Atrial Myocardial Deformation Properties in Obese Nonhypertensive Children Giovanni Di Salvo, MD, PhD, FESC, Giuseppe Pacileo, MD, Emanuele Miraglia Del Giudice, MD, Francesco Natale, MD, Giuseppe Limongelli, MD, PhD, Marina Verrengia, MD, Alessandra Rea, MD, Fiorella Fratta, MD, Biagio Castaldi, MD, Simona Gala, MD, Filomena Coppola, MD, Maria Giovanna Russo, MD, Pio Caso, MD, FESC, Laura Perrone, MD, and Raffaele Calabro’, MD, Naples, Italy Background: Obesity in adulthood is associated with a higher occurrence of atrial arrhythmias. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on atrial myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the atrial function of healthy children with excess weight who have no other clinically appreciable cause of heart disease, by using the more sensitive ultrasonic- derived strain (S) and S rate imaging. Methods: We studied 320 children divided into two groups: obese children (group O; n = 160; age 12 3 years); and healthy lean children, comparable for age, sex, and pubertal stage (referents; n = 160; mean age 12 3 years). Results: Systolic blood pressure (BP) and diastolic BP, as well as 24-hour systolic BP and 24-hour diastolic BP were comparable between groups. Left ventricular mass/height 2.7 and left atrial dimensions were increased (P .0001) in group O (46 12 g\m 2.7 ) compared with referents (31 14 g\m 2.7 ). Standard echocardiographic indices of global left ventricular systolic function were similar in the two groups. Obese children showed atrial peak systolic S rate (2.5 1.2 s-1 ) values lower (P .0001) than that of referents (4.9 1.6 s-1 ) in both left and right atria. In multivariable analysis, average peak systolic atrial S was significantly correlated with glycemia (P .05, coefficient -0.23), body mass index (P .01, coefficient -0.19), and left ventricular mass (P .05, coefficient -0.17). Conclusions: Our study demonstrated that obesity, in absence of hypertension, is associated with reduced atrial myocardial deformation properties already in childhood involving both right and left atria. The prevalence of obesity has increased dramatically in children and adolescents in both the developed and developing worlds, becoming an important medical problem. 1 It has become clear that many of the cardiovascular abnormalities related to obesity may begin in childhood and adolescence. 1 This is a major concern because many of the processes that lead to morbidity and mortality are slow and chronic. Beginning the disease process earlier in life suggests that morbidity and mortality may occur at a younger age. 1,2 Obesity is associated with an increased risk of atrial fibrillation or flutter 3-5 and recently it has been suggested that atrial fibrillation and atrial flutter should be added to the list of diseases caused by obesity. 4 The incidence of atrial fibrillation has been increasing in the last decades. This increase in incidence can have many causes, and the increasing body mass index (BMI) in the general population may have contributed to the increasing incidence of atrial fibrillation. 4 Several studies in adults already demonstrated that BMI is strongly associated with atrial size and this has been confirmed also in children with hypertension, 6 however, to our knowledge no information is available on atrial function in obese nonhypertensive children. Although atrial fibrillation is uncommon in childhood, obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the early effect of obesity, per se, on atrial morphology and function, excluding the influence of possible comor- bidities. A new echocardiography technique, strain (S) and S rate (SR) imaging, has been added to our capabilities 7-9 and has been proposed as strong index of atrial reservoir function. 10 SR, which reflects the rate of myocardial deformation, has been developed by estimating the spatial gradients in myocardial velocities, whereas S, its integral, determines the total amount of local deforma- tion of a tissue. 7 Both are independent of overall heart motion, cardiac rotation, or motion induced by contraction in adjacent myo- cardial segments, and are a true measure of local deformation. 8,9 Tissue Doppler velocities can be used to obtain an estimate of SR and, from that, of S. It can be mathematically shown that for small (0.1%) instantaneous changes in length, SR can be calculated from From the Second University of Naples, Naples, Italy. Reprint requests: Giovanni Di Salvo, MD, PhD, FESC, Via Omodeo 45, Naples 80128, Italy (E-mail: giodisal@yahoo.it). 0894-7317/$34.00 Copyright 2008 by the American Society of Echocardiography. doi:10.1016/j.echo.2007.05.028 151