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Journal articles on the topic 'Atrial differentiation'

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Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Mesquita, Fernanda C. P., Jacquelynn Morrissey, Po-Feng Lee, Gustavo Monnerat, Yutao Xi, Helen Andersson, Fabio C. S. Nogueira, et al. "Cues from human atrial extracellular matrix enrich the atrial differentiation of human induced pluripotent stem cell-derived cardiomyocytes." Biomaterials Science 9, no. 10 (2021): 3737–49. http://dx.doi.org/10.1039/d0bm01686a.

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Decellularized extracellular matrix (dECM) from human atria preserves key native components that directed the cardiac differentiation of hiPSCs to an atrial-like phenotype, yielding a twofold increase of functional atrial-like cells.

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2

Rautaharju, Pentti M. "Differentiation of atrial flutter from atrial fibrillation." Journal of Electrocardiology 33, no. 2 (April 2000): 203. http://dx.doi.org/10.1016/s0022-0736(00)80078-3.

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3

Davies, M. J., J. Rode, N. Woolf, and D. M. Krikler. "NEUROENDOCRINE DIFFERENTIATION IN ATRIAL MYXOMAS." Lancet 330, no. 8562 (October 1987): 800. http://dx.doi.org/10.1016/s0140-6736(87)92533-5.

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4

Knight, Bradley P., Gregory F. Michaud, S. Adam Strickberger, and Fred Morady. "Electrocardiographic differentiation of atrial flutter from atrial fibrillation by physicians." Journal of Electrocardiology 32, no. 4 (October 1999): 315–19. http://dx.doi.org/10.1016/s0022-0736(99)90002-x.

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5

Muir, T. M., J. Hair, G. C. Inglis, J. W. Dow, G. B. Lindop, and B. J. Leckie. "Dexamethasone-induced differentiation of atrial myocytes in culture." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H722—H729. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h722.

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Atrial and ventricular myocytes from fetal and newborn rats were cultured in medium supplemented with fetal or newborn calf serum with and without glucocorticoid. Myocyte morphology was examined by light and electron microscopy, and the amount of stored and secreted atrial natriuretic peptide (ANP) was measured. Without dexamethasone, neonatal atrial myocytes cultured for 7 days contained myofibrils organized into sarcomeres and numerous endocrine granules containing immunostainable ANP. Secretion of immunoreactive ANP reached a peak between days 7 and 9 of culture. Myocytes from fetal rats secreted ANP but contained few endocrine granules, and myofilaments were poorly organized. By contrast, the addition of dexamethasone (1 nM-1 microM) to the culture medium of newborn myocytes promoted development of numerous endocrine storage granules, mitochondria, and myofibrils with prominent Z-bands. Dexamethasone also increased the cellular content of ANP and ANP-specific mRNA in both atrial and ventricular myocytes. In the presence of dexamethasone myocytes maintained their structural integrity for periods of at least 45 days.

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6

Schwach, Verena, Carla Cofiño-Fabres, Simone A. ten Den, and Robert Passier. "Improved Atrial Differentiation of Human Pluripotent Stem Cells by Activation of Retinoic Acid Receptor Alpha (RARα)." Journal of Personalized Medicine 12, no. 4 (April 13, 2022): 628. http://dx.doi.org/10.3390/jpm12040628.

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Human pluripotent stem cell (hPSC)-derived cardiomyocytes have proven valuable for modeling disease and as a drug screening platform. Here, we depict an optimized protocol for the directed differentiation of hPSCs toward cardiomyocytes with an atrial identity by modulating the retinoic acid signaling cascade in spin embryoid bodies. The crucial steps of the protocol, including hPSC maintenance, embryoid body (EB) differentiation, the induction of cardiac mesoderm, direction toward the atrial phenotype, as well as molecular and functional characterization of the cardiomyocytes, are described. Atrial cardiomyocytes (AMs) can be generated within 14 days. Most importantly, we show that induction of the specific retinoic acid receptor alpha (RARα) increased the efficiency of atrial differentiation to 72% compared with 45% after modulating the retinoic acid (RA) pathway with all-trans RA (atRA). In contrast, the induction of RARβ signaling only had a minor impact on the efficiency of atrial differentiation (from about 45% to 50%). Similarly, the total yield of AM per EB of 5000 hPSCs was increased from 10,350 (2.07 per hPSC) to 16,120 (3.22 per hPSC) while selectively modulating RARα signaling. For further purification of the AMs, we describe a metabolic selection procedure that enhanced the AM percentage to more than 90% without compromising the AM yield (15,542 per EB, equal to 3.11 per hPSC) or functionality of the AMs as evaluated by RNAseq, immunostaining, and optical action potential measurement. Cardiomyocytes with distinct atrial and ventricular properties can be applied for selective pharmacology, such as the development of novel atrial-specific anti-arrhythmic agents, and disease modeling, including atrial fibrillation, which is the most common heart rhythm disorder. Moreover, fully characterized and defined cardiac subtype populations are of the utmost importance for potential cell-based therapeutic approaches.

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7

Kallstrom, Eric, Elizabeth Kallus, Krista Erbe, Michael Rampoldi, Don Le, and Neeley Bryan. "Differentiation of Left Atrial Myxomas by Multimodality Imaging." Journal of Diagnostic Medical Sonography 36, no. 1 (August 27, 2019): 52–63. http://dx.doi.org/10.1177/8756479319872153.

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A tumor is an excessive growth of cells that results from the body’s inability to balance the growth of new cells and the destruction of old cells. Tumors can occur throughout the body and are classified as either benign or malignant. However, cardiac tumors are a rare occurrence. When present, several imaging modalities are available to illustrate their presence and characteristics. Not all cardiac masses look similar and, depending on their size and location, may pose different health risks to the patient. This case series introduces six left atrial myxomas with dissimilar appearances initially detected by transthoracic echocardiography, along with cross-correlation by transesophageal echocardiography, computed tomography, and mechanical resonance imaging.

