Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study.

AIMS: The prevalence of obesity is increasing among children in the developed world. The association of obesity and abnormal cardiac function is still debated. The reported changes may reflect the role of comorbidities that contribute to ventricular dysfunction. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the cardiovascular system, of healthy children with excess weight who have no other clinically appreciable cause of heart disease, using the more sensitive ultrasonic-derived strain and strain rate (SR) imaging. METHODS AND
RESULTS: We studied 300 subjects divided into two groups: (i) obese children (Group O: n=150; age, 12+/-3 years); (ii) healthy lean children comparable for age, sex, and pubertal stage (Referents: n=150; mean age, 12+/-3 years). Systolic (SBP) and diastolic blood pressure (DBP), as well as 24 h-SBP and 24 h-DBP were comparable between groups. Left ventricular (LV) mass/height(2.7) was increased (P<0.0001) in Group O (46+/-12 g/m(2.7)) when compared with Referents (31+/-14 gm(2.7)). Standard echocardiographic indices of global systolic function were similar in the two groups. Intima-media thickness measured at the common carotid artery was not significantly different (P=0.4) in obese children (0.46+/-0.09 mm) when compared with Referents (0.45+/-0.07 mm). Obese children showed regional longitudinal peak systolic myocardial deformation properties (SR=-1.4+/-0.7 s(-1)) lower (P<0.0001) than those of Referents (SR=-2.2+/-0.5) in both left and right ventricle. In multivariable analysis, average peak systolic SR was significantly correlated with homeostasis model assessment of insulin resistance (P<0.01; coefficient, 0.02; SE, 0.011), and insulin serum concentration (P<0.01; coefficient, 0.05; SE, 0.023). Average LV peak systolic strain was significantly correlated with body mass index (P=0.0001; coefficient, 0.06; SE, 0.016), LVM/H(2.7) (P=0.006; coefficient, 0.016; SE, 0.018).
CONCLUSIONS: Our study demonstrated that obesity, in absence of hypertension, is associated with significant reduction in systolic myocardial deformation properties already in childhood involving both right and left ventricle. Obesity not only is a risk factor for later cardiovascular disease, but also is associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties.