshire swine by atrial tachypacing. DF mapping was performed using personalized mapping arrays. Histological analysis and late gadolinium enhanced magnetic resonance imaging were performed to determine structural differences in fibrosis. Results The left atrial epicardium was associated with a significant increase in DF in persistent AF (6.5 ± 0.2 vs. 7.4 ± 0.5 Hz, P = 0.03). The organization index (OI) significantly decreased during persistent AF in both the left atria (0.3 ± 0.03 vs. 0.2 ± 0.03, P = 0.01) and right atria (0.33 ± 0.04 vs. 0.23 ± 0.02, P = 0.02). MRI analysis demonstrated increased ECV values in persistent AF (0.19 vs 0.34, paroxysmal vs persistent, P = 0.05). Tissue sections from the atria showed increase in fibrosis in pigs with persistent AF compared to paroxysmal AF. Staining demonstrated decreased myocardial fiber alignment and loss of anisotropy in persistent AF tissue. Conclusions Changes in tissue organization and fibrosis are observed in the porcine model of persistent AF. Alterations in frequency activity and organization index can be captured with high resolution using flexible electrode arrays.
6
Dosdall, Derek J., Ravi Ranjan, Koji Higuchi, Eugene Kholmovski, Nathan Angel, Li Li, Rob MacLeod, et al. "Chronic atrial fibrillation causes left ventricular dysfunction in dogs but not goats: experience with dogs, goats, and pigs." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 5 (September 1, 2013): H725—H731. http://dx.doi.org/10.1152/ajpheart.00440.2013.
Повний текст джерелаАнотація:
Structural remodeling in chronic atrial fibrillation (AF) occurs over weeks to months. To study the electrophysiological, structural, and functional changes that occur in chronic AF, the selection of the best animal model is critical. AF was induced by rapid atrial pacing (50-Hz stimulation every other second) in pigs ( n = 4), dogs ( n = 8), and goats ( n = 9). Animals underwent MRIs at baseline and 6 mo to evaluate left ventricular (LV) ejection fraction (EF). Dogs were given metoprolol (50–100 mg po bid) and digoxin (0.0625–0.125 mg po bid) to limit the ventricular response rate to <180 beats/min and to mitigate the effects of heart failure. The pacing leads in pigs became entirely encapsulated and lost the ability to excite the heart, often before the onset of sustained AF. LV EF in dogs dropped from 54 ± 11% at baseline to 33 ± 7% at 6 mo ( P < 0.05), whereas LV EF in goats did not drop significantly (69 ± 8% at baseline vs. 60 ± 9% at 6 mo, P = not significant). After 6 mo of AF, fibrosis levels in dog atria and ventricles increased, whereas only atrial fibrosis levels increased in goats compared with control animals. In our experience, the pig model is not appropriate for chronic rapid atrial pacing-induced AF studies. Rate-controlled chronic AF in the dog model developed HF and LV fibrosis, whereas the goat model developed only atrial fibrosis without ventricular dysfunction and fibrosis. Both the dog and goat models are representative of segments of the patient population with chronic AF.
7
Li, Guo-Liang, Guy Fontaine, Jine Wu, Shuanliang Fan, Chaofeng Sun, and Ardan M. Saguner. "Atrial dysplasia in the atria of humans without cardiovascular disease." Journal of Investigative Medicine 67, no. 6 (February 14, 2019): 971–76. http://dx.doi.org/10.1136/jim-2018-000916.
Повний текст джерелаАнотація:
Research on atrial histology of humans without cardiovascular disease is scarce. Therefore, our aim was to study human atrial histology in subjects without cardiovascular disease. Histology of the right atrium, left atrium or atrial septum was studied in eight patients (one newborn infant and seven adults) who died of a non-cardiac cause and who were not known to suffer from any cardiovascular pathology. Staining with hematoxylin phloxine saffron or Masson’s trichrome was performed to have a better identification of fibrosis and H&E for better identification of lymphocytes. Atrial histology was compared with the histology of the left ventricle and was taken from a collection of standard glass slides. Common light microscopic examination and numeric image processing was performed in all samples. Left atrial histology showed a substantial amount of adipocytes and interstitial fibrosis, associated with replacement fibrosis in some of these cases including one case of lymphocytic infiltrates, similar to the histologic changes of the right ventricle (RV) known in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD). Furthermore, we identified a perpendicular orientation of atrial myocardial fibres, which is also a feature of the thin RV free wall. A similar histologic substrate to the RV myocardium known in ARVD is found in the atria of humans without an overt cardiovascular pathology. This may explain the high prevalence of atrial fibrillation in the general population.
8
Sramko, Marek, and Josef Kautzner. "Atrial Fibrosis." Journal of the American College of Cardiology 65, no. 22 (June 2015): 2465. http://dx.doi.org/10.1016/j.jacc.2015.01.067.
Повний текст джерела
9
Nagel, Claudia, Giorgio Luongo, Luca Azzolin, Steffen Schuler, Olaf Dössel, and Axel Loewe. "Non-Invasive and Quantitative Estimation of Left Atrial Fibrosis Based on P Waves of the 12-Lead ECG—A Large-Scale Computational Study Covering Anatomical Variability." Journal of Clinical Medicine 10, no. 8 (April 20, 2021): 1797. http://dx.doi.org/10.3390/jcm10081797.
Повний текст джерелаАнотація:
The arrhythmogenesis of atrial fibrillation is associated with the presence of fibrotic atrial tissue. Not only fibrosis but also physiological anatomical variability of the atria and the thorax reflect in altered morphology of the P wave in the 12-lead electrocardiogram (ECG). Distinguishing between the effects on the P wave induced by local atrial substrate changes and those caused by healthy anatomical variations is important to gauge the potential of the 12-lead ECG as a non-invasive and cost-effective tool for the early detection of fibrotic atrial cardiomyopathy to stratify atrial fibrillation propensity. In this work, we realized 54,000 combinations of different atria and thorax geometries from statistical shape models capturing anatomical variability in the general population. For each atrial model, 10 different volume fractions (0–45%) were defined as fibrotic. Electrophysiological simulations in sinus rhythm were conducted for each model combination and the respective 12-lead ECGs were computed. P wave features (duration, amplitude, dispersion, terminal force in V1) were extracted and compared between the healthy and the diseased model cohorts. All investigated feature values systematically in- or decreased with the left atrial volume fraction covered by fibrotic tissue, however value ranges overlapped between the healthy and the diseased cohort. Using all extracted P wave features as input values, the amount of the fibrotic left atrial volume fraction was estimated by a neural network with an absolute root mean square error of 8.78%. Our simulation results suggest that although all investigated P wave features highly vary for different anatomical properties, the combination of these features can contribute to non-invasively estimate the volume fraction of atrial fibrosis using ECG-based machine learning approaches.
10
Tandon, Karman, David Tirschwell, W. T. Longstreth, Bryn Smith, and Nazem Akoum. "Embolic stroke of undetermined source correlates to atrial fibrosis without atrial fibrillation." Neurology 93, no. 4 (June 25, 2019): e381-e387. http://dx.doi.org/10.1212/wnl.0000000000007827.
Повний текст джерелаАнотація:
ObjectiveTo examine the hypothesis that atrial fibrosis and associated atrial cardiopathy may be in the causal pathway of cardioembolic stroke independently of atrial fibrillation (AF) by comparing atrial fibrosis burden between patients with embolic stroke of undetermined source (ESUS), patients with AF, and healthy controls.MethodsWe used late-gadolinium-enhancement MRI to compare atrial fibrosis in 10 patients with ESUS against 10 controls (no stroke, no AF) and 10 patients with AF. Fibrosis was compared between groups, controlling for stroke risk factors.ResultsMean age was 51 ± 15 years, and 43% of participants were female. Patients with ESUS had more atrial fibrosis than controls (16.8 ± 5.7% vs 10.6 ± 5.7%, p = 0.019) and similar fibrosis compared to patients with AF (17.8 ± 4.8%, p = 0.65). Odds ratios of ESUS per quartile of fibrosis were 3.22 (95% CI [CI] 1.11–9.32, p = 0.031, unadjusted) and 3.17 (95% CI 1.05–9.52, p = 0.041, CHA2DVASc score adjusted). Patients with >12% fibrosis had a higher percentage of ESUS (77.8% vs 27.3%, p = 0.02), and patients with >20% fibrosis had the highest proportion of ESUS (4 of 5).ConclusionsPatients with ESUS exhibit similar atrial fibrosis compared to patients with AF and more fibrosis than healthy controls. Fibrosis is associated with ESUS after controlling for stroke risk factors, supporting the hypothesis that fibrosis is in the causal pathway of cardioembolic stroke independently of AF. Prospective studies are needed to assess the role of anticoagulation in primary and secondary stroke prevention in patients with high atrial fibrosis.
11
Miyauchi, Mizuho, Zhilin Qu, Yasushi Miyauchi, Sheng-Mei Zhou, Hui Pak, William J. Mandel, Michael C. Fishbein, Peng-Sheng Chen, and Hrayr S. Karagueuzian. "Chronic nicotine in hearts with healed ventricular myocardial infarction promotes atrial flutter that resembles typical human atrial flutter." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (June 2005): H2878—H2886. http://dx.doi.org/10.1152/ajpheart.01165.2004.