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8

Wolke, Carmen, Elmer Antileo, and Uwe Lendeckel. "WNT signaling in atrial fibrillation." Experimental Biology and Medicine 246, no. 9 (February 27, 2021): 1112–20. http://dx.doi.org/10.1177/1535370221994086.

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The Wnt signaling pathway regulates physiological processes such as cell proliferation and differentiation, cell fate decisions, and stem cell maintenance and, thus, plays essential roles in embryonic development, but also in adult tissue homeostasis and repair. The Wnt signaling pathway has been associated with heart development and repair and has been shown to be crucially involved in proliferation and differentiation of progenitor cells into cardiomyocytes. The investigation of the role of the Wnt signaling pathway and the regulation of its expression/activity in atrial fibrillation has only just begun. The present minireview (I) provides original data regarding the expression of Wnt signaling components in atrial tissue of patients with atrial fibrillation or sinus rhythm and (II) summarizes the current state of knowledge of the regulation of Wnt signaling components’ expression/activity and the contribution of the various levels of the Wnt signal transduction pathway to the processes of the development, maintenance, and progression of atrial fibrillation.

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9

Yao, Yao, Amanda N. Marra, and Deborah Yelon. "Pathways Regulating Establishment and Maintenance of Cardiac Chamber Identity in Zebrafish." Journal of Cardiovascular Development and Disease 8, no. 2 (January 29, 2021): 13. http://dx.doi.org/10.3390/jcdd8020013.

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The vertebrate heart is comprised of two types of chambers—ventricles and atria—that have unique morphological and physiological properties. Effective cardiac function depends upon the distinct characteristics of ventricular and atrial cardiomyocytes, raising interest in the genetic pathways that regulate chamber-specific traits. Chamber identity seems to be specified in the early embryo by signals that establish ventricular and atrial progenitor populations and trigger distinct differentiation pathways. Intriguingly, chamber-specific features appear to require active reinforcement, even after myocardial differentiation is underway, suggesting plasticity of chamber identity within the developing heart. Here, we review the utility of the zebrafish as a model organism for studying the mechanisms that establish and maintain cardiac chamber identity. By combining genetic and embryological approaches, work in zebrafish has revealed multiple players with potent influences on chamber fate specification and commitment. Going forward, analysis of cardiomyocyte identity at the single-cell level is likely to yield a high-resolution understanding of the pathways that link the relevant players together, and these insights will have the potential to inform future strategies in cardiac tissue engineering.

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10

Hotchkiss, Adam, Tiam Feridooni, Mark Baguma-Nibasheka, Kathleen McNeil, Sarita Chinni, and Kishore B. S. Pasumarthi. "Atrial natriuretic peptide inhibits cell cycle activity of embryonic cardiac progenitor cells via its NPRA receptor signaling axis." American Journal of Physiology-Cell Physiology 308, no. 7 (April 1, 2015): C557—C569. http://dx.doi.org/10.1152/ajpcell.00323.2014.

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The biological effects of atrial natriuretic peptide (ANP) are mediated by natriuretic peptide receptors (NPRs), which can either activate guanylyl cyclase (NPRA and NPRB) or inhibit adenylyl cyclase (NPRC) to modulate intracellular cGMP or cAMP, respectively. During cardiac development, ANP serves as an early maker of differentiating atrial and ventricular chamber myocardium. As development proceeds, expression of ANP persists in the atria but declines in the ventricles. Currently, it is not known whether ANP is secreted or the ANP-NPR signaling system plays any active role in the developing ventricles. Thus the primary aims of this study were to 1) examine biological activity of ANP signaling systems in embryonic ventricular myocardium, and 2) determine whether ANP signaling modulates proliferation/differentiation of undifferentiated cardiac progenitor cells (CPCs) and/or cardiomyocytes. Here, we provide evidence that ANP synthesized in embryonic day (E)11.5 ventricular myocytes is actively secreted and processed to its biologically active form. Notably, NPRA and NPRC were detected in E11.5 ventricles and exogenous ANP stimulated production of cGMP in ventricular cell cultures. Furthermore, we showed that exogenous ANP significantly decreased cell number and DNA synthesis of CPCs but not cardiomyocytes and this effect could be reversed by pretreatment with the NPRA receptor-specific inhibitor A71915. ANP treatment also led to a robust increase in nuclear p27 levels in CPCs compared with cardiomyocytes. Collectively, these data provide evidence that in the developing mammalian ventricles ANP plays a local paracrine role in regulating the balance between CPC proliferation and differentiation via NPRA/cGMP-mediated signaling pathways.

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11

Suffee, Nadine, Thomas Moore-Morris, Patrick Farahmand, Catherine Rücker-Martin, Gilles Dilanian, Magali Fradet, Daigo Sawaki, et al. "Atrial natriuretic peptide regulates adipose tissue accumulation in adult atria." Proceedings of the National Academy of Sciences 114, no. 5 (January 17, 2017): E771—E780. http://dx.doi.org/10.1073/pnas.1610968114.

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The abundance of epicardial adipose tissue (EAT) is associated with atrial fibrillation (AF), the most frequent cardiac arrhythmia. However, both the origin and the factors involved in EAT expansion are unknown. Here, we found that adult human atrial epicardial cells were highly adipogenic through an epithelial–mesenchymal transition both in vitro and in vivo. In a genetic lineage tracing the WT1CreERT2+/−RosatdT+/−mouse model subjected to a high-fat diet, adipocytes of atrial EAT derived from a subset of epicardial progenitors. Atrial myocardium secretome induces the adipogenic differentiation of adult mesenchymal epicardium-derived cells by modulating the balance between mesenchymal Wingless-type Mouse Mammary Tumor Virus integration site family, member 10B (Wnt10b)/β-catenin and adipogenic ERK/MAPK signaling pathways. The adipogenic property of the atrial secretome was enhanced in AF patients. The atrial natriuretic peptide secreted by atrial myocytes is a major adipogenic factor operating at a low concentration by binding to its natriuretic peptide receptor A (NPRA) receptor and, in turn, by activating a cGMP-dependent pathway. Hence, our data indicate cross-talk between EAT expansion and mechanical function of the atrial myocardium.

