Fat depot of the heart: contribution to the development of cardiovascular diseases, visualization methods and the possibilities of it’s correction


Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription Access

Abstract

Abstract. Рresents the possibilities of various visualization methods for assessing heart fat depot in patients with cardiovascular disease, as well as the effect of adipose tissue on myocardial function. The prospects of using the heart fat depot as a therapeutic target are considered on the example of the successful use of various groups of antidiabetic drugs, in particular glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors. Thus, it has been established that an ectopic fat depot makes a certain contribution to atherogenesis due to its effect on lipid metabolism, participation in the formation of a chronic inflammatory reaction of low intensity, potentiation of endothelial dysfunction, and activation of a coagulant shift. In addition, local organ dysfunctions, such as increased intrarenal pressure, mitochondrial disorders, increased lipogenesis, the formation of insulin resistance and lipotoxicity additionally create prerequisites for an increase in cardiovascular risk. Defines diagnostic and useful methods that not only quantitatively, but also qualitatively describe the relationship of fat depot and potential comorbid pathology. The effect of reducing cardiovascular risk, consisting in reducing the amount of epicardial adipose tissue in the studied, was observed when taking the preparation of the biguanide group, as well as its combination with drugs - analogues of glucagon-like peptide 1 and dipeptidyl peptidase-4 inhibitor. A similar effect was also observed in the case of the use of type 2 sodium-glucose cotransporter-2 inhibitors.