Повний текст джерелаАнотація:
The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were administered nicotine (5 mg·kg−1·day−1 sc) for 1 mo using osmotic minipumps. High-resolution epicardial (1,792 bipolar electrodes) and endocardial Halo catheters were used to map activation during induced atrial rhythms. Nicotine promoted inducible sustained AFL at a mean cycle length of 134 ± 10 ms in all MI dogs ( n = 6) requiring pacing and electrical shocks for termination. No AFL could be induced in MI dogs ( n = 6), control (non-MI) dogs ( n = 3) not exposed to nicotine, and dogs with no MI and exposed to nicotine ( n = 3). Activation maps during AFL showed a single reentrant wavefront in the right atrium that rotated either clockwise (60%) or counterclockwise (40%) around the crista terminalis and through the isthmus. Ablation of the isthmus prevented the induction of AFL. Nicotine caused a significant ( P < 0.01) but highly heterogeneous increase in atrial interstitial fibrosis (2- to 10-fold increase in left and right atria, respectively) in the MI group but only a 2-fold increase in the right atrium in the non-MI group. Nicotine also flattened ( P < 0.05) the slope of the epicardial monophasic action potential duration (electrical restitution) curve of both atria in the MI but not in non-MI dogs. Two-dimensional simulation in an excitable matrix containing an isthmus and nicotine's restitutional and reduced gap junctional coupling (fibrosis) parameters replicated the experiments. Chronic nicotine in hearts with MI promotes AFL that closely resembles typical human AFL. Increased atrial interstitial fibrosis and flattened electrical restitution are important substrates for the AFL.
12
Gao, Yuan, Yinglan Gong, and Ling Xia. "Simulation of Atrial Fibrosis Using Coupled Myocyte-Fibroblast Cellular and Human Atrial Models." Computational and Mathematical Methods in Medicine 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/9463010.
Повний текст джерелаАнотація:
Atrial fibrosis is characterized by expansion of extracellular matrix and increase in the number of fibroblasts which has been associated with the development and maintenance of atrial arrhythmias. However, the mechanisms how the fibrosis contributes to atrial arrhythmia remain incompletely understood. In this study, we used a proposed fibroblast model coupled with the human atrial myocyte to investigate the effects of fibrosis on atrial excitability and repolarization at both cellular and macroscopic levels. The 12-lead electrocardiogram (ECG) was also simulated to explore the index of clinical diagnosis for fibrosis. The simulation results showed that the fibrosis can modify action potential morphology of human atrial myocyte, slow down wave propagation, and have rate adaptation, thus causing the atrial electrical heterogeneity. The fibrosis alone was sufficient to cause arrhythmia, induce reentry wave, and result in low amplitude and wide P waves at normal heart rate and significant prolonged and inverse P waves at high heart rate. All these symptoms aggravated when the level of fibrosis increased. Our simulations demonstrated that fibrosis is the substrate of atrial arrhythmia and thereby may be a potential target in the treatment of atrial arrhythmias.
13
Pan, Zhenwei, Tomohiko Ai, Po-Cheng Chang, Ying Liu, Jijia Liu, Mitsunori Maruyama, Mohamed Homsi, et al. "Atrial fibrillation and electrophysiology in transgenic mice with cardiac-restricted overexpression of FKBP12." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 2 (February 1, 2019): H371—H379. http://dx.doi.org/10.1152/ajpheart.00486.2018.
Повний текст джерелаАнотація:
Cardiomyocyte-restricted overexpression of FK506-binding protein 12 transgenic (αMyHC-FKBP12) mice develop spontaneous atrial fibrillation (AF). The aim of the present study is to explore the mechanisms underlying the occurrence of AF in αMyHC-FKBP12 mice. Spontaneous AF was documented by telemetry in vivo and Langendorff-perfused hearts of αMyHC-FKBP12 and littermate control mice in vitro. Atrial conduction velocity was evaluated by optical mapping. The patch-clamp technique was applied to determine the potentially altered electrophysiology in atrial myocytes. Channel protein expression levels were evaluated by Western blot analyses. Spontaneous AF was recorded in four of seven αMyHC-FKBP12 mice but in none of eight nontransgenic (NTG) controls. Atrial conduction velocity was significantly reduced in αMyHC-FKBP12 hearts compared with NTG hearts. Interestingly, the mean action potential duration at 50% but not 90% was significantly prolonged in αMyHC-FKBP12 atrial myocytes compared with their NTG counterparts. Consistent with decreased conduction velocity, average peak Na+ current ( INa) density was dramatically reduced and the INa inactivation curve was shifted by approximately +7 mV in αMyHC-FKBP12 atrial myocytes, whereas the activation and recovery curves were unaltered. The Nav1.5 expression level was significantly reduced in αMyHC-FKBP12 atria. Furthermore, we found increases in atrial Cav1.2 protein levels and peak L-type Ca2+ current density and increased levels of fibrosis in αMyHC-FKBP12 atria. In summary, cardiomyocyte-restricted overexpression of FKBP12 reduces the atrial Nav1.5 expression level and mean peak INa, which is associated with increased peak L-type Ca2+ current and interstitial fibrosis in atria. The combined electrophysiological and structural changes facilitated the development of local conduction block and altered action potential duration and spontaneous AF. NEW & NOTEWORTHY This study addresses a long-standing riddle regarding the role of FK506-binding protein 12 in cardiac physiology. The work provides further evidence that FK506-binding protein 12 is a critical component for regulating voltage-gated sodium current and in so doing has an important role in arrhythmogenic physiology, such as atrial fibrillation.
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Grigoryan, S. V., L. G. Azarapetyan, and K. G. Adamyan. "Myocardial fibrosis and atrial fibrillation." Russian Journal of Cardiology, no. 9 (September 24, 2018): 71–76. http://dx.doi.org/10.15829/1560-4071-2018-9-71-76.
Повний текст джерелаАнотація:
Atrial fibrillation is the most prevalent arrhythmia, and tends to progress. Any structural changes in the heart may lead to its progressive remodelling with increased deposition of connective tissue and fibrosis. Predominance of collagen types I and III synthesis over its degradation leads to accumulation of fibers and to fibrosis. Increase of atrial fibrosis is usually found on autopsy and biopsy. There is relation revealed, of atrial fibrosis grade and postsurgery atrial fibrillation. The mechanisms participating in the structural remodelling and progression of atrial fibrosis are not studied well enough, but there is known role of renin-angiotensinaldosterone system, transforming growth factor, inflammation and matrix metalloproteases. As an alternative, one should consider non-invasive diagnostic methods: magnetic resonance imaging of the heart and biomarkers level measurement. Hyperactivation of the renin-angiotensin-aldosterone system facilitates structural remodelling of the heart and progression of atrial fibrosis. Hyperexpression of the transforming growth factor leads to selective atrial fibrosis, heterogeneity of excitation conduction and fibrillation onset. Matrix metalloproteases are the marker of extracellular degradation. Study of fibrosis biomarkers makes it to increase significantly the efficacy of atrial fibrillation course prediction.
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Selcoki, Yusuf, H. İbrahim Aydin, Tugrul H. Celik, Ahmet Isleyen, Ali Erayman, M. Bora Demircelik, Hilmi Demirin, Aydin Kosus, and Beyhan Eryonucu. "Galectin-3: A biochemical marker to detect paroxysmal atrial fibrillation?" Clinical & Investigative Medicine 39, no. 6 (December 1, 2016): 197. http://dx.doi.org/10.25011/cim.v39i6.27528.
Повний текст джерелаАнотація:
Purpose: Atrial fibrillation (AF) is the most common form of arrhythmia. AF leads to electrical remodelling and fibrosis of the atria; however, the mechanism(s) remain poorly understood. Galectin-3 is a potential mediator of cardiac fibrosis. The present study aimed to examine the relationship between serum galectin-3 levels and paroxysmal AF. Methods: Forty-six patients with paroxysmal AF and preserved left ventricular systolic function, and 38 age- and gender-matched control subjects, were involved in the study. Serum galectin-3 levels were analyzed with an enzyme-linked immunosorbent assay (ELISA). Results: Serum galectin-3 levels (median 1.38 ng/mL; 1.21 ng/mL-1.87 ng/mL; p< 0.001) were significantly elevated in patients with paroxysmal AF compared with the control. Left atrial diameter was significantly higher in patients with paroxysmal AF (41.2±3.0 mm vs. 39.6±3.3 mm). Left atrial diameter was found to be significantly correlated with serum galectin-3 levels in patients with paroxysmal AF (r= 0.378, p= 0.001). Conclusion: Serum galectin-3 levels are significantly elevated and significantly correlated with left atrial diameter in patients with paroxysmal AF.
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Tan, Alex Y., and Peter Zimetbaum. "Atrial Fibrillation and Atrial Fibrosis." Journal of Cardiovascular Pharmacology 57, no. 6 (June 2011): 625–29. http://dx.doi.org/10.1097/fjc.0b013e3182073c78.
