Mechanisms of vibration-induced structural myocardial remodeling

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Abstract

The review analyzes literature data on structural changes in the heart of patients with vibration disease, as detected by echocardiographic methods. Particularly, it highlights concentric remodeling of the left ventricle chambers and disturbances in diastolic function. The review also discusses a 1.2-fold decrease in heart structure intensity compared to healthy individuals (p < 0.05). Furthermore, it examines changes in morphometric and bioenergetic parameters of cardiomyocytes under different experimental vibration modes (7 and 56 sessions at a frequency of 8 Hz), confirming the disruptions in the relationship between the spatial configuration of the heart cavities, contractile ability, and energy supply potential. Loss of cardiac myofibrils represents the transition from myocardial hypertrophy to decompensation, accompanied by an increase in degenerative (dystrophic) signs such as the loss of sarcomeres in cardiomyocytes. Understanding these pathological (morphological) processes requires consideration of various mediators that regulate cell metabolism, proliferation, growth, and survival, including stromal interaction molecule, calcium ATPase of the endo(sarco)plasmic reticulum, inositol-1,4,5-triphosphate receptor, protein that forms CRAC channels, and transient receptor potential canonical. The degradation system of the extracellular matrix, including matrix metalloproteinases and tissue inhibitors, plays a crucial role in structural cardiac remodeling. This system regulates the rate of mRNA synthesis on the DNA matrix by binding to specific DNA regions that control cardiac nutrition and plasticity. The review suggests that these findings can help explain some patterns of cardiac remodeling development in patients with vibration disease and determine the direction of pathogenetically based therapy. This therapy should consider not only the vibration-protective effect of drugs but also their ability to inhibit and regress myocardial remodeling.

About the authors

Victoria V. Vorobieva

Kirov Military Medical Academy; Saint Petersburg State University

Email: v.v.vorobeva@mail.ru
ORCID iD: 0000-0001-6257-7129
SPIN-code: 2556-2770

Dr. Med. Sci. (Pharmacology)

Russian Federation, Saint Petersburg; Saint Petersburg

Olga S. Levchenkova

Smolensk State Medical University

Email: levchenkova-o@yandex.ru
ORCID iD: 0000-0002-9595-6982
SPIN-code: 2888-6150

Dr. Med. Sci. (Pharmacology)

Russian Federation, Smolensk

Karina V. Lenskaya

Saint Petersburg State University

Email: karinavl@mail.ru
ORCID iD: 0000-0002-6407-0927

Dr. Biol. Sci., Professor

Russian Federation, Saint Petersburg

Petr D. Shabanov

Kirov Military Medical Academy

Author for correspondence.
Email: pdshabanov@mail.ru
ORCID iD: 0000-0003-1464-1127
SPIN-code: 8974-7477