About the authors

E. S. Bratilova

Military medical academy of S.M. Kirov

Author for correspondence.
Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

V. A. Kachnov

Military medical academy of S.M. Kirov

Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

V. V. Tyrenko

Military medical academy of S.M. Kirov

Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

I. S. Zheleznyak

Military medical academy of S.M. Kirov

Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

D. V. Cherkashin

Military medical academy of S.M. Kirov

Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

S. V. Kushnarev

Military medical academy of S.M. Kirov

Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

A. D. Sobolev

Military medical academy of S.M. Kirov

Email: vmeda-nio@mil.ru
Russian Federation, Saint Petersburg

References

  1. Архангельская, А.Н. Влияние различных факторов на распространенность избыточной массы тела и ожирения среди лиц опасных профессий / А.Н. Архангельская [и др.] // Вестн. новых мед. технол. – 2016. – Т. 10. – № 4 – С. 2–13.
  2. Дедов, И.И. Жировая ткань как эндокринный орган / И.И. Дедов Г.А. Мельничеко, С.А. Бутрова // Ожирение и метаболизм. – 2006. – Т. 3, № 1. – С. 6–13.
  3. Евдокимов, В.И. Показатели заболеваемости военнослужащих контрактной службы Вооруженных сил Российской Федерации (2003–2016 гг.): монография В.И. Евдокимов, П.П. Сиващенко, С.Г. Григорьев // СПб.: Политехника-принт. – 2018. – № 2. – 80 c.
  4. Муромцева, Г.А. Распространенность факторов риска неинфекционных заболеваний в российской популяции в 2012–2013 гг. Результаты исследования ЭССЕ-РФ / Г.А. Муромцева [и др.] // Кардиоваскулярная терапия и профилактика. – 2014. – Т. 13, № 6. – С. 4–11.
  5. Учасова, Е.Г. Эпикардиальная жировая ткань: патофизиология и роль в развитии сердечно-сосудистых заболеваний / Е.Г. Учасова [и др.] // Бюлл. сиб. мед. – 2018. – Т. 17. – №. 4. – С. 27–30.
  6. Bouchi, R. Luseogliflozin reduces epicardial fat accumulation in patients with type 2 diabetes: a pilot study / R. Bouchi [et al.] // Cardiovascular Diabetology. – 2017. – Vol. 16. – P. 32.
  7. Britton, K.A., Ectopic Fat Depots and Cardiovascular Disease / K.A. Britton, C.S. Fox // Circulation. – 2011. – Vol. 124, № 24. – P. 837–841.
  8. Cho-Kai, W. Myocardial adipose deposition and the development of heart failure with preserved ejection fraction / W. Cho-Kai [et al.] // European Journal of Heart Failure. – 2019. – Vol. 22, № 3. – P. 445–454.
  9. Cornier, M.A. Assessing adiposity: a scientific statement from the American Heart Association / M.A. Cornier [et al.] // Circulation. – 2011. –Vol. 124, № 18. – P. 1996–2019.
  10. Díaz-Rodríguez, E. Effects of dapagliflozin on human epicardial adipose tissue: modulation of insulin resistance, inflammatory chemokine production, and differentiation ability / E. Díaz-Rodríguez [et al.] // Cardiovascular Research. – 2018. – Vol. 114, № 2. – P. 336–346.
  11. Dutour, A. Exenatide decreases liver fat content and epicardial adipose tissue in patients with obesity and type 2 diabetes: a prospective randomized clinical trial using magnetic resonance imaging and spectroscopy / A. Dutour [et al.] // Diabetes, Obesity and Metabolism. – 2016. – Vol. 18, № 9. – P. 882–891
  12. Dutour, A. Secretory type II phospholipase A2 is produced and secreted by epicardial adipose tissue and overexpressed in patients with coronary artery disease / A. Dutour [et al.] // The Journal of Clinical Endocrinology & Metabolism. – 2010. – Vol. 95, № 2. – P. 963– 967.
  13. Eroglu, S. Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease / S. Eroglu [et al.] // Nutrition, Metabolism & Cardiovascular Diseases. – 2009. – Vol. 19, № 3. – P. 211– 217.
  14. Fukuda, T. Ipragliflozin Reduces Epicardial Fat Accumulation in Non-Obese Type 2 Diabetic Patients with Visceral Obesity: A Pilot Study / T. Fukuda [et al.] // Diabetes Therapy. – 2017. – Vol. 8, № 4. – P. 851–861.
  15. Gorter, P.M. Quantification of epicardial and peri-coronary fat using cardiac computed tomography; reproducibility and relation with obesity and metabolic syndrome in patients suspected of coronary artery disease / P.M. Gorter [et al.] // Atherosclerosis. – 2008. – Vol. 197, № 2. – P. 896–903.
  16. Iacobellis, G. Liraglutide causes large and rapid epicardial fat reduction / G. Iacobellis [et al.] // Obesity. – 2017. – Vol. 25, № 2. – P. 311–316.
  17. Iacobellis, G. Echocardiographic epicardial fat: a review of research and clinical applications / G. Iacobellis, H.J. Willens // Journal of the American Society of Echocardiography. – 2009. – Vol. 22, № 12. – P. 1311– 1319.
  18. Lim, S. Links Between Ectopic Fat and Vascular Disease in Humans Arterioscler Thromb / Lim, S., & Meigs, J. B. // Arteriosclerosis, thrombosis, and vascular biology. – 2014. –Vol. 34, № 9. – Р. 1820-1826.
  19. Lima-Martínez, M.M. Effect of sitagliptin on epicardial fat thickness in subjects with type 2 diabetes and obesity: a pilot study / M.M. Lima-Martínez [et al.] // Endocrine. – 2016. – Vol. 51, № 3. – P. 448–455.
  20. Mazurek, T. Human epicardial adipose tissue is a source of inflammatory mediators / T. Mazurek [et al.] // Circulation. – 2003. – Vol. 108, № 20. – P. 2460–2466
  21. McAninch, E.A. Epicardial adipose tissue has a unique transcriptome modified in severe coronary artery disease / E.A. McAninch [et al.] //Obesity. – 2015. – Т. 23. – №. 6. – Р. 1267-1278.
  22. Ng, A.C. Myocardial steatosis and biventricular strain and strain rate imaging in patients with type 2 diabetes mellitus / A.C. Ng, V. Delgado [et al.] //Circulation. – 2010. – Т. 122. – № 24. – Р. 2538-2544.
  23. Ouchi, N. Adipokines in inflammation and metabolic disease / N. Ouchi [et al.] // Nature Reviews Immunology. – 2011. – Vol. 11, № 2. – P. 85–97.
  24. Pradhan, A.D. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus / A.D. Pradhan [et al.] // JAMA. – 2001. – Vol. 286, № 3. – P. 327–334.
  25. Sato, T. The effect of dapagliflozin treatment on epicardial adipose tissue volume / T. Sato [et al.] // Cardiovascular Diabetology. – 2018. – Vol. 17, № 1. – P. 6.
  26. Speliotes, E.K. Fatty liver is associated with dyslipidemia and dysglycemia independent of visceral fat: the Framingham Heart Study / E.K. Speliotes [et al.] // Hepatology. – 2010. – Vol. 51, № 6. – P. 277–283.
  27. Szczepaniak, L.S. Myocardial triglycerides and systolic function in humans: in vivo evaluation by localized proton spectroscopy and cardiac imaging // Magnetic Resonance in Medicine / L.S. Szczepaniak [et al.]. – 2003. – Vol. 49, № 3. – P. 417–423.
  28. Tadros, T.M. Pericardial fat volume correlates with inflammatory markers: the Framingham Heart Study / T.M. Tadros [et al.] // Obesity. – 2010. – Vol. 18, № 5. – P. 1039–1045.
  29. Tosaki, T. Sodium-glucose Co-transporter 2 Inhibitors Reduce the Abdominal Visceral Fat Area and May Influence the Renal Function in Patients with Type 2 Diabetes / T. Tosaki [et al.] // Internal Medicine. – 2017. – Vol. 56, № 6. – P. 597–604.
  30. Yagi, S. Canagliflozin reduces epicardial fat in patients with type 2 diabetes mellitus / S. Yagi [et al.] // Diabetology & Metabolic Syndrome. – 2017. – Vol. 9, № 1. – P. 78.

Supplementary files

Supplementary Files
Action
1. JATS XML
2. Fig. The mechanism of influence of the ectopic fat depot of the body on the development of atherosclerosis: FFA - free fatty acids; TG - triglycerides; LDL - low density lipoprotein; IR - insulin resistance; RAAS - renin-angiotensin-aldosterone system; HPC - heart rhythm disturbances. Adapted from S. Lim [18]

Download (283KB)

Copyright (c) 2020 Bratilova E.S., Kachnov V.A., Tyrenko V.V., Zheleznyak I.S., Cherkashin D.V., Kushnarev S.V., Sobolev A.D.

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies