The consequence of biomarkers of myocardial fibrosis in the prediction of arrhythmias in patients with hypertension in combination with coronary heart disease (literature review)
DOI:
https://doi.org/10.26641/2307-0404.2020.4.221225Ключові слова:
markers of fibrosis, galectin-3, aldosterone, transforming growth factor β-1, hypertension, coronary heart disease, ventricular extrasystoleАнотація
The main morphological structural lesion substrate is myocardial fibrosis. The processes of fibrosis in a certain way are associated with the severity of a variety of cardiac arrhythmias. Myocardial fibrosis may be manifested by prolongation of the QRS complex, frequent ventricular arrhythmias and ventricular tachycardia on the electrocardiogram. Echocardiography is the main tool used to assess the structure and function of the heart, it reveals an increase in the left ventricle, and decrease in ejection fraction and diastolic dysfunction of the left ventricle and an increase in filling pressure. Biological markers are quantitatively defined biological parameters that, as indicators, determine the norm, pathology and result of medecinal correction of the disease (definition of experts from the Biomarkers Definitions Working Group, USA). Changes of biomarkers can be controlled to determine the individual risk of cardiovascular diseases development and measures to normalize them. Among the main causes of fibrosis activation, hyperactivation of the renin-angiotensin-aldosterone system and, as a consequence, the excessive formation of angiotensinogen and aldosterone are considered; increased levels of galectin-3, which contributes to the migration of macrophages, proliferation of fibroblasts and collagen synthesis in cardiomyocytes. Recently, much attention is paid to the study of biochemical markers such as aldosterone, galectin-3 and transforming growth factor- beta-1.Thus, these markers were determined in hypertension, metabolic syndrome, congestive heart failure, hypertrophic cardiomyopathy, myocardial infarction, atrial fibrillation. However, to date studies considering association between frequent ventricular premature beats, as a marker of electrical instability and plasma levels of biomarkers of fibrosis, such as aldosterone, galectin-3and transforming growth factor beta-1, in patients with essential hypertension without / or in combination with coronary heart disease are absent. Based on the aforesaid material,, further thorough study of this problem is promising.Посилання
Polunina YeA, Klimchuk DO, Polunina OS, Sevost'yanova IV, Voronina LP. [The relationship between remodeling of the linear dimensions of the aorta, the left atrium and the level of the c-terminal telopeptide of type I collagen in patients with chronic heart failure]. Astrakhanskiy meditsinskiy zhurnal. 2017;12(2):69-75. Russian.
Voronkov LH, Voytsekhovsʹka KV, Parashchenyuk LP. [Clinical and instrumental characteristics of patients with chronic heart failure and reduced left ventricular ejection fraction depending on weight loss over the past 6 months]. Ukrainian Journal of Cardiology. 2019;26(2):48-56. Ukrainian. doi: https://doi.org/10.31928/1608-635X-2019.2.4856
Ionin VA. [Galectin 3 and aldosterone in patients with atrial fibrillation and metabolic syndrome]. Rossiyskiy kardiologicheskiy zhurnal. 2015;4(120):79-83. Russian. doi: https://doi.org/10.15829/1560-4071-2015-04-79-83
Ionin V, Zaslavskaya Ye, Soboleva, A, Baranova Ye, Listopad O, Nifontov IYe, Konradi AO, Shlyakhto Ye. [Galectin-3 in patients with paroxysmal and persistent atrial fibrillation and metabolic syndrome]. Kardiologiya. 2016;56(6):41-45. Russian. doi: https://doi.org/10.18565/cardio.2016.6.17-22
Dagkhar D. [Diagnostic value of galectin-3 level in patients with hypertrophic cardiomyopathy]. ScienceRise. Medical Science. 2017;4:13-18. Russian.
Zhuravlova LV, Kulikova MV. [Biomarkers of heart failure: new diagnostic possibilities]. Liky Ukrainy. 2019;3(229):13-15. Ukrainian.