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Du, Lili, Mu Qin, Yi Yi, Xiaoqing Chen, Weifeng Jiang, Li Zhou, Daoliang Zhang та ін. "Eplerenone Prevents Atrial Fibrosis via the TGF-β Signaling Pathway". Cardiology 138, № 1 (2017): 55–62. http://dx.doi.org/10.1159/000471918.
Повний текст джерелаАнотація:
Objectives: Eplerenone (EPL), an antagonist of the mineralocorticoid receptor, is beneficial for atrial fibrillation and atrial fibrosis. However, the underlying mechanism remains less well known. We aimed to investigate the effect of EPL on atrial fibrosis using a mouse with selective atrial fibrosis and to explore the underlying mechanisms. Methods: EPL-treated MHC-TGFcys33ser transgenic mice that have selective atrial fibrosis (Tx+EPL mice), as well as control mice, were used for in vivo studies including histological analyses, Western blotting, and qRT-PCR studies. TGF-β1-stimulated atrial fibroblasts were treated with EPL or vehicle for the in vitro studies including Western blotting and qRT-PCR studies. In addition, Smad7 siRNA was used to knock down Smad7. Results: EPL inhibited atrial fibrosis in the Tx mice. In addition, EPL suppressed the expression of fibrosis-related molecules induced by TGF-β1 in vivo and in vitro. This occurred in concert with a downregulation of Smad7 protein expression and an upregulation of p-Smad2/3 protein expression. In addition, knockdown of Smad7 by siRNA abolished the protective roles of EPL. Conclusions: EPL inhibited atrial fibrosis in Tx mice. The underlying mechanism may involve increased protein expression of Smad7, which enhances the inhibitory feedback regulation of TGF-β1/Smad signaling.
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Grigoryan, S. V., L. G. Azarapetyan, and K. G. Adamyan. "Comparative evaluation of markers of inflammation and fibrosis in patients with various clinical forms of atrial fibrillation." Cardiovascular Therapy and Prevention 17, no. 6 (December 20, 2018): 26–31. http://dx.doi.org/10.15829/1728-8800-2018-6-26-31.
Повний текст джерелаАнотація:
Aim. To identify and assess the significance of clinical and functional data characterizing cardiac remodeling, as well as inflammatory and fibrosis markers in patients with various clinical forms that promote the progression of atrial fibrillation (AF).Material and methods. We observed 213 patients with arterial hypertension or in combination with coronary artery disease, who were diagnosed with AF. For the clinical and functional assessment of various clinical forms of AF, the significance of certain clinical, hemodynamic, structural, functional, and immunological risk factors for AF was studied. We used the method of binary logistic regression and calculated the significance of the risk factors odds ratio (OR).Results. We made a database consisting of 33 indicators characterizing the clinical, hemodynamic and structural-functional heart condition, inflammatory and fibrosis markers, the significance of which was ambiguous in various clinical groups of AF patients. We identified enough informativeness of the OR significance for indicators of atrial electrical remodeling, which significantly increases from the paroxysmal AF to the persistent form. It confirms a significant role for the heterogeneity of pulses in the atria during the progression of AF. The degree of structural remodeling of both the atria and ventricles also significantly increases with the progression of AF. We also noted that inflammatory markers have statistically significant role with paroxysmal AF. With persistent AF, the significance of OR for inflammatory markers increases, and with permanent AF, their significance decreases. The significance of the OR in fibrosis marker is significantly high with AF and in the further AF progression, and it significantly increases with the persistent AF form.Conclusion. We determined different degrees of electrical and structural remodeling of the atria and ventricles in patients with various clinical forms of AF. At the same time, there is an increase in the reliability of OR in inflammatory and fibrosis markers. However, in patients with persistent AF, the duration of AF and increase in the significance of the OR in fibrosis marker come to the fore.
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Xiao, Minghan, Meixia Zhang, Mengjun Bie, Xiaowen Wang, Jingwen Guo та Hua Xiao. "Galectin-3 Induces Atrial Fibrosis by Activating the TGF-β1/Smad Pathway in Patients with Atrial Fibrillation". Cardiology 145, № 7 (2020): 446–55. http://dx.doi.org/10.1159/000506072.
Повний текст джерелаАнотація:
Background: Atrial fibrosis plays a critical role in the occurrence and maintenance of atrial fibrillation. The role of TGF-β1 in mediating atrial fibrosis is well documented. The β-galactoside-binding lectin galectin-3 (Gal-3) is mainly produced by macrophages in biological events such as inflammation and angiogenesis. Previous studies have shown that Gal-3 is associated with atrial fibrosis, but the relationship between TGF-β1 and Gal-3 in atrial fibrosis remains unclear. Objective: To determine whether Gal-3 induces atrial fibrosis and atrial fibrillation by activating the TGF-β1/Smad pathway and whether the expression of Gal-3 is mediated by TGF-β1, which can enable assessing the relationship between Gal-3 and TGF-β1 in atrial fibrosis. Methods: In this study, 30 patients’ right atrial appendages were collected and divided into 3 groups: congenital heart disease sinus rhythm group (n = 10, as a control group), rheumatic heart disease sinus rhythm group (n = 10), and rheumatic heart disease atrial fibrillation group (n = 10). Rat atrial fibroblasts were cultured in vitro, and recombinant Gal-3 and recombinant TGF-β1 proteins were added to the cell culture. The expression of Gal-3, TGF-β1, Smad2, and collagen I was detected by Western blotting and quantitative real-time PCR. Atrial tissues were stained with Masson’s trichrome stain to evaluate the extent of atrial fibrosis. The expression of Gal-3 and TGF-β1 was detected by immunohistochemical staining and immunofluorescence staining. Gal-3 and TGF-β1 interaction was demonstrated by immunoprecipitation. Results: The expression levels of Gal-3, TGF-β1, Smad2, and collagen I were elevated in the rheumatic heart disease atrial fibrillation group compared with the congenital heart disease sinus rhythm group and the rheumatic heart disease sinus rhythm group. In cultured atrial fibroblasts, there is a synergistic interaction between Gal-3 and TGF-β1. Gal-3 stimulated the TGF-β1/Smad pathway, and overexpression of TGF-β1 induced Gal-3 expression. Conclusions: Gal-3 and TGF-β1 interact with each other and stimulate the downstream TGF-β1/Smad pathway. This finding suggests that Gal-3 could be an important factor in TGF-β1-induced fibrosis in atrial fibrillation.
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Pan, Jian-an, Hao Lin, Jian-ying Yu, Hui-li Zhang, Jun-feng Zhang, Chang-qian Wang, and Jun Gu. "MiR-21-3p Inhibits Adipose Browning by Targeting FGFR1 and Aggravates Atrial Fibrosis in Diabetes." Oxidative Medicine and Cellular Longevity 2021 (August 25, 2021): 1–16. http://dx.doi.org/10.1155/2021/9987219.
Повний текст джерелаАнотація:
A relationship between excess epicardial adipose tissue (EAT) and the risk of atrial fibrillation (AF) has been reported. Browning of EAT may be a novel approach for the prevention or treatment of AF by attenuating atrial fibrosis. Previous studies have identified microRNA-21 (miR-21) as a regulatory factor in atrial fibrosis. The present study examined the role of different subtypes of miR-21 in adipose browning and atrial fibrosis under hyperglycemic conditions. Wild type and miR-21 knockout C57BL/6 mice were used to establish a diabetic model via intraperitoneal injection of streptozotocin. A coculture model of atrial fibroblasts and adipocytes was also established. We identified miR-21-3p as a key regulator that controls adipocyte browning and participates in atrial fibrosis under hyperglycemic conditions. Moreover, fibroblast growth factor receptor (FGFR) 1, a direct target of miR-21-3p, decreased in this setting and controlled adipose browning. Gain and loss-of-function experiments identified a regulatory pathway in adipocytes involving miR-21a-3p, FGFR1, FGF21, and PPARγ that regulated adipocyte browning and participated in hyperglycemia-induced atrial fibrosis. Modulation of this signaling pathway may provide a therapeutic option for the prevention and treatment of atrial fibrosis or AF in DM.
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Kugler, Szilvia, Gábor Duray, and István Préda. "Új felismerések a pitvarfibrilláció genezisében és fenntartásában: az egyénre szabott kezelés lehetőségei." Orvosi Hetilap 159, no. 28 (July 2018): 1135–45. http://dx.doi.org/10.1556/650.2018.31087.
Повний текст джерелаАнотація:
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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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.
Повний текст джерелаАнотація:
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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Palacio, Laura C., Juan P. Ugarte, Javier Saiz, and Catalina Tobón. "The Effects of Fibrotic Cell Type and Its Density on Atrial Fibrillation Dynamics: An In Silico Study." Cells 10, no. 10 (October 15, 2021): 2769. http://dx.doi.org/10.3390/cells10102769.
