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European Heart Journal Advance Access originally published online on August 11, 2006
European Heart Journal 2006 27(22):2689-2695; doi:10.1093/eurheartj/ehl163
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

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

Giovanni Di Salvo*, Giuseppe Pacileo, Emanuele Miraglia Del Giudice, Francesco Natale, Giuseppe Limongelli, Marina Verrengia, Alessandra Rea, Fiorella Fratta, Biagio Castaldi, Antonello D'Andrea, Paolo Calabrò, Tiziana Miele, Filomena Coppola, Maria Giovanna Russo, Pio Caso, Laura Perrone and Raffaele Calabrò

Second University of Naples, Via Omodeo 45, Naples 80128, Italy

Received 30 January 2006; revised 27 June 2006; accepted 6 July 2006; online publish-ahead-of-print 11 August 2006.

* Corresponding author. Tel: +39 (0) 81 193 638 51; fax: +39 (0) 81 560 56 48. E-mail address: giodisal{at}yahoo.it


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
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/height2.7 was increased (P<0.0001) in Group O (46±12 g/m2.7) when compared with Referents (31±14 gm2.7). 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/H2.7 (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.

Key Words: Children • Obesity • Systolic function • Strain rate imaging


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
The prevalence of obesity has increased dramatically in children and adolescents, in both the developed and developing worlds, becoming an important medical problem.1 Many of the outcomes of obesity have traditionally been viewed as problems of adulthood. However, it has become clear that many of these abnormalities 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 younger age.1,2 Obesity has been associated with heart failure,3 left ventricular (LV) dilation, increased LV wall stress, and compensatory (eccentric) LV hypertrophy.2,4 Most studies reported an abnormal diastolic function5–7 without consistent association with systolic dysfunction,5 and a spectrum of minor cardiovascular changes.2,3 These subclinical manifestations may be important, because treatment to reverse the process is most likely to be effective earlier in the disease.8 However, the reported changes may reflect the role of comorbidities that contribute to LV dysfunction [e.g. hypertension, diabetes, coronary artery disease (CAD), and obstructive sleep apnoea], as well as altered loading, especially, as conventional echo-Doppler measures are load-dependent.

A new echocardiography technique, strain (S) and strain rate (SR) imaging, has been added to our capabilities and has been proposed as strong index of myocardial contractility.9–11 SR imaging, 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 deformation of a tissue.9 Both are independent of overall heart motion, cardiac rotation, or motion induced by contraction in adjacent myocardial segments, and are a true measure of local deformation.9,10 Regional S and SR calculation has been shown to quantify regional myocardial function in normal children12 and in children with congenital heart disease.13–15 Moreover, it has been demonstrated that S and SR imaging are able to early detect subclinical myocardial abnormalities in adult patients with hypertension,16–18 diabetes,19,20 obesity,8 or metabolic syndrome,21 still in the presence of a normal LV ejection fraction (EF). Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the early effect of obesity, per se, on myocardial function, excluding the influence of possible comorbidities. We, therefore, sought to define in non-hypertensive children the preclinical effects of isolated obesity on the cardiovascular system, by examining LV function using the more sensitive ultrasonic-derived S and SR imaging.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Limitations
 Conclusions
 References
 