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12

Chen, Tangting, Miaoling Li, Xuehui Fan, Jun Cheng, and Liqun Wang. "Sodium Tanshinone IIA Sulfonate Prevents Angiotensin II-Induced Differentiation of Human Atrial Fibroblasts into Myofibroblasts." Oxidative Medicine and Cellular Longevity 2018 (July 24, 2018): 1–10. http://dx.doi.org/10.1155/2018/6712585.

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Differentiation of atrial fibroblasts into myofibroblasts plays a critical role in atrial fibrosis. Sodium tanshinone IIA sulfonate (DS-201), a water-soluble derivative of tanshinone IIA, has been shown to have potent antifibrotic properties. However, the protective effects of DS-201 on angiotensin II- (Ang II-) induced differentiation of atrial fibroblasts into myofibroblasts remain to be elucidated. In this study, human atrial fibroblasts were stimulated with Ang II in the presence or absence of DS-201. Then, α-smooth muscle actin (α-SMA), collagen I, and collagen III expression and reactive oxygen species (ROS) generation were measured. The expression of transforming growth factor-β1 (TGF-β1) and the downstream signaling of TGF-β1, such as phosphorylation of Smad2/3, were also determined. The results demonstrated that DS-201 significantly prevented Ang II-induced human atrial fibroblast migration and decreased Ang II-induced α-SMA, collagen I, and collagen III expression. Furthermore, increased production of ROS and expression of TGF-β1 stimulated by Ang II were also significantly inhibited by DS-201. Consistent with these results, DS-201 significantly inhibited Ang II-evoked Smad2/3 phosphorylation and periostin expression. These results and the experiments involving N-acetyl cysteine (antioxidant) and an anti-TGF-β1 antibody suggest that DS-201 prevent Ang II-induced differentiation of atrial fibroblasts to myofibroblasts, at least in part, through suppressing oxidative stress and inhibiting the activation of TGF-β1 signaling pathway. All of these data indicate the potential utility of DS-201 for the treatment of cardiac fibrosis.

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13

Sutton, Kathy, Said El Haou, Sarah Williams, Harsha Devalla, Sonja Stoelzle-Feix, Krisztina Juhasz, Leo Doerr, et al. "Differentiation and validation of human iPSC-derived atrial cardiomyocytes." Journal of Pharmacological and Toxicological Methods 93 (September 2018): 168. http://dx.doi.org/10.1016/j.vascn.2018.01.544.

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14

Kornej, Jelena, Samira Zeynalova, Petra Büttner, Ralph Burkhardt, Yoon Ju Bae, Anja Willenberg, Ronny Baber, et al. "Differentiation of atrial fibrillation progression phenotypes using Troponin T." International Journal of Cardiology 297 (December 2019): 61–65. http://dx.doi.org/10.1016/j.ijcard.2019.09.006.

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15

Hu, Xiao Feng, Rui Zhan, Shanhu Xu, Junjun Wang, Jiong Wu, Xiaoli Liu, Yaguo Li, and Linhui Chen. "Growth differentiation factor 15 is associated with left atrial/left atrial appendage thrombus in patients with nonvalvular atrial fibrillation." Clinical Cardiology 41, no. 1 (January 2018): 34–38. http://dx.doi.org/10.1002/clc.22844.

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16

Rajala, Kristiina, Mari Pekkanen-Mattila, and Katriina Aalto-Setälä. "Cardiac Differentiation of Pluripotent Stem Cells." Stem Cells International 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/383709.

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The ability of human pluripotent stem cells to differentiate towards the cardiac lineage has attracted significant interest, initially with a strong focus on regenerative medicine. The ultimate goal to repair the heart by cardiomyocyte replacement has, however, proven challenging. Human cardiac differentiation has been difficult to control, but methods are improving, and the process, to a certain extent, can be manipulated and directed. The stem cell-derived cardiomyocytes described to date exhibit rather immature functional and structural characteristics compared to adult cardiomyocytes. Thus, a future challenge will be to develop strategies to reach a higher degree of cardiomyocyte maturationin vitro, to isolate cardiomyocytes from the heterogeneous pool of differentiating cells, as well as to guide the differentiation into the desired subtype, that is, ventricular, atrial, and pacemaker cells. In this paper, we will discuss the strategies for the generation of cardiomyocytes from pluripotent stem cells and their characteristics, as well as highlight some applications for the cells.

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17

Chang, Wei-Ting, Jhih-Yuan Shih, Yu-Wen Lin, Zhih-Cherng Chen, Jun-Neng Roan, and Chih-Hsin Hsu. "Growth differentiation factor-15 levels in the blood around the pulmonary artery is associated with hospitalization for heart failure in patients with pulmonary arterial hypertension." Pulmonary Circulation 10, no. 4 (October 2020): 204589402096294. http://dx.doi.org/10.1177/2045894020962948.

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Despite no significant differences of growth differentiation factor-15 expressions in peripheral, right atrial, and right ventricular blood, in the pulmonary arterial blood, there was a significantly high level of growth differentiation factor-15 in Group I pulmonary arterial hypertension patients subsequently developing heart failure. During right heart catheterization, collecting pulmonary blood samples is suggested to measure growth differentiation factor-15.

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18

Song, Xianghe, Danni Liu, Jian Cui, Manqian Zhou, Hui Wang, Na Liu, Xin Qi, and Zongjin Li. "Identification of Stem-Like Cells in Atrial Myxoma by Markers CD44, CD19, and CD45." Stem Cells International 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/2059584.

