Speckle tracking echocardiography in the diagnosis of early left ventricular systolic dysfunction in type II diabetic mice

BMC Cardiovascular Disorders

Yi-jia Li¹  Qi-wei Sun¹  Bo Jiang¹  Ning Ma¹  Ya Yang¹  Jiao Yang¹  Rong-juan Li¹ 

[1] Beijing Institute of Heart, Lung and Blood Vessel Disease, Beijing, China

关键词: Cardiac function;    Strain;    Echocardiography;    db/db mice;    Diabetic cardiomyopathy;   

Others  :  1088432
DOI  :  10.1186/1471-2261-14-141

 received in 2014-07-02, accepted in 2014-10-03,  发布年份 2014

【 摘 要 】

s

Background

The leptin receptor-deficient db/db mouse is a well-established type II diabetes animal model used to investigate diabetic cardiomyopathy. Previous reports have documented diabetic cardiomyopathy is accompanied by cardiac structural and functional abnormalities. To better elucidate early or subtle changes in cardiac performance in db/db mice, we used speckle tracking echocardiography to assess systolic myocardial strain in vivo with diabetic db/db mice in order to study early changes of left ventricle contractile function in type II diabetes model.

Methods

Male diabetic db/db mice and age-matched control mice from C57BL/6J strain at 8,12 and 16 weeks of age were subjected to echocardiography. At the midpapillary level in the parasternal left ventricular short-axis view, end diastolic and systolic left ventricular diameter, interventricular septal thickness and posterior wall thicknesses, ejection fraction, fractional shortening were determined by M-mode echocardiography. Using speckle-tracking based strain analysis of two-dimensional echocardiographic images acquired from the parasternal short-axis views at the mid-papillary level, systolic global radial and circumferential strain values were analyzed.

Results

There was no significant difference in interventricular septal thickness, posterior wall thicknesses, end diastolic and systolic left ventricular diameter, ejection fraction and fractional shortening between db/db and age-matched control mice at 8,12 or 16 weeks of age (P > 0.05). At 8 and 12 weeks of age, there was no significant difference in left ventricular radial strain and circumferential strain between db/db mice and age-matched controls (P > 0.05). But at 16 weeks of age, the left ventricular radial strain and circumferential strain in db/db mice were lower than in control mice (P < 0.01).

Conclusion

The present study shows that speckle tracking echocardiography can be used to evaluate cardiac functional alterations in mouse models of cardiovascular disease. Radial and circumferential strain are more sensitive and can be used for detection of early left ventricular contractile dysfunction in db/db type II diabetic mice.

【 授权许可】

   
2014 Li et al.; licensee BioMed Central Ltd.

【 图 表 】

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【 参考文献 】

• [1]Cavaghan MK, Ehrmann DA, Polonsky KS: Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. J Clin Invest 2000, 106:329-333.
• [2]Shehadeh A, Regan TJ: Cardiac consequences of diabetes mellitus. Clin Cardiol 1995, 18:301-305.
• [3]Taffet GE, Hartley CJ, Wen X, Pham T, Michael LH, Entman ML: Noninvasive indexes of cardiac systolic and diastolic function in hyperthyroid and senescent mouse. Am J Physiol Heart Circ Physiol 1996, 270:H2204-H2209.
• [4]Fein FS, Kornstein LB, Strobeck JE, Capasso JM, Sonnenblick EH: Altered myocardial mechanics in diabetic rats. Circ Res 1980, 47(6):922-933.
• [5]Joffe II, Travers KE, Perreault-Micale CL, Hampton T, Katz SE, Morgan JP, Douglas PS: Abnormal cardiac function in the streptozotocin-induced non-insulin-dependent diabetic rat: noninvasive assessment with doppler echocardiography and contribution of the nitric oxide pathway. J Am Coll Cardiol 1999, 34(7):2111-2119.
• [6]Hoit BD, Castro C, Bultron G, Knight S, Matlib MA: Noninvasive evaluation of cardiac dysfunction by echocardiography in streptozotocin-induced diabetic rats. J Card Fail 1999, 5(4):324-333.
• [7]Thompson EW: Structural manifestations of diabetic cardiomyopathy in the rat and its reversal by insulin treatment. Am J Anat 1988, 182(3):270-282.
• [8]Rubler S, Dlugash J, Yuceoglu YZ, Kumral T, Branwood AW, Grishman A: New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol 1972, 30(6):595-602.
• [9]Regan TJ, Lyons MM, Ahmed SS, Levinson GE, Oldewurtel HA, Ahmad MR, Haider B: Evidence for cardiomyopathy in familial diabetes mellitus. J Clin Invest 1977, 60(4):884-899.
• [10]Friedman NE, Levitsky LL, Edidin DV, Vitullo DA, Lacina SJ, Chiemmongkoltip P: Echocardiographic evidence for impaired myocardial performance in children with type I diabetes mellitus. Am J Med 1982, 73(6):846-850.
• [11]Nunoda S, Genda A, Sugihara N, Nakayama A, Mizuno S, Takeda R: Quantitative approach to the histopathology of the biopsied right ventricular myocardium in patients with diabetes mellitus. Heart Vessels 1985, 1(1):43-47.
• [12]Penpargkul S, Schaible T, Yipintsoi T, Scheuer J: The effect of diabetes on performance and metabolism of rat hearts. Circ Res 1980, 47:911-921.
• [13]Tomlinson KC, Gardiner SM, Hebden RA, Bennett T: Functional consequences of streptozotocin-induced diabetes mel-litus, with particular reference to the cardiovascular system. Pharmacol Rev 1992, 44:103-179.
• [14]Yu Z, Tibbits GL, McNeill JH: Cellular functions of diabetic cardiomyocytes: contractility, rapid-cooling contracture, and ryanodine binding. Am J Physiol Heart Circ Physiol 1994, 266:H2082-H2089.
• [15]Pierce GN, Maddaford TG, Russell JC: Cardiovascular dysfunction in insulin-dependent and non-insulin-dependent an-imal models of diabetes mellitus. Can J Physiol Pharmacol 1997, 75:343-350.
• [16]Aasum E, Hafstad AD, Severson DL, Larsen TS: Age-dependent changes in metabolism, contractile function, and ischemic sensitivity in hearts from db/db mice. Diabetes 2003, 52:434-441.
• [17]Carley AN, Semeniuk LM, Shimoni Y, Aasum E, Larsen TS, Berger JP, Severson DL: Treatment of type 2 diabetic db/db mice with a novel PPAR agonist improves cardiac metabolism but not contractile function. Am J Physiol Endocrinol Metab 2004, 286:E449-E455.
• [18]Le Quang K, Bouchareb R, Lachance D, Laplante MA, Husseini DE, Boulanger MC, Fournier D, Fang XP, Avramoglu RK, Pibarot P, Deshaies Y, Sweeney G, Mathieu P, Marette A: Early development of calcific aortic valve disease and left ventricular hypertrophy in a mouse model of combined dyslipidemia and type 2 diabetes mellitus. Arterioscler Thromb Vasc Biol 2014, 34(10):2283-2291.