Patients
Non-syndromically obese children (age range of 6–15 years), with no history of hypertension, diabetes mellitus, endocrinological disorders, hereditary diseases, or systemic inflammatory diseases, were recruited from a specialist clinic for management of overweight and obesity, based at a tertiary university referral center. Children with habitual snoring and observed apnoea (according to parent recall) were excluded from the study. Obesity was defined when body mass index (BMI), calculated as weight in kilograms divided by the square of height in meters, exceeded the 97th percentile for sex and age according to the reference values.22 To exclude organic heart disease, patients underwent a clinical history and examination as well as resting and exercise stress ECG and transthoracic echocardiography. To allow interpretation of ambulatory blood pressure measurements (ABPM) data, by ABPM normative data,23 only children with a height between 115 and 185 cm were included. Only subjects with systolic (SBP) and diastolic blood pressure (DBP) (both in at least three different occasions) <90th percentile for age, sex, and height,24 and 24 h-SBP, 24 h-DBP <90th percentile for sex and height23 were included in the study. In all, we studied 300 subjects divided into two groups: (i) Obese children (Group O: n=150; mean age: 12±3 years); (ii) Referent healthy subjects, comparable for age and sex, recruited from the community with no family history of hypertension and obesity (Referents: n=150; mean age 12±3 years). The sample size in our study was based on previous studies8,24 as well as practicability. Volunteer controls were all recruited in Naples (Italy), were selected from our departments of paediatric cardiology among children investigated for dizziness, or minor orthostatic complaints, or for sport eligibility. None of the control subjects had cardiovascular structural or functional abnormalities or received any medication. We ensured comparability of the two groups using frequency matching,25 for age, sex, and pubertal status, approximately matching one patient with one control. All were non-smokers and without any pharmacologic treatment. The number of patients initially assessed for inclusion into the study was 300; of them 100 did not meet the inclusion criteria, 10 refused to give their informed consent, 20 refused to perform ABMP study, and 20 were excluded for poor image quality at standard echocardiographic evaluation. The number of Referents initially assessed for inclusion was 150; of them 22 refused to perform ABPM and were replaced by 22 new appropriate referents. All studies were performed in accordance with the rules of the Ethical Committee, Second University of Naples. All parents gave their written informed consent to participate in the study.

Clinical assessment
Demographic details of age, gender, and blood pressures (BP) were obtained from standard measurements and questionnaires. Anthropometric measurements (weight, height) were obtained, and BMI was calculated (body weight in kilograms divided by height in meters squared). The mean of the SD scores (Z-score) relative to BMI percentiles was 3.43±1.9 (range 2.1–8.3). The average age at obesity onset was 4.7±2.5 years (range 1–11 years). To assess the age of obesity onset during early childhood, the records of the patients were reviewed. In these records, the anthropometric measurements made in the paediatrician's surgeries within the ambit of children's health balances made annually are reported. Body weights were evaluated by balance beam scale, and wall-mounted stadiometers were used to measure the height. All the measurements were repeated twice.

The pubertal development was determined according to Marshall and Tanner and categorized into two groups (prepubertal: boys with pubic hair and gonadal stage I, girls with pubic hair stage and breast stage I; pubertal: boys with pubic hair and/or gonadal stage ≥ II and girls with pubic hair stage and/or breast stage ≥ II). The blood pressure was measured by one investigator using a validated protocol.23 SBP and DBP were measured twice at the right arm after a 10 min rest in the supine position using a calibrated sphygmomanometer and averaged. The cuff size, which was based on the length and circumference of the upper arm, was chosen to be as large as possible without having the elbow skin crease obstructing the stethoscope.26

Biochemistry
In all the obese children, insulin and glucose levels were measured (after an overnight fast >12 h). The insulin assay used a competitive protein-binding radioimmunoassay. Glucose was measured using the glucose-oxidase method with the Hitachi 704 Chemistry Analyzer. Inter- and intra-assay variations for the serum concentrations of these variables were <5%. Homeostasis model assessment of insulin resistance (HOMA-IR) measures, which correlate with estimates of insulin resistance measured by euglycaemic clamp technique, were used as index of insulin resistance.27

ABPM study
A SpaceLabs model 90207 monitor (SpaceLabs Inc., Redmond, WA, USA) weighing 340 g (including batteries) was used for ABPM. Our methodology for ABPM studies has already been extensively described.28

Echocardiographic image acquisition and analysis
Images were gathered with a standard ultrasound machine (GE System Seven) with a 3.5-MHz phased-array probe (M3S). All the echocardiographic studies were digitally stored and all the measurements were performed off-line by two independent observers (G.D.S. and F.N.) who were blind to the clinical status of the subjects.