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Atrial myxoma is the most frequent tumor arising mainly in atrial septum and its origin remains uncertain. It has been reported that a subpopulation of stem-like cells are present in benign tumors and responsible for tumor initiation and maintenance. In this study, we investigated whether stem-like cells could contribute to the atrial cardiac myxoma. Immunohistology data confirmed that a population of cells bearing the surface markers CD19, CD45, and CD44 resided in a mucopolysaccharide-rich matrix of myxoma. Moreover, we isolated myxoma cells with phase-bright culture method and confirmed that myxoma derived cells express robust level of CD19, CD45, and CD44. Furthermore, the pluripotency of this population of cells also was validated by cardiomyocytes and smooth muscle cells differentiation in vitro. Our results indicate that primary cardiac myxoma may arise from mesenchymal stem cells with the ability to generate tumors with multilineage differentiation. In conclusion, this study for the first time verified that stem-like cells are present in atrial myxoma and this population of cells may have the capacity for myxoma initiation and progression.

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19

Balabanovich, T. I., V. I. Shyshko, and V. R. Shulika. "CIRCULATING SERUM LEVELS OF GROWTH DIFFERENTIATION FACTOR-15 IN NON-VALVULAR ATRIAL FIBRILLATION PATIENTS WITH CONCOMITANT OBSTRUCTIVE SLEEP APNEA/HYPOPNEA SYNDROME." Biological Markers in Fundamental and Clinical Medicine (collection of abstracts) 2, no. 2 (November 15, 2018): 35–36. http://dx.doi.org/10.29256/v.02.02.2018.escbm27.

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20

Sarraf, Lara S., James A. Roth, and Kristina M. Ropella. "Differentiation of atrial rhythms from the electrocardiogram with coherence spectra." Journal of Electrocardiology 35, no. 1 (January 2002): 59–67. http://dx.doi.org/10.1054/jelc.2002.29944.

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21

SATIN, J., D. BADER, and R. DEHAAN. "Local cues influence atrial and ventricular differentiation of precardiac mesoderm." Journal of Molecular and Cellular Cardiology 19 (1987): S16. http://dx.doi.org/10.1016/s0022-2828(87)80673-9.

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22

Malakhov, A. I., S. I. Schookin, V. I. Ivancov, and A. N. Tikhomirov. "A Combined Algorithm for Identification and Differentiation of Atrial Flutter and Atrial Fibrillation Based on ECG Analysis." Biomedical Engineering 47, no. 1 (May 2013): 14–17. http://dx.doi.org/10.1007/s10527-013-9324-y.

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23

Kohtz, D. S., N. R. Dische, T. Inagami, and B. Goldman. "Growth and partial differentiation of presumptive human cardiac myoblasts in culture." Journal of Cell Biology 108, no. 3 (March 1, 1989): 1067–78. http://dx.doi.org/10.1083/jcb.108.3.1067.

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A cell culture model for human cardiac myogenesis is introduced. Human fetal myocardial cells were dissociated enzymatically, and cultured in a mitogen-rich medium that promoted the growth of presumptive cardiac myoblasts. Strains of human cardiac myoblasts were generated from different anatomical regions of the fetal heart. The cells could be cultured for at least 30 generations, or frozen and recovered for later use. Differentiation was induced by culturing the cardiac myoblasts in a mitogen-poor medium. Differentiation of cardiac myoblasts was marked primarily by transcriptional activation of the atrial natriuretic factor (ANF) gene. Evidence is presented that posttranscriptional processing of ANF transcripts is affected by the anatomical origin of the cardiac myoblasts and the presence of cocultured neuronal cells. Cardiac myoblasts induced to differentiate in culture synthesized only low levels of sarcomeric myosin and cardiac alpha-actin, suggesting that differentiation of these cells progresses through two phases: an initial, noncontractile phase that is represented by the differentiating cultured cells; and a later contractile phase, in which myofibrillar assembly is accentuated and modulated by secondary signals from the cardiac milieu.

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24

Eckstein, Jan, Vanessa Sciacca, Hermann Körperich, Lech Paluszkiewicz, Elena Weise Valdés, Wolfgang Burchert, Muhammed Gerçek, et al. "Cardiovascular Magnetic Resonance Imaging-Based Right Atrial Strain Analysis of Cardiac Amyloidosis." Biomedicines 10, no. 12 (November 22, 2022): 3004. http://dx.doi.org/10.3390/biomedicines10123004.

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Background: Cardiac amyloidosis (CA) manifests in a hypertrophic phenotype with a poor prognosis, making differentiation from hypertrophic cardiomyopathy (HCM) challenging and delaying early treatment. The extent to which magnetic resonance imaging (MRI) quantifies the right atrial strain (RAS) and strain rate (RASR), providing valuable diagnostic information, is not yet clinically established. Aims: This study assesses diagnostic differences in the longitudinal RAS and RASR between CA and HCM patients, control subjects (CTRL) and CA subtypes in addition to the impact of atrial fibrillation (AF) on the right atrial function in CA patients. The RAS and RASR of tricuspid regurgitation (TR) patients are used to assess the potential for diagnostic overlap. Methods: RAS and RASR quantification was conducted via MRI feature-tracking for biopsy-confirmed CA patients with subtypes identified. Strain parameters were compared for CTRL, HCM and TR patients. Post hoc testing identified intergroup differences. Results: In total, 41 CA patients were compared to 47 CTRL, 20 HCM and 31 TR patients. Reservoir (R), conduit and booster RAS and RASRs allow for significant differentiation (p < 0.001) between CA and HCM patients (R: 10.6 ± 14.3% vs. R: 33.5 ± 16.3%) and CTRL (R: 44.6 ± 15.7%). Booster and reservoir RAS and RASRs qualified as reliable diagnostic tests (AUC > 0.8). CA patients with AF, in contrast to sinus rhythm, demonstrated a significantly impaired reservoir RAS and RASR and booster RASR. The discriminative power of RAS for CA vs. TR was insufficient (R: 10.6% ± 14.3% vs. 7.0% ± 6.0%, p = 0.069). Differentiation between 21 transthyretin and 20 light-chain amyloidosis subtypes was not achievable (R: 0.7% ± 1.0% vs. 0.7% ± 1.0%, p = 0.827). Conclusion: The MRI-derived RAS and RASR are impaired in CA patients and may support noninvasive differentiation between CA, HCM and CTRL.

