A Case-Control Study assessing Serum Galectin 3 level in Atrial Fibrillation Patients
DOI:
https://doi.org/10.59675/U115Abstract
As a worldwide issue of concern, atrial fibrillation (AF) casts a huge burden on the health care system. Not only being an arrhythmia of high frequency and prevalence, but also due to the chronicity of some its types. It is imperative to increase the understanding of the pathophysiological basis behind atrial fibrillation or at least the processes that sub serves as a prerequisite for its development. Cardiac remodeling and fibrotic changes may derange the conductive properties of the myocardium and hence import an arrhythmogenic conditioning state. Galectin-3 (Gal-3) has a wide spectrum of biological activities. It can be utilized as a tool for screening many cardiac conditions especially those associated with fibrotic states.
Aim of study: this study was designated to explore the association between atrial fibrillation and serum galectin-3 levels. It was of a case-control type that comprised a cohort of 58 patients with atrial fibrillation, together with 30 controls without it. Patients were categorized into two categories depending upon whether they have a persistent or permanent atrial fibrillation. Serum galectin-3 was measured using ELISA technique, and the results were compared among the three groups.
Results: The Gal-3 was found to be higher in patients with permanent AF (p < .0001) where it recorded 19.27 ± 4.58 ng/ml. The rise in the marker concentration was statistically significant when compared to the 13.54 ± 4.9 ng/ml and 12.14 ± 4.69 ng/ml for the persistent AF and control groups, respectively. Likewise, patients with permanent AF had significantly higher values of left atrial diameter (LAD) (p < .0001) with a mean of 4.68 ± 0.37 cm, 4.09 ± 0.3, and 3.54 ± 0.32, for the permanent AF, persistent AF, and the control groups, respectively. Additionally, the LAD revealed a slight positive correlation with the Gal-3 level, r (56) = 0.386, p < 0.003, with an r2 of 0.149. On the other hand, there was a significant reduction in the left ventricular ejection fraction (LVEF %) in patients with permanent AF, p < 0.0001. The LVEF% was 53.27 ± 7.35 %, versus 62.13 ± 6.75 %, and 63.39 ± 5.77% for permanent AF, persistent AF, and control groups, respectively.
In conclusion, serum Gal-3 is elevated in conditions of both, long-standing AF as well as newly diagnosed AF. The marker correlated positively with the LAD and negatively with LVEF%. Furthermore, LVEF% revealed a moderate negative correlation with serum Gal-3 concentrations. The study concluded that as the left atrium increases in size, this will impose a deleterious effect on the left ventricle and will be reflected as an increasing level of the marker. Hence, Gal-3 can be used as a tool for evaluating fibrotic changes in patients with AF especially the chronic types.
Downloads
References
Kornej J, Börschel CS, Benjamin EJ, Schnabel RB. Epidemiology of Atrial Fibrillation in the 21st Century. 2020; 127(1):4-20. DOI: https://doi.org/10.1161/CIRCRESAHA.120.316340
Mahtani AU, Nair DGJMC. Supraventricular tachycardia. 2019; 103(5):863-79. DOI: https://doi.org/10.1016/j.mcna.2019.05.007
