期刊论文详细信息
Cardiovascular Diabetology
Insulin resistance and subclinical abnormalities of global and regional left ventricular function in patients with aortic valve sclerosis
Yasuki Kihara1  Takayuki Hidaka1  Eiji Kunita1  Hideya Yamamoto1  Hiroto Utsunomiya1 
[1] Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan
关键词: Visceral adipose tissue;    Speckle-tracking echocardiography;    Insulin resistance;    Cardiac function;    Aortic valve sclerosis;   
Others  :  793049
DOI  :  10.1186/1475-2840-13-86
 received in 2014-02-13, accepted in 2014-04-20,  发布年份 2014
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【 摘 要 】

Background

Insulin resistance, as a key mediator of metabolic syndrome, is thought to be associated with pathogenesis of calcific aortic valve disease and altered left ventricular (LV) function and structure. However, in patients with aortic valve sclerosis (AVS), the association between insulin resistance and subclinical impairment of LV function is not fully elucidated.

Methods

We studied 57 patients (mean age 70 ± 8 years, 22 women) with asymptomatic AVS but normal LV ejection fraction in echocardiography. LV longitudinal and circumferential strain and strain rate was analyzed using two-dimensional speckle tracking echocardiography. Patients with uncontrolled hypertension and diabetes mellitus, chronic kidney disease, and concomitant coronary artery disease were excluded. They were divided into the insulin-resistant group (AVS+IR; N = 28) and no insulin-resistant group (AVS-IR; N = 29) according to the median value of homeostatic model assessment index. Computed tomography scans were also performed to measure the aortic valve calcium score and the visceral adipose tissue (VAT) area. In addition, age- and sex- adjusted 28 control subjects were recruited for the comparison.

Results

There were no significant differences in LV ejection fraction or mass index among the groups. The AVS+IR group had a higher aortic valve calcium score (median 94 versus 21, P = 0.022) and a larger VAT area (113 ± 42 cm2 versus 77 ± 38 cm2, P = 0.001) than the AVS-IR group. Notably, LV global longitudinal strain, strain rate (SR), and early diastolic SR were significantly lower in the AVS+IR group than in the AVS-IR group and in control subjects (strain: -16.2 ± 1.6% versus -17.2 ± 1.2% and -18.9 ± 0.8%; SR: -1.18 ± 0.26 s-1 versus -1.32 ± 0.21 s-1 and -1.52 ± 0.08 s-1; early diastolic SR: -1.09 ± 0.23 s-1 versus -1.23 ± 0.18 s-1 and -1.35 ± 0.12 s-1; P < 0.05 for all comparison), whereas circumferential function were not significantly different. Multiple linear regression analyses revealed insulin resistance as an independent determinant of LV longitudinal strain (P = 0.017), SR (P = 0.047), and early diastolic SR (P = 0.049) regardless of LV mass index or VAT area.

Conclusions

Insulin resistance is a powerful independent predictor of subclinical LV dysfunction regardless of concomitant visceral obesity and LV hypertrophy. Thus, it may be a novel therapeutic target to prevent subsequent heart failure in patients with AVS.