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25

Bhatia, Snigdha, Amna Qasim, Amyn K. Jiwani, and Ashraf M. Aly. "Benign Structures Mimicking Right Atrial Masses on Prenatal Ultrasound." Case Reports in Pediatrics 2021 (January 12, 2021): 1–4. http://dx.doi.org/10.1155/2021/8889941.

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Advances in imaging have resulted in more frequent reporting of primitive right atrial structures which can sometimes mimic cardiac tumors in prenatal ultrasound. Prominent crista terminalis and Chiari network are examples of these structures. We describe two cases of pregnant women referred to the fetal cardiology clinic for fetal echocardiography for right atrial masses seen on prenatal ultrasound suspicious of tuberous sclerosis. The first case subsequently diagnosed as crista terminalis and the second case as a prominent Chiari network. Postnatal ECHO confirmed the benign nature of these structures. It is important to differentiate tumors from prominent benign structures in the right atrium in fetal ECHO. The location and the similar echogenicity to the adjacent atrial tissue are clues for differentiation of these structures from atrial tumors.

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Willems, Leen, Annick Daniëls, Yanick Fanton, Loes Linsen, Lize Evens, Virginie Bito, Jeroen Declercq, Jean-Luc Rummens, Karen Hensen, and Marc Hendrikx. "Differentiation of Human Cardiac Atrial Appendage Stem Cells into Adult Cardiomyocytes: A Role for the Wnt Pathway?" International Journal of Molecular Sciences 21, no. 11 (May 30, 2020): 3931. http://dx.doi.org/10.3390/ijms21113931.

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Human cardiac stem cells isolated from atrial appendages based on aldehyde dehydrogenase activity (CASCs) can be expanded in vitro and differentiate into mature cardiomyocytes. In this study, we assess whether Wnt activation stimulates human CASC proliferation, whereas Wnt inhibition induces cardiac maturation. CASCs were cultured as described before. Conventional PCR confirmed the presence of the Frizzled receptors. Small-molecule inhibitors (IWP2, C59, XAV939, and IWR1-endo) and activator (CHIR99021) of the Wnt/β -catenin signaling pathway were applied, and the effect on β-catenin and target genes for proliferation and differentiation was assessed by Western blot and RT-qPCR. CASCs express multiple early cardiac differentiation markers and are committed toward myocardial differentiation. They express several Frizzled receptors, suggesting a role for Wnt signaling in clonogenicity, proliferation, and differentiation. Wnt activation increases total and active β-catenin levels. However, this does not affect CASC proliferation or clonogenicity. Wnt inhibition upregulated early cardiac markers but could not induce mature myocardial differentiation. When CASCs are committed toward myocardial differentiation, the Wnt pathway is active and can be modulated. However, despite its role in cardiogenesis and myocardial differentiation of pluripotent stem-cell populations, our data indicate that Wnt signaling has limited effects on CASC clonogenicity, proliferation, and differentiation.

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SEÇİNTİ, İlke Evrim, Didar GÜRSOY, Metin Onur BEYAZ, and İyad FANSA. "Undifferentiated pleomorphic sarcoma with focal myogenic differentiation mimicking left atrial myxoma." Journal of Surgery and Medicine 6, no. 4 (April 1, 2022): 1. http://dx.doi.org/10.28982/josam.992197.

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28

Kleinsorge, Mandy, and Lukas Cyganek. "Subtype-Directed Differentiation of Human iPSCs into Atrial and Ventricular Cardiomyocytes." STAR Protocols 1, no. 1 (June 2020): 100026. http://dx.doi.org/10.1016/j.xpro.2020.100026.

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29

Lin, Huili, Jingsheng Zheng, Kenneth Khaw, Edward Wrobleski, John Saia, Gerald Ukrainski, Patrick O'Beirne, Lannae Ewing, Chad Bousanti, and Lawrence Wehner. "Right Atrial Cardiac Varix Mimicking Myxoma: Differentiation Using Three-Dimensional Echocardiography." Annals of Thoracic Surgery 97, no. 6 (June 2014): e181. http://dx.doi.org/10.1016/j.athoracsur.2014.02.086.

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30

Park, Jeong-Wook, Yeong-Woong Ha, Sung-Hwan Kim, and Yong-Seog Oh. "Diagnostic utility of atrial entrainment for differentiation of long RP tachycardia." Heart Rhythm 17, no. 9 (September 2020): 1629–31. http://dx.doi.org/10.1016/j.hrthm.2020.04.025.

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31

Vugt, Stijn Van, Goaris Aarts, Jeroen Jaspers Focks, Lucie Bloem, Freek Verheugt, and Marc Brouwer. "NOVEL APPROACH FOR RISK DIFFERENTIATION IN ATRIAL FIBRILLATION PATIENTS WITH POLYPHARMACY." Journal of the American College of Cardiology 69, no. 11 (March 2017): 486. http://dx.doi.org/10.1016/s0735-1097(17)33875-5.

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32

Gizatulina, T. P., N. Yu Khorkova, L. U. Martyanova, T. I. Petelina, E. V. Zueva, N. E. Shirokov, D. V. Krinochkin, and E. A. Gorbatenko. "The level of growth differentiation factor 15 as a predictor of left atrial thrombosis in patients with nonvalvular atrial fibrillation." Kardiologiia 61, no. 7 (July 31, 2021): 44–54. http://dx.doi.org/10.18087/cardio.2021.7.n1588.