Lippi G, Sanchis-Gomar F, Cervellin G. Global epidemiology of atrial fibrillation: An increasing epidemic and public health challenge. International journal of stroke : official journal of the International Stroke Society. 2021; 16(2):217-21. DOI: https://doi.org/10.1177/1747493019897870
Kapłon-Cieślicka A, Budnik M, Gawałko M, Peller M, Gorczyca I, Michalska A, et al. Atrial fibrillation type and renal dysfunction as important predictors of left atrial thrombus. 2019; 105(17):1310-5. DOI: https://doi.org/10.1136/heartjnl-2018-314492
Xintarakou A, Tzeis S, Psarras S, Asvestas D, Vardas PJEE. Atrial fibrosis as a dominant factor for the development of atrial fibrillation: facts and gaps. 2020;22(3):342-51. DOI: https://doi.org/10.1093/europace/euaa009
Li CY, Zhang JR, Hu WN, Li SNJIJoMM. Atrial fibrosis underlying atrial fibrillation. 2021; 47(3):1-. DOI: https://doi.org/10.3892/ijmm.2020.4842
Piñeiro-Llanes J, Suzuki-Hatano S, Jain A, Medina VAP, Cade WT, Pacak CA, et al. Matrix produced by diseased cardiac fibroblasts affects early myotube formation and function. 2022; 152:100-12. DOI: https://doi.org/10.1016/j.actbio.2022.08.060
Rubanenko O, Shchukin Y, Rubanenko AJEHJ. Genetic polymorphisms of matrix metalloproteinase-9, tissue inhibitor of matrix metalloproteinase-1 and development of postoperative atrial fibrillation in elderly patients. 2021; 42(Supplement_1):ehab724. 0284. DOI: https://doi.org/10.1093/eurheartj/ehab724.0284
Reese-Petersen AL, Olesen MS, Karsdal MA, Svendsen JH, Genovese FJMb. Atrial fibrillation and cardiac fibrosis: A review on the potential of extracellular matrix proteins as biomarkers. 2020; 91:188-203. DOI: https://doi.org/10.1016/j.matbio.2020.03.005
Klesen A, Jakob D, Emig R, Kohl P, Ravens U, Peyronnet RJHE. Cardiac fibroblasts. 2018; 29(1):62-9. DOI: https://doi.org/10.1007/s00399-018-0553-3
Wijesurendra RS, Casadei BJH. Mechanisms of atrial fibrillation. 2019; 105(24):1860-7. DOI: https://doi.org/10.1136/heartjnl-2018-314267
Ma Z-G, Yuan Y-P, Wu H-M, Zhang X, Tang Q-ZJIjobs. Cardiac fibrosis: new insights into the pathogenesis. 2018; 14(12):1645. DOI: https://doi.org/10.7150/ijbs.28103
Ng HH, Leo CH, Parry LJ, Ritchie RHJFiP. Relaxin as a therapeutic target for the cardiovascular complications of diabetes. 2018; 9:501. DOI: https://doi.org/10.3389/fphar.2018.00501
Sullivan RD, Houng AK, Gladysheva IP, Fan T-HM, Tripathi R, Reed GL, et al. Corin overexpression reduces myocardial infarct size and modulates cardiomyocyte apoptotic cell death. 2020; 21(10):3456. DOI: https://doi.org/10.3390/ijms21103456
Wong CKS, Falkenham A, Myers T, Légaré J-FJJotR-A-AS. Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor-β signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis. 2018; 19(1):1470320318759358. DOI: https://doi.org/10.1177/1470320318759358
Shen J, Xing W, Liu R, Zhang Y, Xie C, Gong FJBmb. MiR-32-5p influences high glucose-induced cardiac fibroblast proliferation and phenotypic alteration by inhibiting DUSP1. 2019; 20(1):1-13. DOI: https://doi.org/10.1186/s12867-019-0135-x
Blanda V, Bracale UM, Di Taranto MD, Fortunato GJIJoMS. Galectin-3 in cardiovascular diseases. 2020; 21(23):9232. DOI: https://doi.org/10.3390/ijms21239232
Gehlken C, Suthahar N, Meijers WC, de Boer RAJHfc. Galectin-3 in heart failure: an update of the last 3 years. 2018; 14(1):75-92. DOI: https://doi.org/10.1016/j.hfc.2017.08.009