Conventional Doppler echocardiography
Images were obtained in the standard tomographic views of the LV [parasternal long- and short-axis, apical four-chamber (A4C) and two-chamber views (A2C)]. Using pulsed-wave Doppler, mitral inflow velocities, peak early diastolic velocity (E), peak late diastolic velocity (A), E/A ratio, E deceleration time (DT), A wave DT, A duration, and isovolumic relaxation time (IVRT) were measured. The pulmonary venous flow was examined with the sample volume positioned just at the orifice of the right upper pulmonary vein. The following Doppler velocities were obtained: peak velocity during ventricular systole (Sp), peak velocity during ventricular diastole (Dp), their ratio, and the peak reverse flow (Ap). Left atrium (LA) width was measured during systole along the parasternal long-axis (PLAX) view from the two-dimensional-guided M-mode tracing. LV diameter and wall thickness were measured from the two-dimensional targeted M-mode echocardiographic tracings in the parasternal short axis, according to the criteria of the American Society of Echocardiography.29 LV end-diastolic and end-systolic volumes and the LVEF at rest were computed from A2C and A4C views, using a modified Simpson's biplane method. Each representative value was obtained from the average of three measurements. LV mass was determined and indexed to height (meters) to the power of 2.7.30 LV end-systolic circumferential wall stress was calculated according to a previously validated formula.31 To assess global right ventricular (RV) longitudinal function, from the standard apical view, the atrioventricular ring displacement was measured for lateral tricuspid ring (TAPSE) by conventional M-mode methods.32 RV pressure was estimated from the velocity in the tricuspid regurgitant jet, always adding 10 mmHg as estimate of right atrial pressure.33 Intima-media thickness (IMT) was measured at the common carotid artery according to a previously described procedure.34

Colour Doppler myocardial imaging study
Real-time two-dimensional colour Doppler myocardial imaging data to assess longitudinal function were recorded from the interventricular septum and the LV inferior wall from standard apical views. We studied these two walls because they had the best alignment to the direction of longitudinal motion. Radial function for the LV posterior wall was recorded using PLAX view. RV regional longitudinal function was studied from RV free wall from the A4C view. All data were acquired at a frame rate of 200±15 frames/s (GE, System Seven; 3.5 MHz). This frame rate was necessary to resolve cardiac mechanical events and to average out the influence of any random noise in the Doppler velocity signal. An appropriate velocity scale was chosen to avoid colour Doppler myocardial imaging data aliasing. The narrowest image sector angle possible (usually 30°) was used to achieve the maximum colour Doppler frame rate possible.

For apical views, care was taken to maintain each wall in the centre of the ultrasound sector in an attempt to align, as near as possible, to the direction of longitudinal motion. For parasternal view, care was paid to keeping the posterior LV wall perpendicular to the ultrasound beam to be aligned, as near as possible, to radial motion. Data from three consecutive cardiac cycles (to be used for subsequent analysis) were recorded during normal quiet respiration. Pulsed-wave tissue Doppler of the septal annulus was used for the measurement of early peak diastolic mitral annular velocity (e'). The E/e' ratio was calculated.

Offline analysis
Colour Doppler myocardial imaging data were stored in digital format and analysed offline using dedicated software (Echopac, GE Vingmed, Horten, Norway). From this one-dimensional ultrasound data set, three parameters were calculated: local velocity, local SR, and its integral, local S. Myocardial velocity measures the local motion of a tissue, SR the local rate of deformation, and S determines the total amount of local deformation of a tissue. Longitudinal SRs were estimated by measuring the spatial velocity gradient over a computation area of 7 mm. Radial SRs were estimated using a computation area of 3 mm. To derive SR profiles from the different segments, the region of interest was maintained in a constant position within the segment being interrogated using a proprietary semi-automated tracking algorithm. End-diastole was defined to be at the onset of the electrocardiographic QRS complex. The timing of ventricular ejection was obtained using an anatomic grey scale M-mode cursor positioned visually in the underlying gray scale data set. The timing of this event was measured by placing the cursor at the level of aortic/pulmonary cusps, for the LV and RV, respectively. From the averaged data, peak systolic S, SR, and myocardial velocity values were measured.