• [19]Semeniuk LM, Kryski AJ, Severson DL: Echocardiographic assessment of cardiac function in diabeticdb/db and transgenic db/db-hGLUT4 mice. Am J Physiol Heart Circ Physiol 2002, 283:H976-H982.
• [20]Cognet T, Vervueren PL, Dercle L, Bastié D, Richaud R, Berry M, Marchal P, Gautier M, Fouilloux A, Galinier M, Carrié D, Massabuau P, Berry I, Lairez O: New concept of myocardial longitudinal strain reserve assessed by a dipyridamole infusion using 2D-strain echocardiography: the impact of diabetes and age, and the prognostic value. Cardiovasc Diabetol 2013, 12:84. BioMed Central Full Text
• [21]Sahn DJ, De Maria A, Kisslo J, Weyman A: Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978, 58:1072-1083.
• [22]Belke DD, Larsen TS, Gibbs EM, Severson DL: Altered metabolism causes cardiac dysfunction in perfused hearts from diabetic (db/db) mice. Am J Physiol 2000, 279:E1104-E1113.
• [23]Aasum E, Belke DD, Severson DL, Riemersma R, Cooper M, Andreassen M, Larsen TS: Cardiac function and metabolism in type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-α activator. Am J Physiol 2002, 283:H949-H957.
• [24]Hoit BD: Echocardiographic characterization of the cardiovascular phenotype in rodent models. Toxicol Pathol 2006, 34:105-110.
• [25]Lairez O, Lonjaret L, Ruiz S, Marchal P, Franchitto N, Calise D, Fourcade O, Mialet-Perez J, Parini A, Minville V: Anesthetic regimen for cardiac function evaluation by echocardiography in mice: comparison between ketamine, etomidate and isoflurane versus conscious state. Lab Anim 2013, 47(4):284-290.
• [26]van Bilsen M, Daniels A, Brouwers O, Janssen BJ, Derks WJ, Brouns AE, Munts C, Schalkwijk CG, van der Vusse GJ, van Nieuwenhoven FA: Hypertension is a conditional factor for the development of cardiac hypertrophy in type 2 diabetic mice. PLoS One 2014, 9(1):e85078.
• [27]Barouch LA, Berkowitz DE, Harrison RW, O’Donnell CP, Hare JM: Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice. Circulation 2003, 108(6):754-759.
• [28]Ng AC, Delgado V, Bertini M, van der Meer RW, Rijzewijk LJ, Hooi Ewe S, Siebelink HM, Smit JW, Diamant M, Romijn JA, de Roos A, Leung DY, Lamb HJ, Bax JJ: Myocardial steatosis and biventricular strain and strain rate imaging in patients with type 2 diabetes mellitus. Circulation 2010, 122(24):2538-2544.
• [29]Ernande L, Rietzschel ER, Bergerot C, De Buyzere ML, Schnell F, Groisne L, Ovize M, Croisille P, Moulin P, Gillebert TC, Derumeaux G: Impaired myocardial radial function in asymptomatic patients with type 2 diabetes mellitus: a speckle-trackingimaging study. J Am Soc Echocardiogr 2010, 23(12):1266-1272.
• [30]Bauer M, Cheng S, Jain M, Ngoy S, Theodoropoulos C, Trujillo A, Lin FC, Liao R: Echocardiographic speckle-tracking-based strain imaging for rapid cardiovascular phenotyping in mice. Circ Res 2011, 108:908-916.
• [31]Popovic ZB, Benejam C, Bian J, Mal N, Drinko J, Lee K, Forudi F, Reeg R, Greenberg NL, Thomas JD, Penn MS: Speckle-tracking echocardiography correctly identifies segmental left ventricular dysfunction induced by scarring in a rat model of myocardial infarction. Am J Physiol Heart Circ Physiol 2007, 292:H2809-H2816.
• [32]Peng Y, Popovic ZB, Sopko N, Drinko J, Zhang Z, Thomas JD, Penn MS: Speckle tracking echocardiography in the assessment of mouse models of cardiac dysfunction. Am J Physiol Heart Circ Physiol 2009, 297:H811-H820.
• [33]Butterfield NN, Graf P, Ries CR, MacLeod BA: The effect of repeated isoflurane anesthesia on spatial and psychomotor performance in young and aged mice. Anesth Analg 2004, 98:1305-1311.
• [34]Matsuda Y, Ohsaka K, Yamamoto H: Comparison of newly developed inhalation anesthesia system and intraperitoneal anesthesia on the hemodynamic state in mice. Biol Pharm Bull 2007, 30:1716-1720.
• [35]Lygate CA, Fischer A, Sebag-Montefiore L, Wallis J, ten Hove M, Neubauer S: The creatine kinase energy transport system in the failing mouse heart. J Mol Cell Cardiol 2007, 42:1129-1136.