van der Velde AR, Meijers WC, Ho JE, Brouwers FP, Rienstra M, Bakker SJ, et al. Serial galectin-3 and future cardiovascular disease in the general population. 2016; 102(14):1134-41. DOI: https://doi.org/10.1136/heartjnl-2015-308975
Dong R, Zhang M, Hu Q, Zheng S, Soh A, Zheng Y, et al. Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review). International journal of molecular medicine. 2018; 41(2):599-614. DOI: https://doi.org/10.3892/ijmm.2017.3311
Bouzas-Mosquera A, Broullón FJ, Álvarez-García N, Méndez E, Peteiro J, Gándara-Sambade T, et al. Left atrial size and risk for all-cause mortality and ischemic stroke. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2011; 183(10):E657-64. DOI: https://doi.org/10.1503/cmaj.091688
Kim I-S, Choi Y-J, Choi E-Y, Min P-K, Yoon YW, Lee BK, et al. Comparison of risk profiles for new-onset atrial fibrillation between patients aged< 60 and≥ 60 years. 2021; 16(11):e0258770. DOI: https://doi.org/10.1371/journal.pone.0258770
Bosch NA, Cimini J, Walkey AJJC. Atrial fibrillation in the ICU. 2018; 154(6):1424-34. DOI: https://doi.org/10.1016/j.chest.2018.03.040
Prabhu S, Voskoboinik A, Kaye DM, Kistler PMJH, Lung, Circulation. Atrial fibrillation and heart failure—cause or effect? 2017; 26(9):967-74. DOI: https://doi.org/10.1016/j.hlc.2017.05.117
Abi-Samra F, Gutterman DJHfr. Cardiac contractility modulation: a novel approach for the treatment of heart failure. 2016; 21(6):645-60. DOI: https://doi.org/10.1007/s10741-016-9571-6
Singam NSV, Fine C, Fleg JLJCC. Cardiac changes associated with vascular aging. 2020; 43(2):92-8. DOI: https://doi.org/10.1002/clc.23313
Hernández-Romero D, Vílchez JA, Lahoz Á, Romero-Aniorte AI, Jover E, García-Alberola A, et al. Galectin-3 as a marker of interstitial atrial remodelling involved in atrial fibrillation. Sci Rep. 2017; 7:40378. DOI: https://doi.org/10.1038/srep40378
Wu Q-Q, Xiao Y, Yuan Y, Ma Z-G, Liao H-H, Liu C, et al. Mechanisms contributing to cardiac remodelling. 2017; 131(18):2319-45. DOI: https://doi.org/10.1042/CS20171167
Pitoulis FG, Nunez-Toldra R, Xiao K, Kit-Anan W, Mitzka S, Jabbour RJ, et al. Remodelling of adult cardiac tissue subjected to physiological and pathological mechanical load in vitro. 2022;118(3):814-27. DOI: https://doi.org/10.1093/cvr/cvab084
Lam CS, Rienstra M, Tay WT, Liu LC, Hummel YM, van der Meer P, et al. Atrial fibrillation in heart failure with preserved ejection fraction: association with exercise capacity, left ventricular filling pressures, natriuretic peptides, and left atrial volume. 2017; 5(2):92-8. DOI: https://doi.org/10.1016/j.jchf.2016.10.005
Seko Y, Kato T, Haruna T, Izumi T, Miyamoto S, Nakane E, et al. Association between atrial fibrillation, atrial enlargement, and left ventricular geometric remodeling. 2018; 8(1):1-8. DOI: https://doi.org/10.1038/s41598-018-24875-1
Harada M, Melka J, Sobue Y, Nattel S. Metabolic Considerations in Atrial Fibrillation - Mechanistic Insights and Therapeutic Opportunities. Circulation journal: official journal of the Japanese Circulation Society. 2017; 81(12):1749-57. DOI: https://doi.org/10.1253/circj.CJ-17-1058
Pirahanchi Y, Jessu R, Aeddula NR. Physiology, Sodium Potassium Pump: StatPearls Publishing, Treasure Island (FL); 2022 2022.
Downloads
Published
Issue
Section
License
Copyright (c) 2023 Academic International Journal of Medical Update
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