Повний текст джерелаАнотація:
Remodeling in atrial fibrillation (AF) underlines the electrical and structural changes in the atria, where fibrosis is a hallmark of arrhythmogenic structural alterations. Fibrosis is an important feature of the AF substrate and can lead to abnormal conduction and, consequently, mechanical dysfunction. The fibrotic process comprises the presence of fibrotic cells, including fibroblasts, myofibroblasts and fibrocytes, which play an important role during fibrillatory dynamics. This work assesses the effect of the diffuse fibrosis density and the intermingled presence of the three types of fibrotic cells on the dynamics of persistent AF. For this purpose, the three fibrotic cells were electrically coupled to cardiomyocytes in a 3D realistic model of human atria. Low (6.25%) and high (25%) fibrosis densities were implemented in the left atrium according to a diffuse fibrosis representation. We analyze the action potential duration, conduction velocity and fibrillatory conduction patterns. Additionally, frequency analysis was performed in 50 virtual electrograms. The tested fibrosis configurations generated a significant conduction velocity reduction, where the larger effect was observed at high fibrosis density (up to 82% reduction in the fibrocytes configuration). Increasing the fibrosis density intensifies the vulnerability to multiple re-entries, zigzag propagation, and chaotic activity in the fibrillatory conduction. The most complex propagation patterns were observed at high fibrosis densities and the fibrocytes are the cells with the largest proarrhythmic effect. Left-to-right dominant frequency gradients can be observed for all fibrosis configurations, where the fibrocytes configuration at high density generates the most significant gradients (up to 4.5 Hz). These results suggest the important role of different fibrotic cell types and their density in diffuse fibrosis on the chaotic propagation patterns during persistent AF.
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Liu, Yang, Haichen Lv, Ruopeng Tan, Xiangbo An, Xiao-Hui Niu, Yue-Jian Liu, Xiaolei Yang, Xiaomeng Yin та Yun-Long Xia. "Platelets Promote Ang II (Angiotensin II)-Induced Atrial Fibrillation by Releasing TGF-β1 (Transforming Growth Factor-β1) and Interacting With Fibroblasts". Hypertension 76, № 6 (грудень 2020): 1856–67. http://dx.doi.org/10.1161/hypertensionaha.120.15016.
Повний текст джерелаАнотація:
Hypertension is a risk factor of atrial fibrillation (AF), and a certain number of patients with hypertension were found with an enlarged left atrium. Platelet activation is found in patients with hypertension or pressure overload/Ang II (angiotensin II)-induced hypertensive animal models and contribute to ventricular fibrosis. Whether hypertension-induced atrial fibrosis is mediated by platelets remains unknown. Our previous experimental data showed that platelet-derived TGF-β1 (transforming growth factor-β1) was reduced in patients with hypertensive AF. The present study is to investigate whether platelet-derived TGF-β1 promotes Ang II-induced atrial fibrosis and AF. Platelet activation and atrial platelet accumulation were measured in sinus rhythm controls, normotensive AF, and patients with hypertensive AF. Ang II (1500 ng/kg per minute, 3 weeks) infused mice with pharmacological (clopidogrel) and genetic platelet inhibition (TGF-β1 deletion in platelets) were used. Platelet activation, atrial structural remodeling, atrial electrical transmission, AF inducibility, inflammation, and fibrosis were measured in mice. We found that circulating platelets were activated in patients with hypertensive AF. A large amount of platelet was accumulated in the atriums of patients with hypertensive AF. Both clopidogrel treatment and platelet-specific deletion of TGF-β1 attenuated Ang II-induced structural remodeling, atrial electrical transmission, AF inducibility, as well as atrial inflammation and fibrosis than mice without interventions. Furthermore, clopidogrel blocked atrial platelet accumulation and platelet-fibroblast conjugation. Platelets promoted atrial fibroblast differentiation in cell culture. Profibrotic actions of platelets are largely via activation of atrial fibroblasts by releasing TGF-β1 and inducing platelet-fibroblast conjugation, and platelet inhibition is sufficient to inhibit atrial fibrosis and AF inducibility.
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Kis, Zsuzsanna, Astrid Amanda Hendriks, Taulant Muka, Wichor M. Bramer, Istvan Kovacs, and Tamas Szili-Torok. "The Role of Atrial Fibrosis Detected by Delayed - Enhancement MRI in Atrial Fibrillation Ablation." Current Medical Imaging Formerly Current Medical Imaging Reviews 16, no. 2 (January 24, 2020): 135–44. http://dx.doi.org/10.2174/1573405614666180806130327.
Повний текст джерелаАнотація:
Introduction: Atrial Fibrillation (AF) is associated with remodeling of the atrial tissue, which leads to fibrosis that can contribute to the initiation and maintenance of AF. Delayed- Enhanced Cardiac Magnetic Resonance (DE-CMR) imaging for atrial wall fibrosis detection was used in several studies to guide AF ablation. The aim of present study was to systematically review the literature on the role of atrial fibrosis detected by DE-CMR imaging on AF ablation outcome. Methods: Eight bibliographic electronic databases were searched to identify all published relevant studies until 21st of March, 2016. Search of the scientific literature was performed for studies describing DE-CMR imaging on atrial fibrosis in AF patients underwent Pulmonary Vein Isolation (PVI). Results: Of the 763 citations reviewed for eligibility, 5 articles (enrolling a total of 1040 patients) were included into the final analysis. The overall recurrence of AF ranged from 24.4 - 40.9% with median follow-up of 324 to 540 days after PVI. With less than 5-10% fibrosis in the atrial wall there was a maximum of 10% recurrence of AF after ablation. With more than 35% fibrosis in the atrial wall there was 86% recurrence of AF after ablation. Conclusion: Our analysis suggests that more extensive left atrial wall fibrosis prior ablation predicts the higher arrhythmia recurrence rate after PVI. The DE-CMR imaging modality seems to be a useful method for identifying the ideal candidate for catheter ablation. Our findings encourage wider usage of DE-CMR in distinct AF patients in a pre-ablation setting.
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Opie, Lionel H. "Tedisamil in Coronary Disease: Additional Benefits in the Therapy of Atrial Fibrillation?" Journal of Cardiovascular Pharmacology and Therapeutics 8, no. 1_suppl (March 2003): S33—S37. http://dx.doi.org/10.1177/107424840300800105.
Повний текст джерелаАнотація:
Atrial fibrillation has recently come into clinical and research focus. In particular, ventricular rate control has been carefully compared with atrial rhythm control. Additionally, the recent discovery of atrial stunning has initiated clinical and research interest in atrial remodeling. Atrial fibrillation is more likely to occur when the atria are damaged by increased fibrosis. The ideal way to prevent atrial fibrillation and the risk of repetition is by tackling the root causes, such as ischemic heart disease, heart failure, and left ventricular hypertrophy. Tedisamil is an unusual antifibrillatory compound that has a novel mechanism of action by inhibiting the transient outward current (Ito) and the repolarizing potassium currents in the sinoatrial node. Tedisamil works acutely against atrial fibrillation. Importantly, atrial fibrillation is often caused by or related to cardiac ischemia, and conversely, ischemia is caused by the increased oxygen demand of atrial fibrillation. Hence, the double properties of tedisamil as a drug that both inhibits atrial fibrillation and acts in an anti-ischemic mode are an attractive basis for future clinical research.
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Matějková, Adéla, and Ivo Šteiner. "Association of Atrial Fibrillation with Morphological and Electrophysiological Changes of the Atrial Myocardium." Acta Medica (Hradec Kralove, Czech Republic) 59, no. 2 (2016): 43–49. http://dx.doi.org/10.14712/18059694.2016.88.
Повний текст джерелаАнотація:
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. For long time it was considered as pure functional disorder, but in recent years, there were identified atrial locations, which are involved in the initiation and maintenance of this arrhythmia. These structural changes, so called remodelation, start at electric level and later they affect contractility and morphology. In this study we attempted to find a possible relation between morphological (scarring, amyloidosis, left atrial (LA) enlargement) and electrophysiological (ECG features) changes in patients with AF. We examined grossly and histologically 100 hearts of necropsy patients – 54 with a history of AF and 46 without AF. Premortem ECGs were evaluated. The patients with AF had significantly heavier heart, larger LA, more severely scarred myocardium of the LA and atrial septum, and more severe amyloidosis in both atria. Severity of amyloidosis was higher in LAs vs. right atria (RAs). Distribution of both fibrosis and amyloidosis was irregular. The most affected area was in the LA anterior wall. Patients with a history of AF and with most severe amyloidosis have more often abnormally long P waves. Finding of long P wave may contribute to diagnosis of a hitherto undisclosed atrial fibrillation.
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Falkenberg, Max, James A. Coleman, Sam Dobson, David J. Hickey, Louie Terrill, Alberto Ciacci, Belvin Thomas, et al. "Identifying locations susceptible to micro-anatomical reentry using a spatial network representation of atrial fibre maps." PLOS ONE 17, no. 6 (June 23, 2022): e0267166. http://dx.doi.org/10.1371/journal.pone.0267166.