Ivanov VP, Shcherbak OV, Maslovsky VYu, Shcherbak VP. [Current opportunities and practical reality in the prognosis of myocardial dysfunction in patients with myocardial infarction]. Acta medica Leopoliensia. 2015;4:76-84. Ukrainian.
Karetnikova VN, Kastalap VV, Kosareva SN, Barbarash OL. [Myocardial fibrosis: current aspects of the problem]. Terapevticheskiy arkhiv. 2017;89(1):88-93. Russian. doi: https://doi.org/10.17116/terarkh201789188-93
Kozhukhov SM, Parkhomenko OM. [Heart failure with preserved left ventricular ejection fraction]. Medytsyna neotlozhnykh sostoyanyy. 2016;1:126-30. Ukrainian.
Myasoyedova YeI, Polunina OS, Sevost'yanova IV, Voronina LP, Zaklyakova LV. [Markers of myocardial fibrosis in patients with ischemic cardiomyopathy: relationship with the severity of symptoms of chronic heart failure]. Astrakhanskiy meditsinskiy zhurnal. 2016;11(4):93-99. Russian.
Ruzhanska VO, Syvak VH, Lozynsʹka MS, Zhebel VM. [Galectin-3 as a marker of myocardial function in men 40-60 years without cardiovascular pathology, carriers of polymorphic genes at1r]. Problemy ekolohiyi ta medytsyny. 2018;22(1-2):33-37. Ukrainian.
Tseluyko VI, Daghar S. [Level of galectin-3 in patients with hypertrophic cardiomyopathy]. Sertse i sudini. 2016;4:47-52. Russian.
Neefs J, van den Berg NWE, Limpens J, Berger WR, Boekholdt SM, Sanders P, de Groot JR. Aldosterone pathway blockade to prevent atrial fibrillation: a systematic review and meta-analysis. International journal of cardiology. 2017;231:55-161. doi: https://doi.org/10.1016/j.ijcard.2016.12.029
Aro AL. Will electrocardiographic detection of myocardial fibrosis work?. 2020;0:1-2. doi: https://doi.org/10.1136/heartjnl-2020-316646
Reese-Petersen AL, Olesen MS, Karsdal M, Svendsen JH, Genovese F. Atrial Fibrillation and Cardiac Fibrosis: A Review on the Potential of Extracellular Matrix Proteins as Biomarkers. Matrix Biology. 2020;S0945-053X(20):30026-30033. doi: https://doi.org/10.1016/j.matbio.2020.03.005
Bengel FM, Ross TL.Emerging imaging targets for infiltrative cardiomyopathy: Inflammation and fibrosis. Journal of Nuclear Cardiology. 2019;26(1):208-16. doi: https://doi.org/10.1007/s12350-018-1356-y
Tang Z, Zeng L, Lin Y, Han Z, Gu J, Wang C, Zhang H. Circulating galectin-3 is associated with left atrial appendage remodelling and thrombus formation in patients with atrial fibrillation. Heart, Lung and Circulation. 2019;28(6):923-31. doi: https://doi.org/10.1016/j.hlc.2018.05.094
Shomanova Z, Ohnewein B, Schernthaner C, et al. Classic and Novel Biomarkers as Potential Predictors of Ventricular Arrhythmias and Sudden Cardiac Death. Journal of Clinical Medicine. 2020;9(2):578. doi: https://doi.org/10.3390/jcm9020578
Liu T, Song D, Dong J. et al. Current understanding of the pathophysiology of myocardial fibrosis and its quantitative assessment in heart failure. Front Physiol. 2017;8:238. doi: https://doi.org/10.3389/fphys.2017.00238
Cypen J, Ahmad T, Testani JM, DeVore AD. Novel biomarkers for the risk stratification of heart failure with preserved ejection fraction. Current heart failure reports. 2017;14(5):434-43. doi: https://doi.org/10.1007/s11897-017-0358-4
DeLeon-Pennell KY, Meschiari CA, Jung M, Lindsey ML. Matrix metalloproteinases in myocardial infarction and heart failure. Prog Mol Biol Transl Sci. 2017;147:75-100. doi: https://doi.org/10.1016/bs.pmbts.2017.02.001