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Aim To study the role of blood concentration of growth differentiation factor 15 (GDF-15) as a predictor of left atrial/left atrial appendage (LA/LAA) thrombosis in patients with nonvalvular atrial fibrillation (AF).Material and methods 538 patients with nonvalvular AF were admitted to the Tyumen Cardiology Research Center in 2019–2020 for radiofrequency ablation and elective cardioversion. According to findings of transesophageal echocardiography (EcoCG), 42 (7.8%) of these patients had LA/LAA thrombosis and 79 (14.7%) of them had the effect of spontaneous echo contrast (SEC). This comparative, cross-sectional, cohort study included at the initial stage 158 successively hospitalized patients with nonvalvular AF: group 1 (with LA/LAA thrombosis, n=42) and group 2 (without LA/LAA thrombosis and without SEC, n=116). To eliminate significant differences in age between the groups, an additional inclusion criterium was introduced, age from 45 to 75 years. Finally, 144 patients were included into the study: group 1 (with LA/LAA thrombosis, n=42, mean age 60.9±7.2 years) and group 2 (without LA/LAA thrombosis and without SEC, n=116, mean age 59.5±6.0 years). 93 (91%) patients in group 1 and 40 (95%) patients in group 2 had arterial hypertension (p=0.4168); 53 (52%) and 29 (^(%), respectively, had ischemic heart disease (p=0.0611). The groups did not differ in sex, profile of major cardiovascular diseases, or frequency and range of oral anticoagulant treatment. General clinical evaluation, EchoCG, and laboratory tests, including measurements of blood concentrations of GDF-15 and NT-proBNP, were performed.Results In the group with LA/LAA thrombosis, 1) persistent AF prevailed whereas paroxysmal AF was more frequently observed in patients without thrombosis; 2) a tendency toward more pronounced chronic heart failure was observed; 3) tendencies toward a high median CHA2DS2‑VASc score and toward a greater proportion of patients with scores ≥3 were observed. According to EchoCG findings, group 1 had higher values of sizes and volumes of both atria and the right ventricle, left ventricular (LV) end-systolic volume and size, pulmonary artery systolic blood pressure, and LV myocardial mass index. LV ejection fraction (EF) was in the normal range in both groups but it was significantly lower for patients with LA/LAA thrombosis, 59.1±5.1 and 64.0±7.3, respectively (p=0.00006). Concentrations of GDF-15 (p=0.00025) and NT-proBNP were significantly higher in group 1 than in group 2 (p=0.000001). After determining the threshold values for both biomarkers using the ROC analysis, two independent predictors of LA/LAA thrombosis were obtained by the stepwise multiple regression analysis: GDF-15 >935.0 pg/ml (OR=4.132, 95 % CI 1.305–13.084) and LV EF (OR=0.859, 95 % CI 0.776–0.951). The ROC analysis assessed the model quality as good: AUC=0.776 (p<0.001), sensitivity 78.3 %, specificity 78.3 %.Conclusion For patients with nonvalvular AF, both increased GDF-15 (>935.0 pg/ml) and LV EF are independent predictors for LA/LAA thrombosis.

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Zhang, Y., S. A. Shafiq, and D. Bader. "Detection of a ventricular-specific myosin heavy chain in adult and developing chicken heart." Journal of Cell Biology 102, no. 4 (April 1, 1986): 1480–84. http://dx.doi.org/10.1083/jcb.102.4.1480.

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In the present study, a monoclonal antibody (McAb), ALD19, generated against myosin of slow tonic muscle, was shown to react with the heavy chain of ventricular myosin in the adult chicken heart. With this antibody, it was possible to detect a ventricular-specific myosin during myocardial differentiation and to show that the epitope recognized by ALD19 was present from the earliest stages of ventricular differentiation and maintained throughout development only in the ventricle. A second McAb, specific for atrial myosin heavy chain (MHC) (Gonzalez-Sanchez, A., and D. Bader, 1984, Dev. Biol., 103:151-158), was used as a control to detect an atrial-specific myosin in the caudal portion of the developing heart at Hamburger-Hamilton stage 15. It was found that the appearance of ventricular MHC predated the expression of atrial MHC by approximately 1 d in ovo and that specific MHCs were always differentially distributed. While a common primordial MHC may be present in the early heart, this study showed the tissue-specific expression of a ventricular MHC during the initial stages of heart development and its differential accumulation throughout development.

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Рождественский, Mikhail Rozhdestvenskiy, Юргель, and E. Yurgel. "Proinflammatory potential for quantitative differentiation of various forms of atrial fibrillation in hypertensive patients in the medico-social examination of disability." Journal of New Medical Technologies. eJournal 9, no. 2 (July 6, 2015): 0. http://dx.doi.org/10.12737/11522.

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In this article the authors examine changes in the levels of tumor necrosis factor alpha and nitric oxide in the blood in patients with atrial fibrillation and hypertension. The study included 66 patients aged 60 to 75 years compared with the control group of 25 people. The results suggest that endothelial dysfunction is developed in patients. It is manifested by changes in the levels of tumor necrosis factor alpha and nitric oxide in the blood. The studied parameters can be the markers of severity and indicate a differentiated approach to various forms of atrial fibrillation. On the severity, an atrial fibrillation is clinically subdivided into paroxysmal, persis-tent and permanent (up to 30, 60 and 80 points, respectively).

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AL-HAMDI, AMAR Talib. "Artifacts in electrocardiogram interpreted as cardiac arrhythmias: Reports of clinical cases." Journal of the Faculty of Medicine Baghdad 62, no. 4 (February 21, 2021): 104–9. http://dx.doi.org/10.32007/jfacmedbagdad.6241767.

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Background: Artifact waves in the ECG and Holter recording are not rare in clinical practice and can be mistaken for tachyarrhythmia. Objective: To orient the practicing physicians to differentiate these artifacts from cardiac arrhythmias. Patients and Methods: Thirteen patients with incorrectly diagnosed cardiac arrhythmias by ECG or Holter recording then distinguished to be ECG artifacts were included in this study. The patients were collected from the author’s private practice in the northern Iraqi governorate of Sulaimanya during the period from June 2015 to August 2020. The differentiation of the artifact waves from the arrhythmias were made by careful inspection of the ECG, identification of the R waves within the artifact waves and correlating the artifact waves with the patient’s symptoms. Results: The artifacts were mistaken for ventricular fibrillation in two patients, ventricular tachycardia in four, atrial fibrillation in two, atrial flutter in four, and in one patient bradycardia of high grade atrio-ventricular block. Conclusion: Distinguishing artifact in ECG and differentiating them from cardiac arrhythmia is important to avoid mismanagement.