【 授权许可】

   
2014 Utsunomiya et al.; licensee BioMed Central Ltd.

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【 参考文献 】
  • [1]Otto CM, Lind BK, Kitzman DW, Gersh BJ, Siscovick DS: Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med 1999, 341:142-147.
  • [2]Nightingale AK, Horowitz JD: Aortic sclerosis: not an innocent murmur but a marker of increased cardiovascular risk. Heart 2005, 91:1389-1393.
  • [3]Utsunomiya H, Yamamoto H, Kunita E, Kitagawa T, Ohashi N, Oka T, Yamazato R, Horiguchi J, Kihara Y: Combined presence of aortic valve calcification and mitral annular calcification as a marker of the extent and vulnerable characteristics of coronary artery plaque assessed by 64-multidetector computed tomography. Atherosclerosis 2010, 213:166-172.
  • [4]Owens DS, Budoff MJ, Katz R, Takasu J, Shavelle DM, Carr JJ, Heckbert SR, Otto CM, Probstfield JL, Kronmal RA, O’Brien KD: Aortic valve calcium independently predicts coronary and cardiovascular events in a primary prevention population. JACC Cardiovasc Imaging 2012, 5:619-625.
  • [5]Despres JP, Lemieux I: Abdominal obesity and metabolic syndrome. Nature 2006, 444:881-887.
  • [6]Capoulade R, Clavel MA, Dumesnil JG, Chan KL, Teo KK, Tam JW, Cote N, Mathieu P, Despres JP, Pibarot P: Insulin resistance and LVH progression in patients with calcific aortic stenosis: a substudy of the ASTRONOMER trial. JACC Cardiovasc Imaging 2013, 6:165-174.
  • [7]Capoulade R, Clavel MA, Dumesnil JG, Chan KL, Teo KK, Tam JW, Cote N, Mathieu P, Despres JP, Pibarot P: Impact of metabolic syndrome on progression of aortic stenosis: influence of age and statin therapy. J Am Coll Cardiol 2012, 60:216-223.
  • [8]Cadeddu C, Nocco S, Piano D, Deidda M, Cossu E, Baroni MG, Mercuro G: Early impairment of contractility reserve in patients with insulin resistance in comparison with healthy subjects. Cardiovasc Diabetol 2013, 12:66. BioMed Central Full Text
  • [9]Sironi AM, Pingitore A, Ghione S, De Marchi D, Scattini B, Positano V, Muscelli E, Ciociaro D, Lombardi M, Ferrannini E, Gastaldelli A: Early hypertension is associated with reduced regional cardiac function, insulin resistance, epicardial, and visceral fat. Hypertension 2008, 51:282-288.
  • [10]Mahmod M, Bull S, Suttie JJ, Pal N, Holloway C, Dass S, Myerson SG, Schneider JE, De Silva R, Petrou M, Sayeed R, Westaby S, Clelland C, Francis JM, Ashrafian H, Karamitsos TD, Neubauer S: Myocardial steatosis and left ventricular contractile dysfunction in patients with severe aortic stenosis. Circ Cardiovasc Imaging 2013, 6:808-816.
  • [11]Lindman BR, Arnold SV, Madrazo JA, Zajarias A, Johnson SN, Perez JE, Mann DL: The adverse impact of diabetes mellitus on left ventricular remodeling and function in patients with severe aortic stenosis. Circ Heart Fail 2011, 4:286-292.
  • [12]Stevens LA, Coresh J, Greene T, Levey AS: Assessing kidney function–measured and estimated glomerular filtration rate. N Engl J Med 2006, 354:2473-2483.
  • [13]Executive summary of the third report of The National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult treatment panel III) JAMA 2001, 285:2486-2497.
  • [14]Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC: Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985, 28:412-419.
  • [15]Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise J, Solomon S, Spencer KT, St John Sutton M, Stewart W: Recommendations for chamber quantification. Eur J Echocardiogr 2006, 7:79-108.
  • [16]Hung CL, Verma A, Uno H, Shin SH, Bourgoun M, Hassanein AH, McMurray JJ, Velazquez EJ, Kober L, Pfeffer MA, Solomon SD: Longitudinal and circumferential strain rate, left ventricular remodeling, and prognosis after myocardial infarction. J Am Coll Cardiol 2010, 56:1812-1822.
  • [17]Ohashi N, Yamamoto H, Horiguchi J, Kitagawa T, Hirai N, Ito K, Kohno N: Visceral fat accumulation as a predictor of coronary artery calcium as assessed by multislice computed tomography in Japanese patients. Atherosclerosis 2009, 202:192-199.
  • [18]Page A, Dumesnil JG, Clavel MA, Chan KL, Teo KK, Tam JW, Mathieu P, Despres JP, Pibarot P: Metabolic syndrome is associated with more pronounced impairment of left ventricle geometry and function in patients with calcific aortic stenosis: a substudy of the ASTRONOMER (Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin). J Am Coll Cardiol 2010, 55:1867-1874.