Повний текст джерелаАнотація:
Micro-anatomical reentry has been identified as a potential driver of atrial fibrillation (AF). In this paper, we introduce a novel computational method which aims to identify which atrial regions are most susceptible to micro-reentry. The approach, which considers the structural basis for micro-reentry only, is based on the premise that the accumulation of electrically insulating interstitial fibrosis can be modelled by simulating percolation-like phenomena on spatial networks. Our results suggest that at high coupling, where micro-reentry is rare, the micro-reentrant substrate is highly clustered in areas where the atrial walls are thin and have convex wall morphology, likely facilitating localised treatment via ablation. However, as transverse connections between fibres are removed, mimicking the accumulation of interstitial fibrosis, the substrate becomes less spatially clustered, and the bias to forming in thin, convex regions of the atria is reduced, possibly restricting the efficacy of localised ablation. Comparing our algorithm on image-based models with and without atrial fibre structure, we find that strong longitudinal fibre coupling can suppress the micro-reentrant substrate, whereas regions with disordered fibre orientations have an enhanced risk of micro-reentry. With further development, these methods may be useful for modelling the temporal development of the fibrotic substrate on an individualised basis.
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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.
Повний текст джерелаАнотація:
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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Jalife, José, and Kuljeet Kaur. "Atrial remodeling, fibrosis, and atrial fibrillation." Trends in Cardiovascular Medicine 25, no. 6 (August 2015): 475–84. http://dx.doi.org/10.1016/j.tcm.2014.12.015.
Повний текст джерела
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Nagel, Claudia, Olaf Dössel, and Axel Loewe. "Sensitivity and Generalization of a Neural Network for Estimating Left Atrial Fibrotic Volume Fractions from the 12-lead ECG." Current Directions in Biomedical Engineering 7, no. 2 (October 1, 2021): 307–10. http://dx.doi.org/10.1515/cdbme-2021-2078.
Повний текст джерелаАнотація:
Abstract Features extracted from P waves of the 12-lead electrocardiogram (ECG) have proven valuable for noninvasively estimating the left atrial fibrotic volume fraction associated with the arrhythmogenesis of atrial fibrillation. However, feature extraction in the clinical context is prone to errors and oftentimes yields unreliable results in the presence of noise. This leads to inaccurate input values provided to machine learning algorithms tailored at estimating the amount of atrial fibrosis with clinical ECGs. Another important aspect for clinical translation is the network’s generalization ability regarding new ECGs. To quantify a network’s sensitivity to inaccurately extracted P wave features, we added Gaussian noise to the features extracted from 540,000 simulated ECGs consisting of P wave duration, dispersion, terminal force in lead V1, peak-to-peak amplitudes, and additionally thoracic and atrial volumes. For assessing generalization, we evaluated the network performance for train-validation-test splits divided such that ECGs simulated with the same atria or torso geometry only belonged to either the training and validation or the test set. The root mean squared error (RMSE) of the network increased the most in case of noisy torso volumes and P wave durations. Large generalization errors with a RMSE difference between training and test set of more than 2% fibrotic volume fraction only occurred if very high or low atria and torso volumes were left out during training. Our results suggest that P wave duration and thoracic volume are features that have to be measured accurately if employed for estimating atrial fibrosis with a neural network. Furthermore, our method is capable of generalizing well to ECGs simulated with anatomical models excluded during training and thus meets an important requirement for clinical translation.
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Xintarakou, Anastasia, Stylianos Tzeis, Stelios Psarras, Dimitrios Asvestas, and Panos Vardas. "Atrial fibrosis as a dominant factor for the development of atrial fibrillation: facts and gaps." EP Europace 22, no. 3 (January 30, 2020): 342–51. http://dx.doi.org/10.1093/europace/euaa009.
Повний текст джерелаАнотація:
Abstract Atrial fibrillation (AF), the most commonly diagnosed arrhythmia, affects a notable percentage of the population and constitutes a major risk factor for thromboembolic events and other heart-related conditions. Fibrosis plays an important role in the onset and perpetuation of AF through structural and electrical remodelling processes. Multiple molecular pathways are involved in atrial substrate modification and the subsequent maintenance of AF. In this review, we aim to recapitulate underlying molecular pathways leading to atrial fibrosis and to indicate existing gaps in the complex interplay of atrial fibrosis and AF.
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Sánchez, Francisco Javier, Esther Pueyo, and Emiliano Raúl Diez. "Strain Echocardiography to Predict Postoperative Atrial Fibrillation." International Journal of Molecular Sciences 23, no. 3 (January 25, 2022): 1355. http://dx.doi.org/10.3390/ijms23031355.
Повний текст джерелаАнотація:
Postoperative atrial fibrillation (POAF) complicates 15% to 40% of cardiovascular surgeries. Its incidence progressively increases with aging, reaching 50% in octogenarians. This arrhythmia is usually transient but it increases the risk of embolic stroke, prolonged hospital stay, and cardiovascular mortality. Though many pathophysiological mechanisms are known, POAF prediction is still a hot topic of discussion. Doppler echocardiogram and, lately, strain echocardiography have shown significant capacity to predict POAF. Alterations in oxidative stress, calcium handling, mitochondrial dysfunction, inflammation, fibrosis, and tissue aging are among the mechanisms that predispose patients to the perfect “atrial storm”. Manifestations of these mechanisms have been related to enlarged atria and impaired function, which can be detected prior to surgery. Specific alterations in the atrial reservoir and pump function, as well as atrial dyssynchrony determined by echocardiographic atrial strain, can predict POAF and help to shed light on which patients could benefit from preventive therapy.
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Tang, Mirong, Yan Chen, Fuqing Sun та Liangliang Yan. "The Dose-Dependent Effects of Spironolactone on TGF-β1 Expression and the Vulnerability to Atrial Fibrillation in Spontaneously Hypertensive Rats". Cardiology Research and Practice 2021 (27 вересня 2021): 1–8. http://dx.doi.org/10.1155/2021/9924381.
Повний текст джерелаАнотація:
Objective. This study tends to assess the dose-dependent effects of spironolactone on TGF-β1 expression, atrial fibrosis, and the vulnerability to atrial fibrillation in spontaneously hypertensive rats (SHRs) and tries to clarify the association of atrial fibrosis with the vulnerability to atrial fibrillation. Methods. Forty 20-week-old male SHRs were randomly divided into 4 groups (10 rats per group): 3 spironolactone groups were lower-dose group (10 mg·kg−1·d−1, dissolved in 2 ml saline solution, group SL), medium-dose group (40 mg·kg−1·d−1, dissolved in 2 ml saline solution, group SM), higher-dose group (80 mg·kg−1·d−1, dissolved in 2 ml saline solution, group SH) and one hypertension group (2 ml saline solution for stomach gavage, group H). Ten matched homologous WKY rats were set as the control group (group C). After 7 weeks of gavage, a multiple electroconductive physiological recorder was used to detect atrial electrical parameters, including P-wave duration, PR interval, and atrial effective refractory period (AERP), the inducibility, and duration of atrial fibrillation. HE staining was used to determine myocardial cell size. Masson staining was used to detect the deposition of the interstitial collagen fibers in atrial muscle. The expression of TGF-β1 was detected by immunohistochemistry and western blot. Results. Compared with group C, the myocardial cell size, atrial fibrosis, TGF-β1 expression, P-wave duration, PR interval, AERP, inducibility, and duration of atrial fibrillation in group H were conspicuously increased ( p < 0.05); compared with group H, there was no significant difference in the myocardial cell size, atrial fibrosis, TGF-β1 expression, and electrophysiological indexes in group SH upon spironolactone intervention ( p > 0.05); compared with group H, the myocardial cell size, atrial fibrosis, the expression of TGF-β1, P-wave duration, PR interval, the inducibility, and duration of atrial fibrillation in the group SL and group SM were all decreased ( p < 0.05); compared with group SM, the effect in the group SL was more prominent ( p < 0.01). Conclusion. Hypertension can lead to cardiomyocyte hypertrophy, deposition of interstitial fibrosis in myocardial tissue, and an increase in the vulnerability to atrial fibrillation. Spironolactone showed a certain dose-dependent effect in SHRs. Lower-dose spironolactone was superior to higher-dose spironolactone in the aspect of reducing hypertensive atrial fibrosis and TGF-β1 expression, as well as preventing the occurrence of atrial fibrillation.
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Rizvi, Farhan, Alessandra DeFranco, Ramail Siddiqui, Ulugbek Negmadjanov, Larisa Emelyanova, Alisher Holmuhamedov, Gracious Ross, et al. "Chamber-specific differences in human cardiac fibroblast proliferation and responsiveness toward simvastatin." American Journal of Physiology-Cell Physiology 311, no. 2 (August 1, 2016): C330—C339. http://dx.doi.org/10.1152/ajpcell.00056.2016.