Dr. Sci. (Medicine), Professor

Russian Federation, Saint Petersburg

References

  1. Dzau V, Braunwald E. Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. Am Heart J. 1991;121(4 Pt 1):1244–1263. doi: 10.1016/0002-8703(91)90694-d
  2. Korotenko OYu, Filimonov ES. Myocardial deformation and parameters of diastolic function of the left ventricle in workers of coal mining enterprises in the South of Kuzbass with arterial hypertension. Russian Journal of Occupational Health and Indusyrial Ecology. 2020;60(3):151–156. doi: 10.31089/1026-9428-2020-60-3-151-156
  3. Tret’yakov SV, Shpagina LA, Vojtovich TV. To the question of heart remodeling in vibration disease. Russian Journal of Occupational Health and Industrial Ecology. 2003;(3):18–23. (In Russ.)
  4. Tret’yakov SV, Shpagina LA. Prospects of studying structural and functional state of cardiovascular system in vibration disease patients with arterial hypertension. Russian Journal of Occupational Health and Industrial Ecology. 2017;(12):30–34.
  5. Saarkopel LM, Kir´ykov VA, Oshkoderov OA. Role of contemporary biomarkers in vibration disease diagnosis. Russian Journal of Occupational Health and Indusyrial Ecology. 2017;(2):6–11.
  6. Gorchakova TYu, Churanova AN. Current state of mortality of the working-age population in Russia and Europe. Russian Journal of Occupational Health and Indusyrial Ecology. 2020;60(11):756–759. doi: 10.31089/1026-9428-2020-60-11-756-759
  7. Vorobieva VV, Shabanov PD. Cellular mechanisms of hypoxia development in the tissues of experimental animals under varying characteristics of vibration exposure. Reviews on Clinical Pharmacology and Drug Therapy. 2019;17(3):59–70. (In Russ.) doi: 10.17816/RCF17359-70
  8. Kiryakov VA, Pavlovskaya NA, Lapko IV, et al. Impact of occupational vibration on molecular and cell level of human body. Russian Journal of Occupational Health and Industrial Ecology. 2018;9:34–43. doi: 10.31089/1026-9428-2018-9-34-43
  9. Bockeria LA, Bockeria OL, Le TG. Electrophysiological remodeling of the myocardium in heart failure and various heart diseases. Annaly aritmologii. 2010;4:41–48. (In Russ.)
  10. Jiang M, Fan X, Wang Y, Sun X. Effects of hypoxia in cardiac metabolic remodeling and heart failure. Exp Cell Res. 2023;432(1):113763. doi: 10.1016/j.yexcr.2023.113763
  11. Heusch G, Libby P, Gersh B, et al. Cardiovascular remodelling in coronary artery disease and heart failure. Lancet. 2014;383(9932):1933–1943. doi: 10.1016/s0140-6736(14)60107-0
  12. Shishkina LN, Klimovich MA, Kozlov MV. A new approach to analysis of participation of oxidative processes in regulation of metabolism in animal tissues. Biophysics. 2014;59(2):904–909. doi: 10.1134/S0006350914020249
  13. Poteriaeva EL, Smirnova EL, Nikiforova NG. Forecasting the formation and course of vibration disease on basis of genetic metabolic markers study. Russian Journal of Occupational Health and Industrial Ecology. 2015;(6):19–22. EDN: UBEMIT
  14. Malyutina NN, Bolotova AF, Eremeev RB et al. Antioxidant status of blood in patients with vibration disease. Russian Journal of Occupational Health and Industrial Ecology. 2019;(12):978–982. EDN: ZPVTXP doi: 10.31089/1026-9428-2019-59-12-978-982
  15. Vorobieva VV, Shabanov PD. Tissue specific peculiarities of vibration-induced hypoxia of the rabbit heart, liver and kidney. Reviews on Clinical Pharmacology and Drug Therapy. 2016;14(1):46–62. EDN: VVEOGN doi: 10.17816/RCF14146-62
  16. Atamantchuk AA, Kuzmina LP, Khotuleva AG, Kolyaskina MM. Polymorphism of genes of renin-angiotensin-aldosterone system in the development of hypertension in workers exposed to physical factors. Russian Journal of Occupational Health and Industrial Ecology. 2019;59(12): 972–977. EDN: RPZIZJ doi: 10.31089/1026-9428-2019-59-12-972-977
  17. Afanasiev SA, Kondratieva DS, Egorova MV, et al. Features the interaction of functional and metabolic remodeling of myocardium in comorbid course of ischemic heart disease and 2 type diabetes mellitus. Diabetes Mellitus. 2019;22(1):25–34. EDN: ZDDIEP doi: 10.14341/DM9735