Dzialo E, Tkacz K, Blyszczuk P. Crosstalk between TGF-β and WNT signalling pathways during cardiac fibrogenesis. ActaBiochim Pol. 2018;65(3):341-9. doi: https://doi.org/10.18388/abp.2018_2635
Ferreira JP, Duarte K, Montalescot G, et al. Effect of eplerenone on extracellular cardiac matrix biomarkers in patients with acute ST-elevation myocardial infarction without heart failure: insights from the randomized double-blind REMINDER Study. G. Clin Res Cardiol. 2018;107(1):49-59. doi: https://doi.org/10.1007/s00392-017-1157-3
Maron MS, Chan RH, Kapur NK, et al. Effect of spironolactone on myocardial fibrosis and other clinical variables in patients with hypertrophic cardiomyopathy. Am J Med. 2018;131(7):837-41. doi: https://doi.org/10.1016/j.amjmed.2018.02.025
Holmström L, Haukilahti A, Vähätalo J, Kenttä T, Appel H, Kiviniemi A, et al. Electrocardiographic associations with myocardial fibrosis among sudden cardiac death victims. Heart. 2020;0:1-6. doi: https://doi.org/10.1136/heartjnl-2019-316105
Nakao E, Adachi H, Enomoto M, et al. Elevated plasma transforming growth factor β1 levels predict the development of hypertension in normotensives: The 14-year follow-up study. Am J Hypertens. 2017;30(8):808-14. doi: https://doi.org/10.1093/ajh/hpx053
Parviz Y. Iqbal J, Pitt B, et al. Emerging cardiovascular indications of mineralocorticoid receptor antagonists. Trends Endocrinol Metab. 2015;26(4):201-11. doi: https://doi.org/10.1016/j.tem.2015.01.007
Koo HY, El‐Baz LM, House S, et al. Fibroblast growth factor 2 decreases bleomycin‐induced pulmonary fibrosis and inhibits fibroblast collagen production and myofibroblast differentiation. The Journal of pathology. 2018;246(1):54-66. doi: https://doi.org/10.1002/path.5106
Leifheit-Nestler M, Kirchhoff F.Nespor J, et al. Fibroblast growth factor 23 is induced by an activated renin–angiotensin–aldosterone system in cardiac myocytes and promotes the pro-fibrotic crosstalk between cardiac myocytes and fibroblasts. Nephrol Dial Transplant. 2018;33(10):1722-34. doi: https://doi.org/10.1093/ndt/gfy006
Kuga K, Kusakari Y, Uesugi K, Semba K, Urashima T, Akaike T, Minamisawa S. Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1. PloS one. 2020;15(4):e0231905. doi: https://doi.org/10.1371/journal.pone.0231905
Nakano SJ, Siomos AK, Garcia AM, et al. Fibrosis-related gene expression in single ventricle heart disease. J Pediatr. 2017;191:82-90. doi: https://doi.org/10.1016/j.jpeds.2017.08.055
Frangogiannis NG. Transforming growth factor–β in tissue fibrosis. Journal of Experimental Medicine. 2020;217(3):e20190103. doi: https://doi.org/10.1084/jem.20190103
Fu B, Su Y, Ma X, et al. Scoparone attenuates angiotensin II-induced extracellular matrix remodeling in cardiac fibroblasts. J Pharmacol Sci. 2018;137(2):110-5. doi: https://doi.org/10.1016/j.jphs.2018.05.006
Filipe MD, Meijers WC, van der Velde AR, de Boer RA. Galectin-3 and heart failure: prognosis, prediction & clinical utility. Clinica chimica acta. 2015;443:48-56. doi: https://doi.org/10.1016/j.cca.2014.10.009
Gong M, Cheung A, Wang QS, et al. Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis. Journal of Clinical Laboratory Analysis. 2020;34(3):e23104. doi: https://doi.org/10.1002/jcla.23104