Statistics
All the analyses were performed using a commercially available package (SPSS, Rel 11.0 2002, Chicago: SPSS Inc.). Qualitative data were compared using Mantel–Haenszel's test. Continuous variables were compared using paired t-test and Wilcoxon matched pairs test. The correlations were studied by linear regression analysis. In addition, to identify significant predictors of average LV peak systolic S and SR in obese children, their individual association with clinical relevant variables was assessed by multivariable Cox regression analyses. The following variables were included into the analysis: clinical data (duration of obesity, BMI, SBP, 24 h-SBP), biochemical parameters (HOMA-IR, insulin serum concentration, glycaemia), echocardiographic indexes (LVM/H2.7, LV diameters, IVRT, carotid IMT). These variables were selected according to their clinical relevance and potential impact on prognosis, as shown by earlier studies.1–4 Variable selection was performed in the multivariable Cox regression as an interactive stepwise backward elimination method, each time excluding the one variable with the highest P-value according to Wald statistics. The assumption of linearity was checked graphically by studying the smoothed martingal residuals from the null model plotted against the covariate variables. The linearity assumptions were satisfied. The Hosmer–Lemeshow goodness-of-fit test was used to check that the model adequately fit the data. Model was cross-validated by the bootstrap technique (200 runs).35 The null hypothesis was rejected for a P-value<0.01. Reproducibility was determined in 60 randomly selected subjects (30 patients and 30 controls). Inter- and intra-observer variability was examined using both Pearson's bivariate two-tailed correlations and Bland-Altman analysis. Relation coefficients, 95% confidence limits, and percent errors were reported.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Limitations
 Conclusions
 References
 
Clinical characteristics
Table 1 summarizes the clinical characteristics of the two groups. The normal lean children did not significantly differ from obese children in age, sex, pubertal stage, heart rate, and BP.


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  		Table 1 General characteristics of the studied sample

 
Standard echocardiographic study
LV mass corrected for height2.7 was increased (P<0.0001) in Group O when compared with Referents (Table 2). LV and LA diameters were significantly increased in obese children when compared with Referents. Global indices of systolic function were similar in the two groups. IVRT was significantly (P<0.0001) prolonged in obese children when compared with Referents. LV end-systolic circumferential wall stress was significantly (P<0.0001) increased in obese children when compared with Referents. IVRT significantly correlated with BMI (P=0.007; r=0.54). Mitral annular velocity (e'), and E/e' were significantly different between obese children and Referents (P<0.0001), and significantly correlated with BMI (P=0.003; r=0.68; P=0.01; r=0.61, respectively). RV pressure and RV global systolic function, assessed by TAPSE, were similar between groups (P=0.2). Common carotid IMT was not significantly increased in obese children (P=0.4). No significant correlations were found between IMT and BMI, fasting glucose and insulin serum concentrations, HOMA-IR and duration of obesity. A 24 h-SBP was significantly correlated with IMT.


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  		Table 2 Standard echocardiographic characteristics of the studied sample

 
CDMI study
All the S and SR tracings were acceptable for the analysis. There were significant (P<0.0001) differences between Referents and the obese children for regional longitudinal myocardial deformation properties (Tables 3 and 4), whereas radial deformation properties were similar (Tables 3 and 4). RV deformation properties were significantly reduced in Group O when compared with Referents (Tables 3 and 4). No significant post-systolic shortening was found in our patients. Peak systolic myocardial velocities were not significantly different between Group O and Referents (Table 5).


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  		Table 3 Peak systolic SR (s–1) values of the studied sample

 

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  		Table 4 Peak systolic strain (%) values of the studied sample

 

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  		Table 5 Peak systolic myocardial velocity (cm/s) values of the studied sample

 
Average longitudinal myocardial SR was significantly correlated with HOMA-IR (P=0.006; r=0.21), insulin serum concentration (P=0.007; r=0.19), duration of obesity (P=0.0055; r=0.19), and LVM/H2.7 (P=0.006; r=0.21). Average longitudinal S was significantly correlated with BMI (P=0.003; r=0.45), duration of obesity (P=0.006; r=0.54), and LVM/H2.7 (P=0.006; r=0.58).

Reproducibility
Pearson's correlations—peak systolic SR: r=0.88, P=0.0001; peak systolic S: r=0.92, P=0.00001; carotid IMT: r=0.95, P<0.00001. Bland–Altman analysis—peak systolic SR (95%CI+3.1, percent error 3.5%); peak systolic S (95%CI+2.5, percent error 2.3%); carotid IMT (95%CI+2.1, percent error 2.2%).

