AGE FEATURES OF COLLAGEN EXCHANGE MARKERS IN PATIENTS WITH HEART FAILURE WITH INTERMEDIATE EMISSION FACTION ON THE BACKGROUND OF METABOLIC SYNDROME

DOI: https://doi.org/10.29296/25877305-2020-06-07
Download full text PDF
Issue: 
6
Year: 
2020

Professor О. Osipova(1), MD; Professor O. Drapkina(2), MD, Corresponding Member of the Russian Academy of Sciences; R. Shepel(2); Е. Gosteva(3), Candidate of Medical Sciences; O. Godlevskaya(4), Candidate of Medical Sciences; О. Belousova(1), Candidate of Medical Sciences; (1)Belgorod State National Research University (2)National Medical Research Centre for Therapy and Preventive Medicine, Moscow (3)N.N. Burdenko Voronezh State Medical University (4)Kharkov Medical Academy of Postgraduate Education, Ukraine

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
Keywords: 
cardiology
myocardial fibrosis
heart failure with mid-range ejection fraction
metabolic syndrome
TIMP-1
MMP-1
MMP-9

It appears your Web browser is not configured to display PDF files. Download adobe Acrobat или click here to download the PDF file.

References: 
  1. Osipova O.A. Nagibina A.I., Komisov A.A. i dr. Patomorfologicheskie mehanizmy reguljatsii obrazovanija miokardial'nogo fibroza u bol'nyh hronicheskoj serdechnoj nedostatochnost'ju na fone ishemicheskoj bolezni serdtsa. Cerdechnaja nedostatochnost'. 2016; 17 (5): 357–64 [Osipova O.A. Nagibina A.I., Komisov A.A. et al. Pathomorphological mechanisms for regulation of myocardial fibrosis formation in patients with chronic heart failure with underlying ischemic heart disease. Serdechnaja nedostatochnost’. 2016; 17 (5): 357–64 (in Russ.)]. 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. Dushina A.G., Lopina E.A., Libis R.A. Osobennosti hronicheskoj serdechnoj nedostatochnosti v zavisimosti ot fraktsii vybrosa levogo zheludochka. Rossijskij kardiologicheskij zhurnal. 2019; 2: 7–11 [Dushina A.G., Lopina E.A., Libis R.A. Features of chronic heart failure depending on the left ventricular ejection fraction. Russian Journal of Cardiology. 2019; 2: 7–11 (in Russ.)] https://doi.org/10.15829/1560-4071-2019-2-7-11
  5. Skorodumova E.G., Kostenko V.A., Skorodumova E.A. i dr. Portret patsienta s promezhutochnoj fraktsiej vybrosa levogo zheludochka na fone ostroj dekompensatsiii serdechnoj nedostatochnosti. Vestnik SZGMU im. I.I. Mechnikova. 2018; 10 (2): 87–91 [Skorodumova E.G., Kostenko V.A., Skorodumova E.A. et al. Portrait of the patient with intermediate ejection fraction of the left ventricle on the background of acute decompencation of heart failure. Bulletin of the North-Western State Medical University named after I.I. Mechnikov. 2018; 10 (2): 87–91 (in Russ.)]. 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 Ó. 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. Osipova O.A., Plaksina K.G., Komisov A.A. i dr. Patogeneticheskie mehanizmy uchastija mezhkletochnogo matriksa miokarda v remodelirovanii serdtsa u bol'nyh hronicheskoj serdechnoj nedostatochnost'ju. Nauchnye vedomosti Belgorodskogo gosudarstvennogo universiteta. Serija: Meditsina. Farmatsija. 2015; 22 (219): 18–25 [Osipova O.A., Plaksina K.G., Komisov A.A. et al. Patogeneticheskie mehanizmy uchastija mezhkletochnogo matriksa miokarda v remodelirovanii serdca u bol’nyh hronicheskoj serdechnoj nedostatochnost’ju. Nauchnye vedomosti Belgorodskogo gosudarstvennogo universiteta. Serija: Medicina. Farmacija. 2015; 22 (219): 18–25 (in Russ.)]
  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. Błaszczyk 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