  18. Shpagina LA, Gerasimenko ON, Novikova II, et al. Clinical, functional and molecular characteristics of vibration disease in combination with arterial hypertension. Russian Journal of Occupational Health and Industrial Ecology. 2022;62(3):146–158. EDN: CNLUQW doi: 10.31089/1026-9428-2022-62-3-146-158
  19. Shpigel AS, Vakurova NV Neurohumoral dysregulation in vibration disease (response features of hormonal complexes to the introduction of tyroliberin). Russian Journal of Occupational Health and Industrial Ecology. 2022;61(1):29–35. EDN: DEGJGA doi: 10/31089/1026-9428-2022-62-129-35
  20. Melentev AV, Serebryakov PV, Zheglova AV. Influence of noise and vibration on nervous regulation of heart. Russian Journal of Occupational Health and Industrial Ecology. 2018;(9):19–23. EDN: YJGUST doi: 10.31089/1026-9428-2018-9-19-23
  21. Yamshchikova AV, Fleishman AN, Gidayatova MO, et. al. Features of vegetative regulation in vibration disease patients, studied on basis of active orthostatic test. Russian Journal of Occupational Health and Industrial Ecology. 2018;(6):11–14. EDN: XQMXAL doi: 10.31089/1026-9428-2018-6-11-15
  22. Vorobieva VV, Levchenkova OS, Shabanov PD. Biochemical mechanisms of the energy-protective action of blockers of slow high-threshold L-type calcium channels. Reviews on Clinical Pharmacology and Drug Therapy. 2022; 20(4):395–405. (In Russ.) EDN: YECCVH doi: 10.17816/RCF204395-405
  23. Grigoriev AI, Tonevitsky AG. Molecular mechanisms of stress adaptation: immediate early genes. Russian journal of physiology. 2009;95(10):1041–1057. EDN: OIZSVD
  24. Vorobieva VV, Shabanov PD. Vibration and vibroprotectors. Vol. 6. In: Pharmacology of extreme conditions: in 12 volumes. Ed. by P.D. Shabanov. Saint Petersburg: Inform-Navigator, 2015. 416 p. (In Russ.)
  25. Bondarev OI, Bugaeva MS, Mikhailova NN. Pathomorphology of heart muscle vessels in workers of the main professions of the coal industry. Russian Journal of Occupational Health and Industrial Ecology. 2019;59(6):335–341. EDN: GSSKJG doi: 10.31089/1026-9428-2019-59-6-335-341
  26. Rukavishnikov VS, Bodienkova GM, Kurchevenko SI, et al. Role of neuroautoimmune integration in pathogenesis of vibration disease. Russian Journal of Occupational Health and Indusyrial Ecology. 2017;1:17–20. EDN: XYEXFZ
  27. Vorobieva VV, Levchenkova OS, Shabanov PD. Pathophysiological mechanisms of neurological disorders in experimental animals exposed to vibration. Reviews on Clinical Pharmacology and Drug Therapy. 2020;18(3):213–224. EDN: ANNCVO doi: 10.17816/RCF183213-224
  28. Nattel S, Li D. Ionic remodeling in the heart: pathophysiological significance and new therapeutic opportunities for atrial fibrillation. Circ Res. 2000;87(6):440–447. doi: 10.1161/01.res.87.6.440
  29. Ginsburg KS, Bers DM. Modulation of excitation contraction coupling by isoproterenol in cardiomyocytes with controlled SR Ca2+ load and Ca2+ current trigger. J Physiol. 2004;556(Pt 2):463–480. doi: 10.1113/jphysiol.2003.055384
  30. Talukder MA, Kalyanasundaram A, Zuo L, et al. Is reduced SERCA2a expression detrimental or benefi cial to postischemic cardiac function and injury? Evidence from heterozygous SERCA2a knockout mice. Am J Physiol Heart Circ Physiol. 2008; 294(3): H1426–H1434. doi: 10.1152/ajpheart.01016.2007
  31. Lou Q, Janardhan A, Efimov IR. Remodeling of calcium handling in human heart failure. Adv Exp Med Biol. 2012;740:1145–1174. doi: 10.1007/978-94-007-2888-2_52
  32. Yano M, Yamamoto T, Ikeda Y, Matsuzaki M. Mechanisms of Disease: ryanodine receptor defects in heart failure and fatal arrhythmia. Nat Clin Pract Cardiovasc Med. 2006;3(1):43–52. doi: 10.1038/ncpcardio0419
  33. Tkachenko SB, Beresten NF. Tissue Doppler study of myocardium. Moscow: Real’noe vremya; 2006. 215 p. (In Russ.)
  34. Syomin FA, Khabibullina AR, Tsaturyan AK. Numerical modeling of the work of the left ventricle of the heart in the circulatory system: the effects of changes in the frequency of contractions and apical myocardial infarction. Biophysics. 2022;67(4):763–775. EDN: IULMNY doi: 10.31857/S0006302922040159
  35. Vorobieva VV, Shabanov PD. Morphological changes in the myocardium, liver and kidneys of rabbits after exposure of general vibration and pharmacological defense with succinate. Morphological Newsletter. 2011;(1):16–20. EDN: NMZIUV
