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Background: Atrial fibrillation (AF) is accompanied by progressive epicardial fibrosis, dissociation of electrical activity between the epicardial layer and the endocardial bundle network, and transmural conduction (breakthroughs). However, causal relationships between these phenomena have not been demonstrated yet. Our goal was to test the hypothesis that epicardial fibrosis suffices to increase endo-epicardial dissociation (EED) and breakthroughs (BT) during AF.
Methods: We simulated the effect of fibrosis in the epicardial layer on EED and BT in a detailed, high-resolution, three-dimensional model of the human atria with realistic electrophysiology. The model results were compared with simultaneous endo-epicardial mapping in human atria. The model geometry, specifically built for this study, was based on MR images and histo-anatomical studies. Clinical data were obtained in four patients with longstanding persistent AF (persAF) and three patients without a history of AF.
Results: The AF cycle length (AFCL), conduction velocity (CV), and EED were comparable in the mapping studies and the simulations. EED increased from 24.1 ± 3.4 to 56.58 ± 6.2% ( < 0.05), and number of BTs per cycle from 0.89 ± 0.55 to 6.74 ± 2.11% ( < 0.05), in different degrees of fibrosis in the epicardial layer. In both mapping data and simulations, EED correlated with prevalence of BTs. Fibrosis also increased the number of fibrillation waves per cycle in the model.
Conclusion: A realistic 3D computer model of AF in which epicardial fibrosis was increased, in the absence of other pathological changes, showed increases in EED and epicardial BT comparable to those in longstanding persAF. Thus, epicardial fibrosis can explain both phenomena.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047215 | PMC |
http://dx.doi.org/10.3389/fphys.2020.00068 | DOI Listing |
Mol Med
December 2024
Guang'anmen Hospital, Chinese Academy of Chinese Medical Sciences, No.5 Beixian'ge Street, Xicheng District, Beijing, 100053, China.
Aims: Atrial fibrillation (AF) has high mortality and morbidity rates. However, the intracellular molecular complexity of the atrial tissue of patients with AF has not been adequately assessed.
Methods And Results: We investigated the cellular heterogeneity of human atrial tissue and changes in differentially expressed genes between cells using single-cell RNA sequencing, fluorescence in situ hybridization, intercellular communication, and cell trajectory analysis.
Cureus
November 2024
Department of Cardiovascular Medicine, Dokkyo Medical University, Mibu, JPN.
Background: ω-3 polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (EPA, C20:5ω3) and docosahexaenoic acid (DHA, C22:6ω3), are widely regarded as cardioprotective. EPA, but not DHA, has been reported to prevent fibrosis in heart failure. The relationship between the ω-3 PUFA fraction in epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT) and vascular inflammation in patients with cardiovascular disease remains unclear.
View Article and Find Full Text PDFCirc Res
December 2024
Division of Molecular Cardiovascular Biology, Department of Pediatrics, University of Cincinnati and Cincinnati Children's Hospital Medical Center, OH. (A.K.Z.J., R.K.K., R.J.V., S.-C.J.L., S.L.K.B., Y.K., K.M.G., K.W., M.A.S., T.A.B., J.D.M.).
Background: TCF21 (transcription factor 21) is a bHLH (basic helix-loop-helix) protein required for the developmental specification of cardiac fibroblasts (CFs) from epicardial progenitor cells that surround the embryonic heart. In the adult heart, TCF21 is expressed in tissue-resident fibroblasts and is downregulated in response to injury or stimuli leading to myofibroblast differentiation. These findings led to the hypothesis that TCF21 regulates fibroblast differentiation in the adult mammalian heart to affect fibrosis.
View Article and Find Full Text PDFAm Heart J Plus
December 2024
University of Pittsburgh Medical Center, Pittsburgh, PA, United States of America.
Research (Wash D C)
November 2024
Bioinspired Engineering and Biomechanics Center (BEBC), Xi'an Jiaotong University, Xi'an 710049, P.R. China.
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