2013


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2013/№5

Peculiarities of myocardial remodeling and functions in patients with epicardial obesity

Veselovskaya N.G., Chumakova G.A., Ott A.V., Gritsenko O.V., Trubina E.V.

Keywords: myocardial remodeling, risk factors, CHF, epicardial obesi

DOI: 10.18087 / rhfj.2013.5.1821

Background. Mechanisms of lipotoxic myocardial injury and remodeling in epicardial obesity (EO) are understudied. Aim. Studying the interrelation between the epicardial adipose tissue thickness (EATt) and myocardial structure and function parameters. Materials and methods. The study included 104 male patients (54.8±8.2 years) with IHD, II–III class exertional angina and underlying obesity (BMI 34.26±2.80 kg / m²). The following groups were isolated: group 1 with EATt ≥7 mm (n=49) and group 2 with EATt <7 mm (n=55). Visceral adipose tissue adipokines (leptin, adiponectin, resistin) were measured in all patients. EO degree was evaluated using echoCG (measurement of linear EATt behind the RV free wall in the end of systole). Results. In group 1, mean EDV and ESV values were 132.67±15.67 and 51.89±8.31 ml. These values were significantly greater than for group 2 patients, 124.45±12.69 ml (р=0.005) and 43.76±6.54 ml (р=0.002), respectively. In addition, left atrial (LA) and RV EDR dimensions were greater in patients with EATt ≥7 mm than in patients with EATt <7 mm (44.37±4.97 mm and 29.31±3.48 mm vs. 40.54±2.98 mm, р=0.001 and 25.43±3.12 mm, respectively, р=0.001). Type 1 diastolic dysfunction (DD) was observed in 28.5 % (n=14) of group 1 patients and in 14 % (n=8) of group 2 patients. In addition, type 2 DD was found in two patients (4 %) of group 1; in patients of group 2, this DD type was not observed. Conclusion. EO is an important pathogenetic mechanism of myocardial remodeling and a modifiable RF for CHF development and progression.
  1. Zhou YT, Grayburn P, Karim A et al. Lipotoxic heart disease in obese rats: implications for human obesity. Proc Natl Acad Sci U S A. 2000;97 (4):1784–1789.
  2. Kenchaiah S, Evans JC, Levy D et al. Obesity and the risk of heart failure. N Engl J Med. 2002;347 (5):305–313.
  3. Ritchie RH. Evidence for a causal role of oxidative stress in the myocardial complications of insulin resistance. Heart Lung Circ. 2009;18 (1):11–18.
  4. Silaghi A, Achard V, Paulmyer-Lacroix O et al. Expression of adrenomedullin in human epicardial adipose tissue:role of coronary status. Am J Physiol Endocrinol Metab. 2007;293 (5):1443–1450.
  5. Iacobellis G, Willens HJ. Echocardiographic Epicardial Fat: A Review of Research and Clinical Applications. JASE. 2009;22 (12):1311–1319.
  6. Mazurek T, Zhang L, Zalewski A et al. Human epicardial adipose tissue is a source of inflammatory mediators. Circulation. 2003;108 (20):2460–2466.
  7. Sade LE, Eroglu S, Bozbas H et al. Relation between epicardial fat thickness and coronary flow reserve in women with chest pain and angiographically normal coronary arteries. Atherosclerosis. 2009;204 (2):580–585.
  8. Ahn SG, Lim HS, Joe DY. Relationship of epicardial adipose tissue by echocardiography to coronary artery disease. Heart. 2008;94 (3):7–13.
  9. Park JS, Ahn SG, Hwang JW et al. Impact of body mass index on the relationship of epicardial adipose tissue to metabolic syndrome and coronary artery disease in an Asian population. Cardiovasc Diabetol. 2010;9:29.
  10. Jeong JW, Jeong MH, Yun KH et al. Echocardiographic epicardial fat thickness and coronary artery disease. Circ J. 2007;71 (4):536–539.
  11. Eroglu S, Sade LE, Yildirir A et al. Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease. Nutr Metab Cardiovasc Dis. 2009;19 (3):211–217.
  12. Rajapurohitam V, Gan XT, Kirshenbaum LA, Karmazyn M. The obesity-associated peptide leptin induces hypertrophy in neonatal rat ventricular myocytes. Circ Res. 2003;93 (4):277–279.
  13. Reilly MP, Lehrke M, Wolfe ML et al. Resistin is an inflammatory marker of atherosclerosis in humans. Circulation. 2005;111 (7):932–939.
  14. Frankel DS, Vasan RS, D'Agostino RB Sr et al. Resistin, adiponectin, and risk of heart failure the Framingham offspring study. J Am Coll Cardiol. 2009;53 (9):754–762.
  15. Kumada M, Kihara S, Sumitsuji S et al. Association of hypo­adiponectinemia with coronary artery disease in men. Arterioscler Thromb Vasc Biol. 2003;23 (1):85–89.
  16. Weyer C, Funahashi T, Tanaka S et al. Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia. J Clin Endocrinol Metab. 2001;86 (5):1930–1935.
  17. Tan KC, Xu A, Chow WS et al. Hypoadiponectinemia is associated with impaired endotheliumdependdent vasodilation. J Clin Endocrinol Metab. 2004;89 (2):765–769.
  18. George J, Patal S, Wexler D et al. Circulating adiponectin concentrations in patients with congestive heart failure. Heart. 2006;92 (10):1420–1424.
  19. Iacobellis G, Leonetti F, Singh N et al. Relationship of epicardial adipose tissue with atrial dimensions and diastolic function in morbidly obese subjects. Int J Cardiol. 2007;115 (2):272–273.
  20. Corradi D, Maestri R, Callegari S et al. The ventricular epicardial fat is related to the myocardial mass in normal, ischemic and hypertrophic hearts. Cardiovasc Pathol. 2004;13 (6):313–316.
  21. Iacobellis G, Ribaudo MC, Zappaterreno A et al. Relation between epicardial adipose tissue and left ventricular mass. Am J Cardiol. 2004;94 (8):1084–1087.
Veselovskaya N.G., Chumakova G.A., Ott A.V. et al. Peculiarities of myocardial remodeling and functions in patients with epicardial obesity. Russian Heart Failure Journal. 2013;14 (5):247-251

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