  36. Egorova IF, Sukhacheva TV, Serov RA, et al. Cardiomyocyte structural rearrangement in patients with dilated cardiomyopathy and valvular heart disease. Arkhiv Patologii. 2012;74(4):3–7. EDN: PEIWQT
  37. Mohrman DE, Heller L. Cardiovascular physiology. Saint Petersburg: Peter; 2000. 249 p.
  38. Braunwald E. Biomarkers in heart failure. New Engl J Med. 2008;358(20):2148–2159. doi: 10.1056/NEJMra0800239
  39. Gerdes AM. Cardiac myocyte remodeling in hypertrophy and progression to failure. J Card Fail. 2002;8(6):S264–S268. doi: 10.1054/jcaf.2002.129280
  40. Wu QQ, Xiao Y, Yuan Y, et al. Mechanisms contributing to cardiac remodelling. Clin Sci (Lond). 2017;131(18):2319–2345. doi: 10.1042/CS201711676
  41. Levchenkova OS, Novikov VE, Parfenov EA, et al. Combined preconditioning reduces the negative influence of cerebral ischemia on the morphofunctional condition of CNS. Bulletin of Experimental Biology and Medicine. 2021;171(4):489–493. EDN: NAETUN doi: 10.1007/s10517-021-05257-6
  42. Hein S, Arnon E, Kostin S, et al. Progression from compensated hypertrophy to failure in the pressure-overloaded human heart: structural deterioration and compensatory mechanisms. Circulation. 2003;107(7):984–991. doi: 10.1161/01.cir.0000051865.66123.b7
  43. Razeghi P, Young ME, Alcorn JL, et al. Metabolic gene expression in fetal and failing human heart. Circulation. 2001;104(24):2923–2931. doi: 10.1161/hc4901.1005269
  44. Sutton MJJSt, Norman S. Left ventricular remodeling after myocardial infarction. Circulation. 2004;101:2981–2986 doi: 10.1161/01.cir.101.25.2981
  45. Spaich S, Katus HA, Backs J. Ongoing controversies surrounding cardiac remodeling: is it black and white — or rather fifty shades of gray? Front Pharmacol. 2015;6:202. doi: 10.3389/fphys.2015.00202
  46. Hohendanner F, McCulloch A, Blatter L, Michailova A. Calcium and IP3 dynamics in cardiac myocytes: experimental and computational perspectives and approaches. Front Pharmacol. 2014;5:35. doi: 10.3389/fphar.2014.00035
  47. Klimanova EA, Sidorenko SV, Tverskoi AM, et al. Search for intracellular sensors involved in the functioning of monovalent cations as secondary messengers. Biokhimiya. 2019;84(11):1592–1609. EDN: KMNUCT doi: 10.1134/S032097251911006X
  48. Guo Y. Comparative analysis reveals distinct and overlapping functions of Mef2c and Mef2d during cardiogenesis in Xenopus laevis. PLoS One. 2014;9(1):e87294. doi: 10.1371/journal.pone.0087294
  49. Meunier J, Hayashi Т. Sigma-1 receptors regulate Bcl-2 expression by reactive oxygen species-dependent transcriptional regulation of nuclear factor kappa B. J Pharmacol Exp Ther. 2010;332(2): 388–397 doi: 10.1124/jpet.109.160960
  50. Tagashira H, Bhuiyan MS, Shinoda Y, et al. Sigma-1 receptor is involved in modification of ER-mitochondria proximity and Ca2+ homeostasis in cardiomyocytes. J Pharmacol Sci. 2023;151(2):128–133. doi: 10.1016/j.jphs.2022.12.005
  51. Gao QJ, Yang В, Chen J, et al. Sigma-1 receptor stimulation with PRE-084 ameliorates myocardial ischemia-reperfusion injury in rats. Chin Med J (Engl). 2018;131(5):539–543. doi: 10.4103/0366-6999.226076
  52. Briasoulis A, Tousoulis D, Papageorgiou N, et al. Novel therapeutic approaches targeting matrix metalloproteinases in cardiovascular disease. Curr Top Med Chem. 2012;12(10):1214–1221. doi: 10.2174/1568026611208011214
  53. Ponikowska B, Iwanek G, Zdanowicz A, et al. Biomarkers of myocardial injury and remodeling in heart failure. J Pers Med. 2022;12(5):799. doi: 10.3390/jpm12050799
  54. Serezshina EK, Obrezan AG Myocardial damage and remodelling biomarkers in the diagnosis of heart failure with a preserved ejection fraction. RMJ. Medical Review. 2019;3(10(1)):23–26. (In Russ.) EDN: PTQLAC
  55. González A, Richards AM, de Boer RA, et al. Cardiac remodelling — Part 1: From cells and tissues to circulating biomarkers. A review from the Study Group on Biomarkers of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2022;24(6):927–943. doi: 10.1002/ejhf.2493
  56. Bogatyreva FM, Kaplunova VYu, Kozhevnikova MV, et al. Correlation between markers of fibrosis and myocardial remodeling in patients with various course of hypertrophic cardiomyopathy. Cardiovascular Therapy and Prevention. 2022;21(3):3140. EDN: EKFVOO doi: 10.15829/1728-8800-2022-3140