Повний текст джерелаАнотація:
Fibroblasts, the most abundant cells in the heart, contribute to cardiac fibrosis, the substrate for the development of arrythmogenesis, and therefore are potential targets for preventing arrhythmic cardiac remodeling. A chamber-specific difference in the responsiveness of fibroblasts from the atria and ventricles toward cytokine and growth factors has been described in animal models, but it is unclear whether similar differences exist in human cardiac fibroblasts (HCFs) and whether drugs affect their proliferation differentially. Using cardiac fibroblasts from humans, differences between atrial and ventricular fibroblasts in serum-induced proliferation, DNA synthesis, cell cycle progression, cyclin gene expression, and their inhibition by simvastatin were determined. The serum-induced proliferation rate of human atrial fibroblasts was more than threefold greater than ventricular fibroblasts with faster DNA synthesis and higher mRNA levels of cyclin genes. Simvastatin predominantly decreased the rate of proliferation of atrial fibroblasts, with inhibition of cell cycle progression and an increase in the G0/G1 phase in atrial fibroblasts with a higher sensitivity toward inhibition compared with ventricular fibroblasts. The DNA synthesis and mRNA levels of cyclin A, D, and E were significantly reduced by simvastatin in atrial but not in ventricular fibroblasts. The inhibitory effect of simvastatin on atrial fibroblasts was abrogated by mevalonic acid (500 μM) that bypasses 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibition. Chamber-specific differences exist in the human heart because atrial fibroblasts have a higher proliferative capacity and are more sensitive to simvastatin-mediated inhibition through HMG-CoA reductase pathway. This mechanism may be useful in selectively preventing excessive atrial fibrosis without inhibiting adaptive ventricular remodeling during cardiac injury.
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Kovács, István, András Mester, Lehel Bordi, Alexandra Stănescu, Sebastian Condrea, Monica Chiţu, Annabell Benedek, and Imre Benedek. "Myocardial Fibrosis and the Risk of Recurrence in Atrial Fibrillation." Journal of Interdisciplinary Medicine 1, no. 3 (December 1, 2016): 259–62. http://dx.doi.org/10.1515/jim-2016-0067.
Повний текст джерелаАнотація:
Abstract Atrial fibrillation (AF) is the most frequent cardiac arrhythmia increasing the risk of stroke and mortality from heart failure. Magnetic resonance imaging was used by several authors for assessment of atrial fibrosis and to predict the rate of recurrence following AF ablation. The aim of this manuscript was to summarize the new data in the literature regarding the role of atrial fibrosis in AF imaging and the role of cardiac fibrosis in predicting AF recurrence after radio-frequency ablation.
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Stychynskyi, Oleksandr S., Pavlo O. Almiz, and Alina V. Topchii. "Atrial Cardiomyopathy: a Role in the Pathogenesis of Atrial Fibrillation and Influence on the Results of Its Treatment." Ukrainian Journal of Cardiovascular Surgery, no. 4 (45) (December 22, 2021): 85–89. http://dx.doi.org/10.30702/ujcvs/21.4512/sa053-8589.
Повний текст джерелаАнотація:
The work is dedicated to the issue of atrial cardiomyopathies (ACs). They have a significant effect on the heart function, provoke rhythm disturbances and increase the risk of thromboembolic complications.
The aim. To analyze the latest publications on the topic.
The material for the analysis were the papers published by the leading arrhythmological clinics.
Discussion. This paper describes the origin of the term “atrial cardiomyopathy”, highlights the conditional classification of changes in the atrial myocardium according to the EHRAS classification. The causes of this nosological form may be some types of gene mutations, as well as hypertension, congestive circulatory failure, diabetes mellitus, myocarditis, etc. ACs play an important role in the occurrence of atrial fibrillation (AF) and also affect its natural course and treatment outcomes. Electroanatomical mapping and magnetic resonance data show significant fibrotic changes in the atria in individuals with this form of arrhythmia. The DECAAF study (Delayed enhancement MRI and atrial fibrillation catheter ablation) showed that fibrotic changes in the atrial myocardium are directly related to the frequency of recurrent arrhythmias after catheter ablation. The DECAAFII study confirmed the effectiveness of the influence on the fibrous substrate in the catheter treatment of AF at stages 1 and 2 of fibrosis. The results of catheter treatment depend on the severity of fibrosis, which shows the importance of taking this factor into account when determining the indications for ablation.
Conclusions. Thus, AC is an important component of the pathogenesis of AF. Improvement of techniques for influencing the fibrous substrate will improve the results of catheter treatment of AF.
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Jiang, Zhiyuan, Guoqiang Zhong, Lina Wen, Yujie Hong, Shu Fang, Peizhen Sun, Shuo Li, Shanshan Li та Guirong Feng. "The Role of Platelet-Derived Growth Factor-B/Platelet-Derived Growth Factor Receptor-β Signaling in Chronic Atrial Fibrillation". Cardiology 133, № 4 (2016): 242–56. http://dx.doi.org/10.1159/000442940.
Повний текст джерелаАнотація:
Objective: To explore the role of platelet-derived growth factor-B (PDGF-B)/platelet-derived growth factor receptor-β (PDGFR-β) signaling in chronic atrial fibrillation (AF). Methods: Thirty-nine AF patients and 33 patients with sinus rhythm (SR) were enrolled. Twenty canines were randomized into 5 groups: control, sham and AF lasting 1, 2 or 4 weeks. The AF canine models were made by rapid atrial pacing. Rat atrial fibroblasts were treated with PDGF-BB or PDGF-BB + PDGFR inhibitor AG1295, respectively. Gene expression in the right atrial appendage of patients, the left atrium of canines and rat atrial fibroblasts was measured by quantitative real-time PCR and Western blot, respectively. The degree of atrial fibrosis was evaluated by Masson trichrome staining. Results: The degree of atrial fibrosis and the expression of PDGF-B, PDGFR-β and collagen type I (COL1) in AF patients significantly increased compared to patients with SR. The degree of atrial fibrosis and the expression of PDGF-B and COL1 in canines increased progressively with the increased duration of AF. The expression of PDGFR-β increased progressively 2 weeks after AF. PDGF-BB promoted the proliferation and COL1 secretion of rat atrial fibroblasts. AG1295 attenuated these effects. Conclusions: Our study suggests that PDGF-B/PDGFR-β signaling, which promotes the proliferation and COL1 secretion of atrial fibroblasts, is an important contributor to atrial fibrosis in AF and may represent a novel target for the intervention of AF.
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Wilber, David J. "Fibrosis and Atrial Fibrillation." JACC: Clinical Electrophysiology 3, no. 5 (May 2017): 530. http://dx.doi.org/10.1016/j.jacep.2017.04.001.
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Gramley, Felix, Johann Lorenzen, Christian Knackstedt, Obaida R. Rana, Erol Saygili, Dirk Frechen, Sven Stanzel, et al. "Age-related atrial fibrosis." AGE 31, no. 1 (October 7, 2008): 27–38. http://dx.doi.org/10.1007/s11357-008-9077-9.
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Sohns, Christian, and Nassir F. Marrouche. "Atrial fibrillation and cardiac fibrosis." European Heart Journal 41, no. 10 (November 12, 2019): 1123–31. http://dx.doi.org/10.1093/eurheartj/ehz786.
Повний текст джерелаАнотація:
Abstract The understanding of atrial fibrillation (AF) evolved from a sole rhythm disturbance towards the complex concept of a cardiomyopathy based on arrhythmia substrates. There is evidence that atrial fibrosis can be visualized using late gadolinium enhancement cardiac magnetic resonance imaging and that it is a powerful predictor for the outcome of AF interventions. However, a strategy of an individual and fibrosis guided management of AF looks promising but results from prospective multicentre trials are pending. This review gives an overview about the relationship between cardiac fibrosis and AF focusing on translational aspects, clinical observations, and fibrosis imaging to emphasize the concept of personalized paths in AF management taking into account the individual amount and distribution of fibrosis.
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Takawale, Abhijit, Martin Aguilar, Yasmina Bouchrit, and Roddy Hiram. "Mechanisms and Management of Thyroid Disease and Atrial Fibrillation: Impact of Atrial Electrical Remodeling and Cardiac Fibrosis." Cells 11, no. 24 (December 14, 2022): 4047. http://dx.doi.org/10.3390/cells11244047.
Повний текст джерелаАнотація:
Atrial fibrillation (AF) is the most common cardiac arrhythmia associated with increased cardiovascular morbidity and mortality. The pathophysiology of AF is characterized by electrical and structural remodeling occurring in the atrial myocardium. As a source of production of various hormones such as angiotensin-2, calcitonin, and atrial natriuretic peptide, the atria are a target for endocrine regulation. Studies have shown that disorders associated with endocrine dysregulation are potential underlying causes of AF. The thyroid gland is an endocrine organ that secretes three hormones: triiodothyronine (T3), thyroxine (T4) and calcitonin. Thyroid dysregulation affects the cardiovascular system. Although there is a well-established relationship between thyroid disease (especially hyperthyroidism) and AF, the underlying biochemical mechanisms leading to atrial fibrosis and atrial arrhythmias are poorly understood in thyrotoxicosis. Various animal models and cellular studies demonstrated that thyroid hormones are involved in promoting AF substrate. This review explores the recent clinical and experimental evidence of the association between thyroid disease and AF. We highlight the current knowledge on the potential mechanisms underlying the pathophysiological impact of thyroid hormones T3 and T4 dysregulation, in the development of the atrial arrhythmogenic substrate. Finally, we review the available therapeutic strategies to treat AF in the context of thyroid disease.
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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.
Повний текст джерелаАнотація:
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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O’Neill, Louisa, Iain Sim, Daniel O’Hare, John Whitaker, Rahul K. Mukherjee, Orod Razeghi, Steven Niederer, et al. "CArdiac MagnEtic resonance assessment of bi-Atrial fibrosis in secundum atrial septal defects patients: CAMERA-ASD study." European Heart Journal - Cardiovascular Imaging, September 26, 2021. http://dx.doi.org/10.1093/ehjci/jeab188.
Повний текст джерелаАнотація:
Abstract Aims Atrial septal defects (ASD) are associated with atrial arrhythmias, but the arrhythmia substrate in these patients is poorly defined. We hypothesized that bi-atrial fibrosis is present and that right atrial fibrosis is associated with atrial arrhythmias in ASD patients. We aimed to evaluate the extent of bi-atrial fibrosis in ASD patients and to investigate the relationships between bi-atrial fibrosis, atrial arrhythmias, shunt fraction, and age. Methods and results Patients with uncorrected secundum ASDs (n = 36; 50.4 ± 13.6 years) underwent cardiac magnetic resonance imaging with atrial late gadolinium enhancement. Comparison was made to non-congenital heart disease patients (n = 36; 60.3 ± 10.5 years) with paroxysmal atrial fibrillation (AF). Cardiac magnetic resonance parameters associated with atrial arrhythmias were identified and the relationship between bi-atrial structure, age, and shunt fraction studied. Bi-atrial fibrosis burden was greater in ASD patients than paroxysmal AF patients (20.7 ± 14% vs. 10.1 ± 8.6% and 14.8 ± 8.5% vs. 8.6 ± 6.1% for right and left atria respectively, P = 0.001 for both). In ASD patients, right atrial fibrosis burden was greater in those with than without atrial arrhythmias (33.4 ± 18.7% vs. 16.8 ± 10.3%, P = 0.034). On receiver operating characteristic analysis, a right atrial fibrosis burden of 32% had a 92% specificity and 71% sensitivity for predicting the presence of atrial arrhythmias. Neither age nor shunt fraction was associated with bi-atrial fibrosis burden. Conclusion Bi-atrial fibrosis burden is greater in ASD patients than non-congenital heart disease patients with paroxysmal AF. Right atrial fibrosis is associated with the presence of atrial arrhythmias in ASD patients. These findings highlight the importance of right atrial fibrosis to atrial arrhythmogenesis in ASD patients.
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Adam, Oliver, Daniel Lavall, Hans-Joachim Schäfers, Michael Böhm, and Ulrich Laufs. "Abstract 1346: Rac1 GTPase Activtiy is Associated with Atrial Fibrosis and Fibrillation." Circulation 116, suppl_16 (October 16, 2007). http://dx.doi.org/10.1161/circ.116.suppl_16.ii_276.
Повний текст джерелаАнотація:
Patients with atrial fibrillation (AF) are characterized by increased atrial fibrosis. The underlying signal transduction is incompletely understood. We hypothesized that activation of Rac1 GTPase contributes to increased fibrosis and atrial fibrillation via activation of NADPH oxidase and production of reactive oxygen species. Methods and Results: Samples of the left atrial appendage were analyzed in 8 patients with AF undergoing mitral valve surgery and 7 patients with sinus rhythm (SR) matched for atrial diameter. Despite same size of the atria, collagen content was significantly higher in AF compared to SR (14.9±2.1% vs. 8.5±1.3%). Expression analysis showed that AF was associated with upregulation of connective tissue growth factor (CTGF). Atria of patients with AF were characterized by significant upregulation of Rac1 total protein expression (Western blot), Rac1 activity (PAK pull-down assays) and a 20-fold upregulation of NADPH oxidase activity compared to SR (2225±500%). In order to test whether Rac1 plays a causal role in the pathogenesis in AF, transgenic mice with cardiac overexpres-sion (αMHC promoter) of Rac1 (RacET) were compared to wildtype (WT) and WT undergoing transaortic constriction (TAC, 360 μm). After 16 months, echocardiography showed similar left ventricular hypertrophy in RacET and TAC. RacET but not TAC exhibited atrial enlargement; 75% of RacET but no WT or TAC showed AF. Interstitial collagen content was significantly increased in the atria of RacET (44±1% of area vs 19±5% in WT). In contrast, interstitial fibrosis in TAC atria did not significantly differ from WT (31±6%). In the left ventricle, both RacET and TAC mice showed an elevated collagen content compared to the control group (WT 9±2%, RacET 29±3%; TAC 24±4%). In all mice, atrial collagen content exceeded ventricular collagen. All effects are significant with p<0.05. Conclusion: Left atria of patients with AF exhibit upregulation of Rac1, increased NADPH oxidase activity and interstitial fibrosis. Cardiac-specific overexpression of Rac1 in mice results atrial fibrosis and fibrillation independent of left ventricular hypertrophy. Rac1-GTPase mediated activation of left atrial NADPH-oxidase may represent a novel target for the prevention of atrial fibrosis.
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Wu, P. C., B. C. Lin, Y. H. Yeh, W. J. Chen, and K. C. Yang. "P2556TXNDC5 is a novel therapeutic target of atrial fibrosis and fibrillation." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz748.0884.
Повний текст джерелаАнотація:
Abstract Background Atrial fibrillation (AF), one of the most common cardiac arrhythmias, increases the risk of stroke, systemic embolization and cardiovascular mortality. Atrial fibrosis, a hallmark of chronic AF, provides substrates to initiate/propagate fibrillation waves in the atria. There, however, lacks effective and specific therapeutics targeting atrial fibrosis. We have recently identified an endoplasmic reticulum (ER) protein thioredoxin domain containing 5 (TXNDC5) as a critical mediator of cardiac ventricular fibrosis. We hypothesized that TXNDC5 could also play an important role in the pathogenesis of atrial fibrosis and fibrillation. Purpose To determine the role of TXNDC5 in atrial fibrosis and fibrillation. Methods and results TXNDC5 transcript and protein levels were both significantly upregulated in the atrial tissue from patients with AF. In addition, TXNDC5 mRNA expression levels were positively correlated with those of transcripts encoding transforming growth factor β1 (TGFβ1) and extracellular matrix (ECM) proteins in human atrial tissue. Knockdown of TXNDC5 in human atrial fibroblasts (hAF) attenuated TGFβ1–induced hAF activation, proliferation and ECM protein upregulation, whereas overexpression of TXNDC5 was sufficient to trigger hAF activation, proliferation and ECM protein production. Further experiments revealed that the fibrogenic effects of TXNDC5 were dependent on c-Jun N-terminal kinase (JNK) signaling. Furthermore, using α-MHC-TGFβcys33ser mice, a transgenic mouse model with cardiac-specific overexpression of constitutively active TGFβ, which develop extensive atrial fibrosis and inducible AF, we showed that TXNDC5 was strongly upregulated in the fibrotic atria of α-MHC-TGFβcys33ser mice and specifically enriched in collagen-secreting atrial fibroblasts. Targeted deletion of TXNDC5 (Txndc5−/−) in α-MHC-TGFβcys33ser mice considerably mitigated the extent of atrial fibrosis. In addition, transesophageal atrial burst pacing induced AF in 75% (3 out of 4) α-MHC-TGFβcys33ser mice, whereas knockout of Txndc5 markedly reduced the inducibility of AF (25%, 3 out of 12) in α-MHC-TGFβcys33ser mice (Figure). TXNDC5 KO Reduces AF Inducibility Conclusion The present study revealed that ER protein TXNDC5 augments atrial fibrosis by promoting cardiac fibroblast proliferation and ECM protein production via JNK signaling activation. Targeted deletion of Txndc5 protects against TGFβ induced atrial fibrosis and AF. Targeting TXNDC5, therefore, could be a promising new therapeutic approach to treat or prevent atrial fibrosis and AF.
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Sim, I., L. O’neill, J. Whitaker, R. Mukherjee, D. O’hare, N. Fitzpatrick, S. Niederer, M. O’neill, M. Shattock, and S. Williams. "Dynamic voltage attenuation identifies atrial fibrosis in a rabbit model: simultaneous assessment with optical mapping and contact electrogram mapping." EP Europace 24, Supplement_1 (May 18, 2022). http://dx.doi.org/10.1093/europace/euac053.624.
