European Heart Journal Advance Access originally published online on May 6, 2007
European Heart Journal 2007 28(13):1662-1663; doi:10.1093/eurheartj/ehm133
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Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study
Department of Ultrasound
The First Affiliated Hospital
College of Medicine
Zhejiang University
79 Qingchun Road
Hangzhou 310003
P.R. China
Tel/Fax: +86 571 8723 6628 E-mail address: zezhou_song{at}126.com
I read with great interest the study by Di Salvo et al.,1 which confirms significant changes in the longitudinal myocardial function of both right ventricle (RV) and left ventricle (LV) in healthy children with excess weight who have no other clinically appreciable cause of heart disease and that obesity, in the absence of hypertension, is associated with significant reduction in systolic myocardial deformation properties already in childhood involving both RV and LV, suggesting that obesity is not only a risk factor for later cardiovascular disease, but also is associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties. The methods and interpretation of the results, however, raise several concerns.
In this study,1 the authors provide observational findings that link obesity, insulin levels, and myocardial disturbances. The authors, however, did not well describe and provide the putative mechanisms that link obesity, insulin levels, and myocardial disturbances, which could affect the precise assessment of opportunity and modality of treatment to reverse the process of this disease. Wong et al.2 consider that a number of putative mechanisms may underlie these morphological changes. (i) Increased stroke volume and cardiac output lead to the dilatation of the heart chambers with eccentric LV hypertrophy. However, the mechanical advantage conferred by the compensatory reduction of myocardial fibre shortening is offset by a concomitant increase in myocardial oxygen consumption and ventricular wall stress. (ii) Insulin resistance may mediate the increased LV mass in obese subjects.3 Wong et al.2 demonstrate some correlation of LV systolic and diastolic measures to fasting insulin level, consistent with previous studies suggesting an association of LV diastolic function with hyperinsulinaemia and glucose intolerance.4 A study on young obese women further supported the notion that insulin resistance and alterations in myocardial substrate metabolism lead to myocardial contractile dysfunction associated with obesity.5 It has been proposed that insulin may also exercise its influence on cardiac geometry owing to its growth-stimulating, sodium retention, and other neuroendocrine effects. (iii) Adipose tissue may contribute to circulating angiotensin II,6 which promotes myocardial tissue growth as well as influences aldosterone, which may mediate myocardial fibrosis. (iv) Obstructive sleep apnoea is common in obese persons and may contribute to heart failure through several mechanisms. In the general community, obstructive sleep apnoea is associated with hypertension, although such patients were excluded from Di Salvo et al.1 and Wong et al.2 studies. Increases in afterload and wall stress associated with the generation of negative intrathoracic pressure during episodes of obstructive apnoea as well as inflammatory cytokines and sympathetic activation are potential mechanisms.7 Therefore, further work is needed to clarify the links between these alterations in the LV characteristics with insulin resistance, volume overload, changes in respiratory workload, and other metabolic mechanisms such as renal sodium retention, oxidative stress, and inflammatory cytokines.2 In conclusion, obesity is an independent risk factor for subclinical LV dysfunction. Better understanding of the pathophysiology of obesity-related LV characteristics will enable us to modify the disease process resulting in the regression of subclinical LV changes.
References
- Di Salvo G, Pacileo G, Giudice EMD, Natale F, Limongelli G, Verrengia M, Rea A, Fratta F, Castaldi B, D'Andrea A, Calabrò P, Miele T, Coppola F, Russo MG, Caso P, Perrone L, Calabrò R. Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study. Eur Heart J (2006) 27:2689–2695.
[Abstract/Free Full Text] - Wong CY, O'Moore-Sullivan T, Leano R, Byrne N, Beller E, Marwick TH. Alterations of left ventricular myocardial characteristics associated with obesity. Circulation (2004) 110:3081–3087.
[Abstract/Free Full Text] - Karason K, Sjostrom L, Wallentin I, et al. Impact of blood pressure and insulin on the relationship between body fat and left ventricular structure. Eur Heart J (2003) 24:1500–1505.
[Abstract/Free Full Text] - Mureddu GF, Greco R, Rosato GF, et al. Relation of insulin resistance to left ventricular hypertrophy and diastolic dysfunction in obesity. Int J Obes Relat Metab Disord (1998) 22:363–368.[CrossRef][Web of Science][Medline]
- Peterson LR, Herrero P, Schechtman KB, et al. Effect of obesity and insulin resistance on myocardial substrate metabolism and efficiency in young women. Circulation (2004) 109:2191–2196.
[Abstract/Free Full Text] - Engeli S, Negrel R, Sharma AM. Physiology and pathophysiology of the adipose tissue renin–angiotensin system. Hypertension (2000) 35:1270–1277.
[Abstract/Free Full Text] - Laaban JP, Pascal-Sebaoun S, Bloch E, et al. Left ventricular systolic dysfunction in patients with obstructive sleep apnea syndrome. Chest (2002) 122:1133–1138.[CrossRef][Web of Science][Medline]
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