Age features of collagen exchange markers in patients with heart failure with intermediate emission faction on the background of metabolic syndrome


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Abstract

In pathological conditions, the activity of matrix metalloproteinases (MMP) increases, which leads to an imbalance between the synthesis and degradation of the extracellular matrix, which provokes the development of fibrosis in the myocardium, which contributes to the occurrence of heart failure. The aim of the study. To evaluate the features of collagen metabolism in elderly patients with chronic heart failure, an intermediate ejection fraction of heart failure with mid-range ejection fraction (HFmrEF) against the background of metabolic syndrome (MS). Material and methods. The study included 180 patients with HFmrEF (40-49%), functional class II according to NYHA (NYHA class II) of ischemic origin. We assessed the age of patients, the presence of MS, and levels of tissue inhibitor metalloproteinases tissue inhibitor metalloproteinas (TIMP-1), MMP-1, MMP-9. Results. Depending on the presence of MS in patients with HFmrEF, there was a significant (p<0.05) increase in MMP-9 with increasing age. The level of MMP-1 in the elderly late adulthood and senile gerontic age significantly increased with age in the presence of MS (p<0.05). In senile patients, the level of TIMP-1 in the group with MS was 13% lower (p<0.05) than without MS. In all age groups, the ratio of MMP-9/TIMP-1 in the presence of MS was higher (p<0.05) than without MS. Conclusions. Increased expression of MMP-9 and decreased expression of TIMP-1 in old age contribute to myocardial remodeling and fibrosis myocardium fibrosis, thereby changing the extracellular matrix of myocardial tissue leading to progression of heart failure. Metabolic syndrome significantly worsens the course of heart failure in the elderly and senile age, a mismatch between the degree of increase in the level of MMP-9 and TIMP-1 is characteristic.

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About the authors

O. A Osipova

Belgorod State National Research University

Email: osipova@bsu.edu.ru
Professor; MD

O. M Drapkina

National Medical Research Centre for Therapy and Preventive Medicine

MD, Corresponding Member of the Russian Academy of Sciences Moscow

R. N Shepel

National Medical Research Centre for Therapy and Preventive Medicine

Candidate of Medical Sciences Moscow

E. V Gosteva

N.N. Burdenko Voronezh State Medical University

Candidate of Medical Sciences

O. M Godlevskaya

Kharkov Medical Academy of Postgraduate Education

Candidate of Medical Sciences Ukraine

O. N Belousova

Belgorod State National Research University

Candidate of Medical Sciences

References

  1. Осипова О.А. Нагибина А.И., Комисов А.А. и др. Патоморфологические механизмы регуляции образования миокардиального фиброза у больных хронической сердечной недостаточностью на фоне ишемической болезни сердца. Сердечная недостаточность. 2016; 17 (5): 357-64 doi: 10.18087/RHFJ.2016.5.2137
  2. Cheng J.M., Akkerhuis K.M., Meilhac O. et al. Circulating osteoglycin and NGAL/MMP9 complex concentrations predict 1-year major adverse cardiovascular events after coronary angiography. Arterioscler. Thromb. Vasc. Biol. 2014; 34 (5): 1078-84. doi: 10.1161/ATVBAHA.114.303486
  3. Ravi Kanth V.V., Nageshwar R. Role of matrix metalloproteinases in physiological processes and disease. Indian J. Med. Res. 2014; 140 (5): 585-7.
  4. Душина А.Г., Лопина Е.А., Либис Р.А. Особенности хронической сердечной недостаточности в зависимости от фракции выброса левого желудочка. Российский кардиологический журнал. 2019; 2: 7-11 https://doi.org/10.15829/1560-4071-2019-2-7-11
  5. Скородумова Е.Г., Костенко В.А., Скородумова Е.А. и др. Портрет пациента с промежуточной фракцией выброса левого желудочка на фоне острой декомпенсациии сердечной недостаточности. Вестник СЗГМУ им. И.И. Мечникова. 2018; 10 (2): 87-91 doi: 10.17816/mechnikov201810287-91
  6. Pascual-Figal D.A. Ferrero-Gregori A., Gomez-Otero I. et al. Mid-range left ventricular ejection fraction: clinical profile and cause of death in ambulatory patients with chronic heart failure. Int. J. Cardiol. 2017; 240: 265-70. DOI: 10.1016 /j.ijcard.2017.03.032
  7. Guisado-Espartero M.E., Salamanca-Bautista P., Aramburu-Bodas Ö. et al. Heart failure with mid-range ejection fraction in patients admitted to internal medicine departments: findings from the RICA registry. Int. J. Cardiol. 2018; 255: 124-8. DOI: 10.1016/ j.ijcard.2017.07.101
  8. Koh A.S., Tay W.T., Teng T.H.K. et al. A comprehensive population-based characterization of heart failure with mid-range ejection fraction. Eur. J. Heart Fail. 2017; 19: 1624-34. DOI: 10.1002 /ejhf.945
  9. Toba H., Lindsey M.L. Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly. Pharmacol. Ther. 2019; 193: 99-120. doi: 10.1016/j.pharmthera.2018.08.014
  10. Srivastava, P.K., Hsu, J.J., Ziaeian, B. et al. Heart Failure With Mid-range Ejection Fraction. Curr. Heart Fail Rep. 2020; 17 (1): 1-8. https://doi.org/10.1007/s11897-019-00451-0
  11. Osipova O.A., Plaksina K.G., Komisov A.A. et al. Pathogenetic mechanisms of participation of the intercellular matrix of the myocardium cardiac remodeling in with chronic heart failure. Cardiology. 2015; 22: 18.
  12. Осипова О.А., Плаксина К.Г., Комисов А.А. и др. Патогенетические механизмы участия межклеточного матрикса миокарда в ремоделировании сердца у больных хронической сердечной недостаточностью. Научные ведомости Белгородского государственного университета. Серия: Медицина. Фармация. 2015; 22 (219): 18-25
  13. Hopps E., Lo Presti R., Montana M. et al. Gelatinases and their tissue inhibitors in a group of subjects with metabolic syndrome. J. Investig. Med. 2013; 61 (6): 978-83. doi: 10.2310/JIM.0b013e318294e9da
  14. Bfaszczyk E, Gawlik A. Neurotrophins, VEGF and matrix metalloproteinases: new markers or causative factors of metabolic syndrome components? Pediatr. Endocrinol. Diab. Metabol. 2016; 22 (3): 125-31. doi: 10.18544/pedm-22.03.0060
  15. Spinale F.G., Coker M.L., Thomas C.V. et al. Time-dependent changes in matrix metalloproteinase activity and expression during the progression of congestive heart failure. Relation to ventricular and myocyte function. Circ. Res. 1998; 82: 482-95. doi: 10.1161/01.res.82.4.482
  16. Schwartzkopff B., Fassbach M., Pelzer B. et al. Elevated serum markers of collagen degradation in patients with mild to moderate dilated cardiomyopathy. Eur. J. Heart Fail. 2002; 4: 439-44. doi: 10.1016/s1388-9842(02)00092-2
  17. Lindsay M.M., Maxwell P., Dunn F.G. TIMP-1: a marker of left ventricular diastolic dysfunction and fibrosis in hypertension. Hypertension. 2002; 40: 136-41. doi: 10.1161/01.hyp.0000024573.17293.23
  18. Morishita T., Uzui H., Mitsuke Ya. et al. Association between matrix metalloproteinase-9 and worsening heart failure events in patients with chronic heart failure. ESC Heart Fail. 2017; 4: 321-30. doi: 10.1002/ehf2.12137

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