Exercise training does not improve myocardial diastolic tissue velocities in Type 2 diabetes

被引:35
作者
Loimaala A. [1 ]
Groundstroem K. [2 ]
Rinne M. [3 ]
Nenonen A. [4 ]
Huhtala H. [5 ]
Vuori I. [3 ]
机构
[1] Clinical Physiology and Nuclear Medicine, Seinäjoki Central Hospital, Seinäjoki
[2] Department of Medicine, Kymenlaakso Central Hospital, Kotka
[3] UKK Institute for Health Promotion Research, Tampere
[4] Clinical Chemistry, Rheumatism Foundation Hospital, Heinola
[5] School of Public Health, University of Tampere
关键词
Fabry Disease; Tissue Doppler Image; Systolic Strain; Tissue Velocity; Early Diastolic Velocity;
D O I
10.1186/1476-7120-5-32
中图分类号
学科分类号
摘要
Background. Myocardial diastolic tissue velocities are reduced already in newly onset Type 2 diabetes mellitus (T2D). Poor disease control may lead to left ventricular (LV) systolic dysfunction and heart failure. The aim of this study was to assess the effects of exercise training on myocardial diastolic function in T2D patients without ischemic heart disease. Methods. 48 men (52.3 ± 5.6 yrs) with T2D were randomized to supervised training four times a week and standard therapy (E), or standard treatment alone (C) for 12 months. Glycated hemoglobin (HbA1c), oxygen consumption (VO2max), and muscle strength (Sit-up) were measured. Tissue Doppler Imaging (TDI) was used to determine the average maximal mitral annular early (Ea) and late (Aa) diastolic as well as systolic (Sa) velocities, systolic strain (ε) and strain rate () from the septum, and an estimation of left ventricular end diastolic pressure (E/Ea). Results. Exercise capacity (VO2max, E 32.0 to 34.7 vs. C 32.6 to 31.5 ml/kg/min, p = .001), muscle strength (E 12.7 to 18.3 times vs. C 14.6 to 14.7 times, p < .001), and HbA1c(E 8.2 to 7.5% vs. C 8.0 to 8.4%, p = .006) improved significantly in the exercise group compared to the controls (ANOVA). Systolic blood pressure decreased in the E group (E 144 to 138 mmHg vs. C 146 to 144 mmHg, p = .04). Contrary to risk factor changes diastolic long axis relaxation did not improve significantly, early diastolic velocity Ea from 8.1 to 7.9 cm/s for the E group vs. C 7.4 to 7.8 cm/s (p = .85, ANOVA). Likewise, after 12 months the mitral annular systolic velocity, systolic strain and strain rate, as well as E/Ea were unchanged. Conclusion. Exercise training improves endurance and muscle fitness in T2D, resulting in better glycemic control and reduced blood pressure. However, myocardial diastolic tissue velocities did not change significantly. Our data suggest that a much longer exercise intervention may be needed in order to reverse diastolic impairment in diabetics, if at all possible. © 2007 Loimaala et al; licensee BioMed Central Ltd.
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共 29 条
[1]  
Burchfiel C.M., Reed D.M., Marcus E.B., Strong J.P., Hayashi T., Association of diabetes mellitus with coronary aterosclerosis and myocardial lesions: An autopsy study from the Honolulu Heart Program, Am J Epidemiol, 137, pp. 1328-1340, (1993)
[2]  
Uusitupa M., Mustonen J.N., Airaksinen K.E., Diabetic heart muscle disease, Ann Med, 22, pp. 377-386, (1990)
[3]  
Diabetes Control T., Trial Research Group C., The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin dependent diabetes mellitus, N Engl J Med, 329, pp. 977-986, (1993)
[4]  
Rubler S., Dlugash J., Yeceoglu Y.Z., Kumral T., Branwood A.W., Grishman A., New type of cardiomyopathy associated with diabetic glomerulosclerosis, Am J Cardiol, 30, pp. 595-602, (1972)
[5]  
Loimaala A., Groundstroem K., Majahalme S., Nenonen A., Vuori I., Impaired myocardial function in newly onset Type 2 diabetes associates with arterial stiffness, Eur J Echocardiography, 7, 5, pp. 341-347, (2006)
[6]  
Fang Z.Y., Yuda S., Anderson V., Short L., Case C., Marwick T.H., Echocardiographic detection of early diabetic myocardial disease, J Am Coll Cardiol, 41, pp. 611-617, (2003)
[7]  
Vinereanu D., Nicolaides E., Boden L., Payne N., Jones C.J.H., Fraser A.G., Conduit arterial stiffness is associated with impaired left ventricular subendocardial function, Heart, 89, pp. 449-451, (2003)
[8]  
Hillis G.S., Moller J.E., Pellikka P.A., Gersh B.J., Wright R.S., Ommen S.R., Reeder G.S., Oh J.K., Noninvasive estimation of left ventricular filling pressure by E/e' is a powerful predictor of survival after acute myocardial infarction, J Am Coll Cardiol, 43, pp. 360-367, (2004)
[9]  
Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS33), Lancet, 352, pp. 837-852, (1998)
[10]  
Patel R., Nagueh S.F., Tsybouleva N., Abdellatif M., Lutucuta S., Kopelen H.A., Quinones M.A., Zoghbi W.A., Entman M.L., Roberts R., Marian A.J., Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy, Circulation, 104, pp. 317-324, (2001)