Повний текст джерелаАнотація:
Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation. Academy of Medical Sciences. Background Bipolar voltage amplitude is a widely-used clinical parameter in atrial electrophysiology procedures. However, voltage amplitude is variable, and it has been shown that increasing activation rate decreases bipolar voltage amplitude in patients with atrial fibrillation. It is not known whether such voltage attenuation is a marker of the presence of atrial fibrosis which could therefore be used to improve intra-procedural assessment of atrial cardiomyopathy. Purpose We sought to investigate the effect of increasing activation rate on bipolar voltage amplitude in both healthy and fibrotic left atrial tissue. Methods 10 New Zealand Rabbits were fed a high cholesterol diet (0.75%) for a period of 12 weeks to create an atrial fibrosis model. 10 Animals were fed normal chow. After terminal anaesthesia the heart was excised, and optical and voltage mapping of the excised left atrial tissue was performed. Blebbistatin was used to maintain cardiac stasis and the voltage sensitive dye RH237 was used for optical mapping. Voltage and optical recordings were made during pacing was from 3 different directions at rates from 2-6Hz and at 3 sites across the atrial tissue. Voltage amplitude was recorded as the mean amplitude over 10 beats during steady-state pacing. Optical recordings were used to measure conduction velocity and action potential characteristics. Only pacing runs showing 1:1 conduction were included in analysis. Atrial fibrosis was assessed using Masson’s Trichrome staining. Results The degree of atrial fibrosis was significantly greater in the atrial fibrosis model compared to healthy controls (15±3.24% vs. 9.74±4.98%, p=0.0069). Median voltage at base rate pacing of 2Hz was not significantly different between control and fibrotic atria (11.63mV, IQR 6.35mV vs. 10.3mV, IQR 6.81mV, p=0.71, respectively). Median voltage was significantly lower at 6Hz than at 2Hz in the control group (9.84mV, IQR 6.87mV, p=0.046). The degree of voltage attenuation between study groups was not significantly different between when pacing at 3hz or 4hz, whereas pacing at 5Hz and 6Hz showed significantly greater attenuation in fibrotic atria. At 5Hz the median reduction in amplitude from baseline in control vs fibrotic atria was 0.88mV, IQR 2.36mV vs 1.92mV, IQR 1.63mV (p=0.031). At 6 Hz the median reduction was 0.94mV, IQR 1.69mV vs 2.68mV, IQR 1.11mV, p=0.013 in control and fibrotic groups respectively. Discussion High cholesterol diet increased atrial fibrosis in a rabbit model. Bipolar voltage amplitude attenuation occurred in both control and fibrotic atria however the degree of voltage attenuation was significantly greater in fibrotic atria. These findings support the further evaluation of dynamic voltage attenuation for intraprocedural identification of atrial fibrosis.
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Yoo, Shin, Edward B. Thorp, Aaron Kunamalla, Gary L. Aistrup, Jason Ng, David Gordon, Bradley Knight, Rod Passman, Jeffrey Goldberger, and Rishi Arora. "Abstract 18342: Development of Fibrotic Substrate for Atrial Fibrillation in Advanced Heart Failure is Driven Not by Inflammation but by Smad2/3 Dependent Replacement Fibrosis." Circulation 132, suppl_3 (November 10, 2015). http://dx.doi.org/10.1161/circ.132.suppl_3.18342.
Повний текст джерелаАнотація:
Introduction: Fibrosis is an important contributor to atrial fibrillation (AF) substrate in heart failure, with TGF-β signaling generating atrial fibrosis. Inflammation is also known to contribute to AF. However, it is not known: a) if inflammation underlies the development of atrial fibrosis, b) if TGF-β signaling is involved in the generation of atrial inflammation and c) what is the relative role of canonical SMAD2/3 versus non-canonical TGF-β-activated kinase 1 (TAK) signaling in the creation of atrial inflammation/fibrosis. Methods: 21 dogs underwent transfection in the posterior left atria of either a plasmid expressing a dominant negative TGF-β type II receptor (pUBC-TGFβ-DN-RII) (N=9) or control vector (pUBC-LacZ) (N=12), followed by 3-4 weeks of right ventricular tachypacing (VTP) (240 bpm). After 3-4 weeks of VTP, the following were assessed: AF by open-chest mapping. Atrial tissue was assessed for signaling (pSMAD2/3 and pTAK) by western blot, fibrosis by trichrome staining and iflammation by CD68 staining. Results: The interstitial fibrosis in LacZ atria was replacement in character (Fig 1A). TGFβ-RII-DN dogs had a significant decrease in replacement fibrosis leading to a decrease in duration of inducible AF (LacZ 63.64 ± 12.12 s vs. TGFβ 26.52 ± 3.79 s, p < 0.05). While both groups demonstrated evidence of inflammation (CD68 staining), there was no difference in inflammation between the groups (Fig 1B). TGFβ-RII-DN dogs had a significant decrease in pSMAD2/3 but not pTAK, compared to pUBC-LacZ dogs. Conclusion: The development of fibrotic substrate for AF in advanced HF is driven not by inflammation but primarily by SMAD2/3 mediated myocardial replacement fibrosis. These findings may have important implications for mechanism-guided therapies for AF, with canonical TGF-β signaling appearing to be an attractive therapeutic target in AF.
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Yamaguchi, Takanori, Toyokazu Otsubo, Yuya Takahashi, Kana Nakashima, Akira Fukui, Kei Hirota, Yumi Ishii, et al. "Atrial Structural Remodeling in Patients With Atrial Fibrillation Is a Diffuse Fibrotic Process: Evidence From High‐Density Voltage Mapping and Atrial Biopsy." Journal of the American Heart Association 11, no. 6 (March 15, 2022). http://dx.doi.org/10.1161/jaha.121.024521.
Повний текст джерелаАнотація:
Background Low‐voltage areas (LVAs) in the atria of patients with atrial fibrillation are considered local fibrosis. We hypothesized that voltage reduction in the atria is a diffuse process associated with fibrosis and that the presence of LVAs reflects a global voltage reduction. Methods and Results We examined 140 patients with atrial fibrillation and 13 patients with a left accessory pathway (controls). High‐density bipolar voltage mapping was performed using a grid‐mapping catheter during high right atrial pacing. Global left atrial (LA) voltage (V GLA ) in the whole LA and regional LA voltage (V RLA ) in 6 anatomic regions were evaluated with the mean of the highest voltage at a sampling density of 1 cm 2 . Patients with atrial fibrillation were categorized into quartiles by V GLA . LVAs were evaluated at voltage cutoffs of 0.1, 0.5, 1.0, and 1.5 mV. Twenty‐eight patients with atrial fibrillation also underwent right atrial septum biopsy, and the fibrosis extent was quantified. Voltage at the biopsy site (V biopsy ) was recorded. V GLA results by category were Q1 (<4.2 mV), Q2 (4.2–5.6 mV), Q3 (5.7–7.0 mV), and Q4 (≥7.1 mV). V RLA at any region was reduced as V GLA decreased. V GLA and V RLA did not differ between Q4 and controls. The presence of LVAs increased as V GLA decreased at any voltage cutoff. Biopsies revealed 11±6% fibrosis, which was inversely correlated with both V biopsy and V GLA ( r =–0.71 and –0.72, respectively). V biopsy was correlated with V GLA ( r =0.82). Conclusions Voltage reduction in the LA is a diffuse process associated with fibrosis. Presence of LVAs reflects diffuse voltage reduction of the LA.
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Chen, Minglong, Weizhu Ju, Daowu Wang, Mingfang Li, Rundi Qi, Lijun Tang, Bing Yang, et al. "Abstract 15018: Idiopathic, Isolated, Fibrotic Atrial Cardiomyopathy: An Overlooked Type of Cardiomyopathy." Circulation 132, suppl_3 (November 10, 2015). http://dx.doi.org/10.1161/circ.132.suppl_3.15018.
Повний текст джерелаАнотація:
Introduction Myocardium fibrosis is a hallmark of cardiomyopathy and a proposed substrate for cardiac arrhythmias. Nevertheless, fibrosis of atrial myocardium and fibrotic atrial cardiomyopathy has not been systemically addressed. Hypothesis We hypothesized that idiopathic, isolated, fibrotic atrial cardiomyopathy (IIF-ACM) is a specific cardiomyopathy, which is characterized by atrial fibrosis and related arrhythmias. Methods In the past 8 years, 34 patients (male 13, mean age 46.5±13.3 yrs) were diagnosed with IIF-ACM based on: 1) clinical evaluation; 2) cardiac image examination; and 3) electro-anatomic mapping detected atrial scarring. Serum biomarkers of collagen metabolism and cardiomyopathy-related genetic screening were performed. Tissue pathology and virus detections were done for two patients. Results During clinical evaluation, electric silent areas were detected in all patients by intra-cardiac electro-anatomical mapping. Among 34 patients, 26 presented with atrial tachycardia (AT), 5 with sick sinus syndrome (SSS) and 3 with atrial standstill. 5 AT patients further developed SSS during the correction of AT by radiofrequency ablation. Late gadolinium-enhancement cardiovascular magnet resonance showed mild to severely dilated atria, without bilateral ventricular scarring or functional impairment. Serum biomarkers of collagen screening demonstrated significant increased collagen synthesis than collagen degradation in IIF-ACM patients. Cardiomyopathy-related genetic screening depicted no clinically relevant mutation. Histological studies showed global fibrosis of atria (Fig. 1). Conclusions We systemically reported 34 patients with IIF-ACM, which is characterized by atrial scarring and relevant arrhythmias. Ventricular functions of note were preserved in all patients. However, the underlying etiology of IIF-ACM remains to be investigated.