  57. Ilov NN, Arnaudova KS, Nechepurenko AA, et al. Role of the cardiac extracellular matrix in the onset and progression of heart failure. Russian Journal of Cardiology. 2021;26(2S):4362. EDN: ELODLF doi: 10.15829/1560-4071-2021-4362
  58. Zambrano MA, Alcaide P. Immune cells in cardiac injury repair and remodeling. Curr Cardiol Rep. 2023;25(5):315–323. doi: 10.1007/s11886-023-01854-1
  59. O’Meara E, Zannad F. Fibrosis biomarkers predict cardiac reverse remodeling. JACC Heart Fail. 2023;11(1):73–75. doi: 10.1016/j.jchf.2022.11.011
  60. Cieplak P, Strongin AY. Matrix metalloproteinases — From the cleavage data to the prediction tools and beyond. Biochim Biophys Acta Mol Cell Res. 2017;1864(11 Pt A):1952–1963. doi: 10.1016/j.bbamcr.2017.03.0109
  61. Deschamps A, Spinale F. Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation. Cardiovasc Res. 2006;69(3):666–676. doi: 10.1016/j.cardiores.2005.10.004
  62. Koduri H, Ng J, Cokic I, et al. Contribution of fibrosis and the autonomic nervous system to atrial fibrillation electrograms in heart failure. Circ Arrhythm Electrophysiol. 2012;5(4):640–649. doi: 10.1161/CIRCEP.111.970095
  63. Galati G, Leone O, Pasquale F, et al. Histological and histometric characterization of myocardial fibrosis in end-stage hypertrophic cardiomyopathy: a clinical-pathological study of 30 explanted hearts. Circ Heart Fail. 2016;9(9):e003090. doi: 10.1161/CIRCHEARTFAILURE.116.003090
  64. Smirnova EL, Poteryaeva EL, Ivanova AA, et al. Association of ID polymorphism of the CASP8 gene with vibration disease. Russian Journal of Occupational Health and Industrial Ecology. 2022;62(12):809–813. (In Russ.) EDN: SRSPYJ doi: 10.31089/1026-9428-2022-62-12-809-813
  65. Chistova NP. The role of candidate gene polymorphisms for endothelial dysfunction and metabolic disorders in the development of cardiovascular diseases under the influence of production factors. Russian Journal of Occupational Health and Industrial Ecology. 2019;62(5): 331–336. EDN: JDNIWU doi: 10.31089/1026-9428-2022-62-5-331-336
  66. Ussov VYu, Bogunetsky AA. Detection of myocardial viability in isсhaemic damage using magnetic resonance and emission tomography. Bulletin of Siberian Medicine. 2013;12(6):154–166. (In Russ.) EDN: RUENRN doi: 10.20538/1682-0363-2013-6-154-166
  67. McMurray JJ. Neprilysin inhibition to treat heart failure: a tale of science, serendipity, and second chances. Eur J Heart Fail. 2015;17(3):242–247. doi: 10.1002/ejhf.250
  68. Sacharczuk W, Dankowski R, Ożegowski S, et al. Evaluation of early left-sided cardiac reverse remodeling under combined therapy of sacubitril-valsartan and spironolactone compared with angiotensin-converting enzyme inhibitors and spironolactone. Front Cardiovasc Med. 2023;10:1103688. doi: 10.3389/fcvm.2023.1103688
  69. Carluccio E, Dini FL, Correale M, et al. Effect of sacubitril/valsartan on cardiac remodeling compared with other renin–angiotensin system inhibitors: a difference-in-difference analysis of propensity-score matched samples. Clin Res Cardiol. 2023. doi: 10.1007/s00392-023-02306-0
  70. Leancă SA, Afrăsânie I, Crișu D, et al. Cardiac reverse remodeling in ischemic heart disease with novel therapies for heart failure with reduced ejection fraction. Life. 2023;13(4):1000. doi: 10.3390/life13041000
  71. Álvarez-Zaballos S, Martínez-Sellés M. Angiotensin-converting enzyme and heart failure. Front Biosci (Landmark Ed). 2023;28(7):150. doi: 10.31083/j.fbl2807150
  72. Nishiya D, Enomoto S, Omura T, et al. The long-acting Ca2+-channel blocker azelnidipine prevents left ventricular remodeling after myocardial infarction. J Pharmacol Sci. 2007;103(4):391–397. doi: 10.1254/jphs.fp0061139
  73. Spasov AA, Vassiliev PM, Lenskaya KV, et al. Hypoglycemic potential of cyclic guanidine derivatives. Pure and Applied Chemistry. 2017;89(8):1007–1016. doi: 10.1515/pac-2016-1024
  74. Huang Yl, Xu Xz, Liu J, et al. Effects of new hypoglycemic drugs on cardiac remodeling: a systematic review and network meta-analysis. BMC Cardiovasc Disord .2023;23(1):293. doi: 10.1186/s12872-023-03324-6

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