DOI: 10.25881/20728255_2022_17_2_4

Authors

SHevchenko YU.L.

Pirogov National Medical and Surgical Center, Moscow

Abstract

Despite the fact that the cause of heart failure is more often cardiomyocyte dysfunction caused by coronary heart disease, inflammatory processes of various etiologies, excessive physical overload, including congenital and acquired heart defects, etc., there is such a group of patients whose etiology remains unclear and there are no obvious signs of myocardial damage according to instrumental and laboratory studies. At the same time, the peculiarity of attempts to treat such patients is the ineffectiveness of heart failure therapy. Long-term clinical practice, numerous scientific and experimental studies have suggested that the cause of such myocardial dysfunction is the immobilizing interstitial fibrosis of the heart.

Conclusion. The immobilizing interstitial fibrosis of the heart can be considered an independent pathology and one of the main causes of the development of chronic heart failure. It is based on the process of changing the connective tissue framework of the myocardium, resulting in the suppression of its work.

Keywords: heart failure, immobilization, connective tissue, interstitial fibrosis.

References

1. Ricard-Blum S. The collagen family. Cold Spring Harb Perspect Biol. 2011; 3(1): a004978. doi: 10.1101/cshperspect.a004978.

2. Halper J. Basic Components of Connective Tissues and Extracellular Matrix: Fibronectin, Fibrinogen, Laminin, Elastin, Fibrillins, Fibulins, Matrilins, Tenascins and Thrombospondins. Adv Exp Med Biol. 2021; 1348: 105-126. doi: 10.1007/978-3-030-80614-9_4.

3. Pinto AR, Ilinykh A, Ivey MJ, et al. Revisiting cardiac cellular composition. Circ Res. 2016; 118: 400-409.

4. Gersch C, Dewald O, Zoerlein M, et al. Mast cells and macrophages in normal C57/BL/6 mice. Histochem Cell Biol. 2002; 118: 41-49.

5. Bajpai G, Schneider C, Wong N, et al. The human heart contains distinct macrophage subsets with divergent origins and functions. Nat Med. 2018; 24: 1234-1245.

6. Epelman S, Lavine KJ, Beaudin AE, et al. Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation. Immunity. 2014; 40: 91-104.

7. Lee JS, Jeong SJ, Kim S, et al. Conventional dendritic cells impair recovery after myocardial infarction. J Immunol. 2018; 201: 1784-1798.

8. Camelliti P, Borg TK, Kohl P. Structural and functional characterisation of cardiac fibroblasts. Cardiovasc Res. 2005; 65: 40-51.

9. Tallquist MD. Cardiac fibroblast diversity. Annu Rev Physiol. 2020; 82: 63-78.

10. Liu X, Wu H, Byrne M, et al. Type III collagen is crucial for collagen I fibrillogenesis and for normal cardiovascular development. Proc Natl Acad Sci U S A. 1997; 94(5): 1852-1856. doi: 10.1073/pnas.94.5.1852.

11. Kuivaniemi H, Tromp G. Type III collagen (COL3A1): Gene and protein structure, tissue distribution, and associated diseases. Gene. 2019; 707: 151-171. doi: 10.1016/j.gene.2019.05.003.

12. Jugdutt BI. Ventricular remodeling after infarction and the extracellular collagen matrix: when is enough enough? Circulation. 2003; 108: 1395-1403.

13. Huang S, Chen B, Su Y, et al. Distinct roles of myofibroblast-specific Smad2 and Smad3 signaling in repair and remodeling of the infarcted heart. J Mol Cell Cardiol. 2019; 132: 84-97.

14. Suthahar N, Meijers WC, Silljé HHW, de Boer RA. From Inflammation to Fibrosis-Molecular and Cellular Mechanisms of Myocardial Tissue Remodelling and Perspectives on Differential Treatment Opportunities. Curr Heart Fail Rep. 2017; 14(4): 235-250. doi:10.1007/s11897-017-0343-y.

15. Krenning G, Zeisberg EM, Kalluri R. The origin of fibroblasts and mechanism of cardiac fibrosis. J Cell Physiol. 2010; 225: 631-7. doi:10.1002/jcp.22322.

16. Frangogiannis NG. Cardiac fibrosis. Cardiovasc Res. 2021; 117(6): 1450-1488. doi:10.1093/cvr/cvaa324].

17. Gao XM, White DA, Dart AM, Du XJ. Post-infarct cardiac rupture: recent insights on pathogenesis and therapeutic interventions. Pharmacol Ther. 2012; 134: 156-179.

18. Dai Z, Aoki T, Fukumoto Y, Shimokawa H. Coronary perivascular fibrosis is associated with impairment of coronary blood flow in patients with non-ischemic heart failure. J Cardiol. 2012; 60: 416-421.

19. Kalkman E, Bilgin Y, Haren P, et al. Determinants of coronary reserve in rats subjected to coronary artery ligation or aortic banding. Cardiovasc Res. 1996; 32: 1088-1095.

20. Kramann R, Schneider RK, DiRocco DP, et al. Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. Cell Stem Cell. 2015; 16: 51-66.

21. Wu L, Ong S, Talor MV, et al. Cardiac fibroblasts mediate IL-17A-driven inflammatory dilated cardiomyopathy. J Exp Med. 2014; 211: 1449-1464. doi: 10.1084/jem.20132126.

22. Dzemeshkevich SL, Stivenson LU. Disfunkciya miokarda i serdechnaya hirurgiya: klassifikaciya, diagnostika, hirurgicheskoe lechenie. M.: GEOTAR-Media, 2009. (In Russ).

For citation

SHevchenko YU.L. The immobilizing interstitial fibrosis of the heart. Part 1. Bulletin of Pirogov National Medical & Surgical Center. 2022;2(17):4-10. (In Russ.) https://doi.org/10.25881/20728255_2022_17_2_4