  • [19]Ng AC, Delgado V, Bertini M, van der Meer RW, Rijzewijk LJ, Shanks M, Nucifora G, Smit JW, Diamant M, Romijn JA, de Roos A, Leung DY, Lamb HJ, Bax JJ: Findings from left ventricular strain and strain rate imaging in asymptomatic patients with type 2 diabetes mellitus. Am J Cardiol 2009, 104:1398-1401.
  • [20]Ceyhan K, Kadi H, Koc F, Celik A, Ozturk A, Onalan O: Longitudinal left ventricular function in normotensive prediabetics: a tissue Doppler and strain/strain rate echocardiography study. J Am Soc Echocardiogr 2012, 25:349-356.
  • [21]Katz R, Budoff MJ, Takasu J, Shavelle DM, Bertoni A, Blumenthal RS, Ouyang P, Wong ND, O’Brien KD: Relationship of metabolic syndrome with incident aortic valve calcium and aortic valve calcium progression: the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes 2009, 58:813-819.
  • [22]Eckel RH, Alberti KG, Grundy SM, Zimmet PZ: The metabolic syndrome. Lancet 2010, 375:181-183.
  • [23]Arishiro K, Hoshiga M, Negoro N, Jin D, Takai S, Miyazaki M, Ishihara T, Hanafusa T: Angiotensin receptor-1 blocker inhibits atherosclerotic changes and endothelial disruption of the aortic valve in hypercholesterolemic rabbits. J Am Coll Cardiol 2007, 49:1482-1489.
  • [24]Cognet T, Vervueren PL, Dercle L, Bastie D, Richaud R, Berry M, Marchal P, Gautier M, Fouilloux A, Galinier M, Carrie 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. Cardiovascular diabetology 2013, 12:84. BioMed Central Full Text
  • [25]Kosmala W, Jedrzejuk D, Derzhko R, Przewlocka-Kosmala M, Mysiak A, Bednarek-Tupikowska G: Left ventricular function impairment in patients with normal-weight obesity: contribution of abdominal fat deposition, profibrotic state, reduced insulin sensitivity, and proinflammatory activation. Circ Cardiovasc Imaging 2012, 5:349-356.
  • [26]Karabay CY, Kocabay G, Kalayci A, Colak Y, Oduncu V, Akgun T, Kalkan S, Guler A, Kirma C: Impaired left ventricular mechanics in nonalcoholic fatty liver disease: a speckle-tracking echocardiography study. Eur J Gastroenterol Hepatol 2014, 26:325-331.
  • [27]Whaley-Connell A, Habibi J, Rehmer N, Ardhanari S, Hayden MR, Pulakat L, Krueger C, Ferrario CM, DeMarco VG, Sowers JR: Renin inhibition and AT(1)R blockade improve metabolic signaling, oxidant stress and myocardial tissue remodeling. Metabolism 2013, 62:861-872.
  • [28]Noyan-Ashraf MH, Shikatani EA, Schuiki I, Mukovozov I, Wu J, Li RK, Volchuk A, Robinson LA, Billia F, Drucker DJ, Husain M: A glucagon-like peptide-1 analog reverses the molecular pathology and cardiac dysfunction of a mouse model of obesity. Circulation 2013, 127:74-85.
  • [29]Domenighetti AA, Danes VR, Curl CL, Favaloro JM, Proietto J, Delbridge LM: Targeted GLUT-4 deficiency in the heart induces cardiomyocyte hypertrophy and impaired contractility linked with Ca(2+) and proton flux dysregulation. J Mol Cell Cardiol 2010, 48:663-672.
  • [30]Sharma N, Okere IC, Duda MK, Chess DJ, O’Shea KM, Stanley WC: Potential impact of carbohydrate and fat intake on pathological left ventricular hypertrophy. Cardiovasc Res 2007, 73:257-268.
  • [31]Mellor KM, Bell JR, Ritchie RH, Delbridge LM: Myocardial insulin resistance, metabolic stress and autophagy in diabetes. Clin Exp Pharmacol Physiol 2013, 40:56-61.
  • [32]Shimizu I, Minamino T, Toko H, Okada S, Ikeda H, Yasuda N, Tateno K, Moriya J, Yokoyama M, Nojima A, Koh GY, Akazawa H, Shiojima I, Kahn CR, Abel ED, Komuro I: Excessive cardiac insulin signaling exacerbates systolic dysfunction induced by pressure overload in rodents. J Clin Invest 2010, 120:1506-1514.
  • [33]Lee RJ, Hinson A, Helgerson S, Bauernschmitt R, Sabbah HN: Polymer-based restoration of left ventricular mechanics. Cell Transplant 2013, 22:529-533.
  • [34]Wisniacki N, Taylor W, Lye M, Wilding JP: Insulin resistance and inflammatory activation in older patients with systolic and diastolic heart failure. Heart 2005, 91:32-37.
  • [35]Kodama K, Tojjar D, Yamada S, Toda K, Patel CJ, Butte AJ: Ethnic differences in the relationship between insulin sensitivity and insulin response: a systematic review and meta-analysis. Diabetes Care 2013, 36:1789-1796.
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