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TADA, HIROSHI, HAKAN ORAL, RADMIRA GREENSTEIN, FRANK PELOSI, BRADLEY P. KNIGHT, S. ADAM STRICKBERGER, and FRED MORADY. "Differentiation of Atrial and Pulmonary Vein Potentials Recorded Circumferentially Within Pulmonary Veins." Journal of Cardiovascular Electrophysiology 13, no. 2 (February 2002): 118–23. http://dx.doi.org/10.1046/j.1540-8167.2002.00118.x.

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Yagishita, Atsuhiko, Hitoshi Hachiya, Koji Higuchi, Tomofumi Nakamura, Koji Sugiyama, Yasuaki Tanaka, Tetsuo Sasano, Mihoko Kawabata, Mitsuaki Isobe, and Kenzo Hirao. "Differentiation of atrial tachycardia from other long RP tachycardias by electrocardiographic characteristics." Journal of Arrhythmia 30, no. 5 (October 2014): 376–81. http://dx.doi.org/10.1016/j.joa.2014.04.002.

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Ito, Shinji, Akihiro Ueda, Kenichiro Murate, Seiko Hirota, Takao Fukui, Tomomasa Ishikawa, Sayuri Shima, et al. "Differentiation of cancer from atrial fibrillation in patients with acute multifocal stroke." Journal of the Neurological Sciences 368 (September 2016): 344–48. http://dx.doi.org/10.1016/j.jns.2016.07.054.

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Schoels, Wolfgang, Laurence D. Sterns, Kirsten D. Freigang, Alex Bauer, Johannes Brachmann, and Wolfgang Kübler. "992–114 Atrial Recordings for the Differentiation of Ventricular and Supraventricular Tachyarrhythmias." Journal of the American College of Cardiology 25, no. 2 (February 1995): 317A. http://dx.doi.org/10.1016/0735-1097(95)92775-z.

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Sciacca, Vanessa, Jan Eckstein, Hermann Körperich, Thomas Fink, Leonard Bergau, Mustapha El Hamriti, Guram Imnadze, et al. "Magnetic-Resonance-Imaging-Based Left Atrial Strain and Left Atrial Strain Rate as Diagnostic Parameters in Cardiac Amyloidosis." Journal of Clinical Medicine 11, no. 11 (June 1, 2022): 3150. http://dx.doi.org/10.3390/jcm11113150.

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Aims: The present study aims to evaluate magnetic-resonance-imaging (MRI)-assessed left atrial strain (LAS) and left atrial strain rate (LASR) as potential parameters for the diagnosis of cardiac amyloidosis (CA), the distinction of clinical subtypes and differentiation from other cardiomyopathies. Methods and results: LAS and LASR were assessed by MRI feature tracking in patients with biopsy-proven CA. LAS and LASR of patients with CA were compared to healthy subjects and patients with hypertrophic cardiomyopathy. LAS and LASR were also analyzed concerning differences between patients with transthyretin (ATTR) and light chain amyloidosis (AL). A total of 44 patients with biopsy-proven CA, 19 patients with hypertrophic cardiomyopathy and 24 healthy subjects were included. In 22 CA patients (50%), histological examination identified ATTR as CA subtype and AL in the remaining patients. No significant difference was observed for reservoir, conduit or booster LAS in patients with AL or ATTR. Reservoir LAS, conduit LAS and booster LAS were significantly reduced in patients with CA and HCM as compared to healthy subjects (p < 0.001). Reservoir LAS and booster LAS were significantly reduced in CA as compared to HCM patients (p < 0.001). A linear correlation was observed between LA global reservoir strain and LA-EF (p < 0.001, r = 0.5), conduit strain and global longitudinal LV strain (p < 0.001, r = 0.5), global booster strain rate and LA-EF (p < 0.001, r = 0.6) and between global booster strain rate and LA area at LVED (p < 0.0001, 0.5). Conclusions: LAS and LASR are severely impaired in patients with CA. The MRI-based assessment of LAS and LASR might allow non-invasive diagnosis and categorization of CA and its distinct differentiation from other hypertrophic phenotypes.

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Liu, Yang, Haichen Lv, Ruopeng Tan, Xiangbo An, Xiao-Hui Niu, Yue-Jian Liu, Xiaolei Yang, Xiaomeng Yin, and 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, no. 6 (December 2020): 1856–67. http://dx.doi.org/10.1161/hypertensionaha.120.15016.

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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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Chlumský, J., and J. Charvát. "Contribution of Distensibility and Intima-Media Thickness to the Etiology of Stroke." Rivista di Neuroradiologia 18, no. 1 (February 2005): 78–81. http://dx.doi.org/10.1177/197140090501800113.

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We evaluated carotid artery distensibility (D) and intima-media thickness (IMT) in patients with stroke (S), and its relationship to diabetes and atrial fibrilation. We measured D and IMT in 89 stroke patients. 59 patients had type II diabetes and 64 patients had atrial fibrillation. D was determined using the Reneman formula (mm/100mm Hg). D was consistently lower in diabetic patients then in non-diabetic patients (0.14 v. 0.17, p=0.039) and showed a relation to IMT. In atrial fibrillation patients IMT was consistently lower (67 v.79 mm, p=0.033) and D was increased (0.19 v. 0.10, p=0.023). Type II diabetes is characterized by wall stiffening and thickening of the carotid artery. D and IMT can contribute to the differentiation of embolic and thrombotic etiology of stroke.

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Amin, Mohamed, Yoshihiro Kushida, Shohei Wakao, Masaaki Kitada, Kazuki Tatsumi, and Mari Dezawa. "Cardiotrophic Growth Factor–Driven Induction of Human Muse Cells Into Cardiomyocyte-Like Phenotype." Cell Transplantation 27, no. 2 (February 2018): 285–98. http://dx.doi.org/10.1177/0963689717721514.