Oz F, Onur I, Elitok A, Ademoglu E, Altun I, Bilge AK, Adalet K. Galectin-3 correlates with arrhythmogenic right ventricular cardiomyopathy and predicts the risk of ventricular arrhythmias in patients with implantable defibrillators. Acta cardiologica. 2017;72(4):453-9. doi: https://doi.org/10.1080/00015385.2017.1335371
Park S, Ranjbarvaziri S, Lay FD, et al. Genetic regulation of fibroblast activation and proliferation in cardiac fibrosis. Circulation. 2018;138(12):1224-35. doi: https://doi.org/10.1161/CIRCULATIONAHA.118.035420
Gonzalez A, Schelbert EB, Diez J, Butler J. Myocardial interstitial fibrosis in heart failure: biological and translational perspectives. J Am Coll Cardiol. 2018;71(15):1696-706. doi: https://doi.org/10.1016/j.jacc.2018.02.021
Goumans MJ, ten Dijke P. TGF-β signaling in control of cardiovascular function. Cold Spring Cold Spring Harb Perspect Biol. 2017;10(2):a022210. doi: https://doi.org/10.1101/cshperspect.a022210
Hopps E, Presti RL, Caimi G. Matrix Metalloproteases in Arterial Hypertension and their Trend after Antihypertensive Treatment. Kidney and Blood Pressure Research. 2017;42(2):347-57. doi: https://doi.org/10.1159/000477785
Junttila MJ. Electrocardiographic Markers of Fibrosis in Cardiomyopathy: A Beginning of a Long Journey. Cardiology. 2020;145(5):309-10. doi: https://doi.org/10.1159/000506507
Kang Q, Li X, Yang M, Fernando T, Wan Z. Galectin-3 in patients with coronary heart disease and atrial fibrillation. Clinica Chimica Acta. 2018;478:166-70. doi: https://doi.org/10.1016/j.cca.2017.12.041
Latchamsetty R, Bogun F. Premature Ventricular Complex Ablation in Structural Heart Disease. Cardiac electrophysiology clinics. 2017;9(1):133-40. doi: https://doi.org/10.1016/j.ccep.2016.10.010
Li L, Zhao Q, Kong W. Extracellular matrix remodeling and cardiac fibrosis. Matrix Biol. 2018;68:490-506. doi: 10.1016/j.matbio.2018.01.013
Lubrano V, Balzan S. Role of oxidative stress-related biomarkers in heart failure: galectin 3, α1-antitrypsin and LOX-1: new therapeutic perspective?. Molecular and cellular biochemistry. 2020;464(1-2):143-52. doi: https://doi.org/10.1007/s11010-019-03656-y
Magnussen C, Blankenberg S. Biomarkers for heart failure: small molecules with high clinical relevance. J InternMed. 2018;283(6):530-43. doi:https://doi.org/10.1111/joim.12756
Arnar DO, Mairesse GH, Boriani G, et al. Management of asymptomatic arrhythmias: a European heart rhythm association (EHRA) consensus document, endorsed by the heart failure association (HFA), heart rhythm society (HRS), Asia Pacific heart rhythm society (APHRS), cardiac arrhythmia society of Southern Africa (CASSA), and Latin America heart rhythm society (LAHRS). EP Europace. 2019;0:1-32. doi: https://doi.org/10.1093/europace/euz046
Cheng R, Dang R, Zhou Y, et al. MicroRNA-98 inhibits TGF-b1-induce differentiation and collagen production of cardiacfibroblasts by targeting TGFBR1. Human Cell. 2017;30(3):192-200. doi: https://doi.org/10.1007/s13577-017-0163-0
Yuan X, Pan J, Wen L, et al. MiR‐590‐3p regulates proliferation, migration and collagen synthesis of cardiac fibroblast by targeting ZEB1. Journal of cellular and molecular medicine. 2020;24(1):227-37. doi: https://doi.org/10.1111/jcmm.14704
