Authors
Shevchenko Yu.L., Plotnitsky A.V., Ulbashev D.S.
Pirogov National Medical and Surgical Center, Moscow
Abstract
Fibrosis of the heart may reflect the activation of reparative or maladaptive processes. When the regulation of collagen fiber synthesis is disrupted, the volume of the interstitial space increases, the interstitial connective tissue changes qualitatively (its density increases, the structure of the “braiding” changes, the location of the fibers changes, etc.) – this often causes cardiac dysfunction: there is mechanical compression of healthy cardiomyocytes from the outside, restriction of their normal movement and functioning. The article presents two clinical observations that demonstrate an example of primary and secondary (induced) immobilizing interstitial cardiac fibrosis.
Primary immobilizing interstitial cardiac fibrosis is based on changes in connective tissue, without initial damage to cardiomyocytes. The development of the disease occurs gradually, starting with a slight increase in the volume of the interstitium, up to the formation of gross fibrosis with compression of arterioles. Secondary (induced) immobilizing interstitial cardiac fibrosis is based on the process of diffuse changes in the interstitial connective tissue as a result of stimulation by its formed postinfarction scars.
Keywords: interstitial fibrosis, heart failure, coronary heart disease.
References
1. Frangogiannis NG. Cardiac fibrosis. Cardiovasc. Res. 2020; 117: 1450-1488. doi: 10.1093/cvr/cvaa324.
2. Eijgenraam TR, Silljé HHW, de Boer RA. Current understanding of fibrosis in genetic cardiomyopathies. Trends Cardiovasc. Med. 2019; 30: 353-361. doi: 10.1016/j.tcm.2019.09.003.
3. Treibel TA, López B, González A, et al. Reappraising myocardial fibrosis in severe aortic stenosis: An invasive and non-invasive study in 133 patients. Eur. Heart J. 2017; 39: 699-709. doi: 10.1093/eurheartj/ehx353.
4. Hinderer S, Schenke-Layland K. Cardiac fibrosis–A short review of causes and therapeutic strategies. Adv. Drug Deliv. Rev. 2019; 146: 77-82. doi: 10.1016/j.addr.2019.05.011.
5. 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.
6. Krejci J, Mlejnek D, Sochorova D, Nemec P. Inflammatory Cardiomyopathy: A Current View on the Pathophysiology, Diagnosis, and Treatment. Biomed. Res. Int. 2016; 2016: 4087632. doi: 10.1155/2016/4087632.
7. Imanaka-Yoshida K, Tawara I, Yoshida T. Tenascin-C in cardiac disease: A sophisticated controller of inflammation, repair, and fibrosis. Am. J. Physiol.-Cell Physiol. 2020; 319: 781-796. doi: 10.1152/ajpcell.00353.2020.
8. Sygitowicz G, Maciejak-Jastrzębska A, Sitkiewicz D. A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation. J. Clin. Med. 2021; 10: 4430. doi: 10.3390/jcm10194430.
9. Cowling RT, Kupsky D, Kahn AM, et al. Mechanisms of cardiac collagen deposition in experimental models and human disease. Transl Res. 2019; 209: 138-155. doi:10.1016/j.trsl. 2019.03.004.
10. Souders CA, Bowers SL, Baudino TA. Cardiac fibroblast: the renaissance cell. Circ Res. 2009; 105: 1164-76.
11. González A, López B, Ravassa S, et al. The complex dynamics of myocardial interstitial fibrosis in heart failure. Focus on collagen cross-linking. Biochim. Et Biophys. Acta Mol. Cell Res. 2019; 1866: 1421-1432. doi: 10.1016/j.bbamcr.2019.06.001.
12. Caulfield JB, Norton P, Weaver RD. Cardiac dilatation associated with collagen alterations. Mol. Cell Biochem. 1992; 116: 171-179. doi: 10.1007/BF00299396.
13. Frangogiannis NG. Cardiac fibrosis: cell biological mechanisms, molecular pathways and therapeutic opportunities. Mol Aspects Med. 2019; 65: 70-99.
14. Prabhu SD Frangogiannis NG. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. Circ Res 2016; 119: 91-112.
15. Frangogiannis NG. The Extracellular Matrix in Ischemic and Nonischemic Heart Failure. Circ. Res. 2019; 125: 117-146. doi: 10.1161/ CIRCRESAHA.119.311148.
16. Dusenbery SM, Jerosch-Herold M, Rickers C, et al. Myocardial extracellular remodeling is associated with ventricular diastolic dysfunction in children and young adults with congenital aortic stenosis. J Am Coll Cardiol. 2014; 63: 1778-85.
17. Schnee JM, Hsueh WA. Angiotensin II, adhesion, and cardiac fibrosis. Cardiovasc Res. 2000; 46: 264-8.
18. Leask A. Getting to the heart of the matter: new insights into cardiac fibrosis. Circ Res. 2015; 116: 1269-76.
19. Wenzl FA, Ambrosini S, Mohammed SA, et al. Inflammation in Metabolic Cardiomyopathy. Front. Cardiovasc. Med. 2021; 8: 742178. doi: 10.3389/fcvm.2021.742178.
20. Imanaka-Yoshida K. Inflammation in myocardial disease: From myocarditis to dilated cardiomyopathy. Pathol. Int. 2020; 70: 1-11. doi: 10.1111/pin.12868.
21. Bovelli D, Plataniotis G, Roila F. Cardiotoxicity of chemotherapeutic agents and radiotherapy-related heart disease: ESMO clinical practice guidelines. Ann Oncol. 2010; 21(5): v277-82.
22. Shevchenko YuL. The immobilizing interstitial fibrosis of the heart. Part I. Bulletin of Pirogov National Medical & Surgical Center. 2022; 17(2): 4-10. (In Russ.) doi:10.25881/20728255_2022_17_2_4.
23. Shevchenko YuL, Plotnitsky AV, Sudilovskaya VV, et al. Morphology and markers of the immobilizing interstitial fibrosis of the heart. Bulletin of Pirogov National Medical & Surgical Center. 2022; 17(3): 84-93. (In Russ.) doi: 10.25881/20728255_2022_17_3_84.
24. Shevchenko YuL, Ulbashev DS. The immobilizing interstitial fibrosis of the heart. Part II. Bulletin of Pirogov National Medical & Surgical Center. 2022; 17(3): 4-10. (In Russ.) doi: 10.25881/20728255_2022_17_3_4.