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Multilineage-differentiating stress-enduring (Muse) cells are endogenous nontumorigenic stem cells collectable as stage-specific embryonic antigen 3 (SSEA-3) + from various organs including the bone marrow and are pluripotent-like. The potential of human bone marrow-derived Muse cells to commit to cardiac lineage cells was evaluated. We found that (1) initial treatment of Muse cells with 5′-azacytidine in suspension culture successfully accelerated demethylation of cardiac marker Nkx2.5 promoter; (2) then transferring the cells onto adherent culture and treatment with early cardiac differentiation factors including wingless-int (Wnt)-3a, bone morphogenetic proteins (BMP)-2/4, and transforming growth factor (TGF) β1; and (3) further treatment with late cardiac differentiation cytokines including cardiotrophin-1 converted Muse cells into cardiomyocyte-like cells that expressed α-actinin and troponin-I with a striation-like pattern. MLC2a expression in the final step suggested differentiation of the cells into an atrial subtype. MLC2v, a marker for a mature ventricular subtype, was expressed when cells were treated with Dickkopf-related protein 1 (DKK-1) and Noggin, inhibitors of Wnt3a and BMP-4, respectively, between steps (2) and (3). None of the steps included exogenous gene transfection, making induced cells feasible for future clinical application.

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Vogel, Britta, Dierk Thomas, Derliz Mereles, Wolfgang Rottbauer, and Hugo A. Katus. "Systemic Embolization and Myocardial Infarction due to Clinically Unrecognized Left Atrial Myxoma." Case Reports in Medicine 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/159024.

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Myxomas are the most common primary tumors of the heart. We report an extraordinary severe case of left atrial myxoma, presenting with stroke, myocardial infarction, and multiple arterial embolism including aorta, splenic and renal arteries, and several peripheral arteries. The patient had previously been diagnosed with systemic vasculitis, a typical but less common finding caused by multiple emboli mimicking vasculitis. The myxoma was removed and atrial septum reconstruction was performed. In summary, early diagnostic differentiation of myxoma from vasculitis is critical, and immediate surgical removal of myxoma is required as the probability of thromboembolic complications increases over time.

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Goya, Masahiko, Yoshito Iesaka, Atsushi Takahashi, Teiichi Yamane, Masakazu Gotoh, Yohkoh Soejima, Yoshihiro Okamoto, et al. "Atrial flutter with negative F wave in inferior limb leads: Differentiation among orthodromic and antidromic common and uncommon atrial flutter." Japanese Journal of Electrocardiology 18, no. 1 (1998): 46–53. http://dx.doi.org/10.5105/jse.18.46.

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Muller, I. I., D. B. Melville, V. Tanwar, W. M. Rybski, A. Mukherjee, M. B. Shoemaker, W. D. Wang, et al. "Functional modeling in zebrafish demonstrates that the atrial-fibrillation-associated gene GREM2 regulates cardiac laterality, cardiomyocyte differentiation and atrial rhythm." Disease Models & Mechanisms 6, no. 2 (December 7, 2012): 332–41. http://dx.doi.org/10.1242/dmm.010488.

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Martin, Kendall E., and Joshua S. Waxman. "Atrial and Sinoatrial Node Development in the Zebrafish Heart." Journal of Cardiovascular Development and Disease 8, no. 2 (February 9, 2021): 15. http://dx.doi.org/10.3390/jcdd8020015.

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Proper development and function of the vertebrate heart is vital for embryonic and postnatal life. Many congenital heart defects in humans are associated with disruption of genes that direct the formation or maintenance of atrial and pacemaker cardiomyocytes at the venous pole of the heart. Zebrafish are an outstanding model for studying vertebrate cardiogenesis, due to the conservation of molecular mechanisms underlying early heart development, external development, and ease of genetic manipulation. Here, we discuss early developmental mechanisms that instruct appropriate formation of the venous pole in zebrafish embryos. We primarily focus on signals that determine atrial chamber size and the specialized pacemaker cells of the sinoatrial node through directing proper specification and differentiation, as well as contemporary insights into the plasticity and maintenance of cardiomyocyte identity in embryonic zebrafish hearts. Finally, we integrate how these insights into zebrafish cardiogenesis can serve as models for human atrial defects and arrhythmias.

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Ray, Ruma, SaumyaR Mallick, Prasenjit Das, Bhaskar Shukla, SS Kothari, and V. Devagourou. "Right atrial myxoma with glandular differentiation: A rare entity in pediatric age group." Annals of Pediatric Cardiology 3, no. 2 (2010): 159. http://dx.doi.org/10.4103/0974-2069.74046.

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Müller, A. L., and D. H. Freed. "MICRORNA-301A TARGETS DICER TO ATTENTUATE PRIMARY C-KIT+ HUMAN ATRIAL CELL DIFFERENTIATION." Canadian Journal of Cardiology 31, no. 10 (October 2015): S144—S145. http://dx.doi.org/10.1016/j.cjca.2015.07.313.

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Zhou, Jing, Zhefeng Kang, Lulu Liu, Yingqiang Guo, and Sai Chen. "Predicting Value of Growth Differentiation Factor 15 and Its Correlations With Atrial Fibrillation." Heart Surgery Forum 23, no. 4 (July 2, 2020): E452—E460. http://dx.doi.org/10.1532/hsf.2355.

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Aims: Despite several clinical risk factors for atrial fibrillation (AF), some newly identified biomarkers may also potentially serve as risk factors for AF. However, none of these factors so far have been adopted in clinical practice. Recently, a number of studies with an attempt to identify the role of growth differentiation factor 15 (GDF-15) in AF have obtained ambiguous results. We try to identify the predicting role of GDF-15 in AF and AF-related complications with meta-analysis or systematic analysis. Methods and results: We enrolled 10 studies, looking at the predicting role of GDF-15 in non-valvular AF using meta-analysis, summarized its role in AF-related major complications, and discussed whether it was dependable to forecast postoperative AF. It turned out that GDF-15 is an independent factor to predict occurrence of AF, while it remains obscure to directly demonstrate its relationship with postoperative AF. For AF patients on anti-platelet treatment, GDF-15 plays a critical role in predicting major bleeding, cardiovascular death and overall death, and improves the current predicting model. Conclusions: Circulating GDF-15 greatly associates with AF and AF-related complications. It should be applied clinically.

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