Nattel S. Molecular and cellular mechanisms of atrial fibrosis in atrial fibrillation. JACC Clin Electrophysiol. 2017;3(5):425-35. doi: https://doi.org/10.1016/j.jacep.2017.03.002
Okyere AD, Tilley DG. Leukocyte-Dependent Regulation of Cardiac Fibrosis. Frontiers in Physiology. 2020;11:301. doi: https://doi.org/10.3389/fphys.2020.00301
Francia P, Adduci C, Semprini L, et al. Osteopontin and galectin‐3 predict the risk of ventricular tachycardia and fibrillation in heart failure patients with implantable defibrillators. Journal of cardiovascular electrophysiology. 2014;25(6):609-16. doi: https://doi.org/10.1111/jce.12364
Ferreira JP, Machu JL, Girerd N, et al. Rationale of the FIBROTARGETS study designed to identify novel biomarkers of myocardial fibrosis. ESC Heart Fail. 2018;5(1):139-48. doi: https://doi.org/10.1002/ehf2.12218
Chow SL, Maisel AS, Anand I, et al. Role of biomarkers for the prevention, assessment, and management of heart failure: a scientific statement from the American Heart Association. Circulation. 2017;135(22):e1054-91. doi: https://doi.org/10.1161/cir.0000000000000490
Dworatzek E, Mahmoodzadeh S, Schriever C, et al. Sex-specific regulation of collagen I and III expression by 17β-Estradiol in cardiac fibroblasts: role of estrogen receptors. Cardiovascular research. 2019;115(2):315-327. doi: https://doi.org/10.1093/cvr/cvy185
Tarbit E, Singh I, Peart JN. Rose’Meyer RB.Biomarkers for the identification of cardiac fibroblast and myofibroblast cells. Heart Fail Rev. 2019;24(1):1-15. doi: https://doi.org/10.1007/s10741-018-9720-1
Miro O, Gonzalez de la Presa B, Herrero-Puente P, et al. The GALA study: relationship between galectin-3 serum levels and short-and long-term outcomes of patients with acute heart failure. Biomarkers. 2017;22(8):731-9. doi: https://doi.org/10.1080/1354750X.2017.1319421
Ma Y, Zou H, Zhu XX, Pang J, Xu Q, Jin QY, Ding YH, Zhou B, Huang DS. Transforming growth factor β: A potential biomarker and therapeutic target of ventricular remodeling. Oncotarget. 2017;8(32):53780. doi: https://doi.org/10.18632/oncotarget.17255
Nielsen SH, Mouton AJ, DeLeon-Pennell KY, et al. Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes. Matrix Biol. 2017;75-76:43-57. doi: https://doi.org/10.1016/j.matbio.2017.12.001
##submission.downloads##
Опубліковано
Як цитувати
Номер
Розділ
Ліцензія
Авторське право (c) 2020 Медичні перспективи
Ця робота ліцензується відповідно до Creative Commons Attribution 4.0 International License.
Submitting manuscript to the journal "Medicni perspektivi" the author(s) agree with transferring copyright from the author(s) to publisher (including photos, figures, tables, etc.) editor, reproducing materials of the manuscript in the journal, Internet, translation into other languages, export and import of the issue with the author’s article, spreading without limitation of their period of validity both on the territory of Ukraine and other countries. This and other mutual duties of the author and all co-authors separately and editorial board are secured by written agreement by special form to use the article, the sample of which is presented on the site.
Author signs a written agreement and sends it to Editorial Board simultaneously with submission of the manuscript.