Multivariable analysis
In multivariable analysis, average LV peak systolic SR was significantly correlated with HOMA-IR (P=0.0003; coefficient, 0.02; SE, 0.011), insulin serum concentration (P=0.006; coefficient, 0.05; SE, 0.023), whereas BMI, LVM/H2.7, duration of obesity, IMT, 24 h-SBP, SBP, glycaemia, LV diameters, and IVRT were not significantly correlated. Average LV peak systolic S was significantly correlated with BMI (P=0.0001; coefficient, 0.06; SE, 0.016), LVM/H2.7 (P=0.006; coefficient, 0.016; SE, 0.018), whereas HOMA-IR, insulin serum concentration, duration of obesity, IMT, 24 h-SBP, SBP, glycaemia, LV diameters, and IVRT were not significantly correlated.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Limitations
 Conclusions
 References
 
To the best of our knowledge, this is the first attempt of using S and SR in obese children. The results of this study show significant changes in the longitudinal myocardial function of both RV and LV in healthy children with excess weight who have no other clinically appreciable cause of heart disease. Our findings indicate that obesity, in the absence of hypertension, is not only a risk factor for later cardiovascular disease, but is also associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties.

Standard echocardiographic study
In our study, the standard echocardiographic evaluation of obese, non-hypertensive children showed well-known morphological findings, such as larger LV and LA diameters, increased LV end-systolic circumferential wall stress, and LVM/H2.7,2–6 although almost all within the normal range. The evaluation of global LV systolic function assessed by LVEF, and global RV function assessed by TAPSE were not able to detect any significant difference between healthy lean children and obese children. Parameters of diastolic function were significantly different in obese children (Table 2) when compared with Referents in agreement with previous studies.3,4

Although the increased preload may influence all these parameters, these significant LV structural and diastolic differences indicate an early sign of cardiac pathology, not yet reflected in robust indices of global systolic function (such as LVEF, peak systolic myocardial velocities), but already detectable by myocardial deformation parameters.

IMT in childhood obesity
The measurement of IMT of the common carotid artery is an acknowledged non-invasive marker for early atherosclerotic changes.36 Whether the thickness of arterial wall increases with BMI is still a matter of debate. Tounian et al.37 reported no statistically significant difference between carotid IMT in 48 children with severe obesity, but normal BP values and lean controls. Conversely, other studies38–43 demonstrated a significant increase in carotid IMT in obese children when compared with lean controls. However, in these studies a strong association between IMT and BP is reported,38,40 and some of these studies included obese children with hypertension,39,40 or with blood pressure values significantly increased when compared with their referents.40 In addition, in most of these studies38,40–43 only casual BP measurements were performed, and in three series38,39,41 a small number of obese children (n<45) were included. In our study, carotid IMT was significantly correlated with 24 h-SBP, but without a statistical difference between obese and lean children. This may be explained by the exclusion of hypertensive obese children from our studied cohort, and may suggest that carotid IMT increases in obese children only when hypertension develops.

Regional systolic myocardial function
Obese children presented significant reduction in peak systolic longitudinal S and SR values in both RV and LV when compared with Referents. As previously demonstrated in a mathematical model,44 peak systolic S and SR values increase with increasing preload as long as contractile function is preserved, and decrease if intrinsic contractility is reduced. Thus, we would have expected an increase in peak systolic S and SR in obese children because of volume overload. Conversely, the significant reduction in systolic myocardial deformation properties we found, suggests that during childhood, obesity, in the absence of hypertension, significantly influence regional myocardial systolic function.

This was confirmed by the significant correlation between SR, HOMA, and insulin serum concentration. Our results are different from previous standard echocardiographic studies, which demonstrates that LV systolic function is preserved in obese patients.4–6 This result may be explained by the low sensitivity of the techniques used, in previous reports, for the assessment of systolic function, such as LVEF, which was normal also in our study. In several clinical and experimental studies, SR demonstrated a superior sensitivity than LVEF and myocardial velocities in detecting early systolic changes.9,13–21

Our data is in agreement with an SR imaging study in 83 obese adult patients.8 However, in this series, the effect of comorbidities cannot be completely excluded, as no ABPM study was performed and CAD was excluded only by exercise ECG in a cohort of obese adults with a mean age >40 years. Indeed, casual BP measurements were characterized by high variability and a small number of measurements obtained in a medical setting may not necessarily reflect the habitual BP of an individual.45 Several investigators have argued that values obtained from ABPM are more indicative of cardiovascular risk than those obtained from casual measurements,45 even in patients completely normotensive by standard criteria.46

Studying the effect of obesity in children, without hypertension (as assessed by both casual BP measurements and ABPM) and without other clinically appreciable cause of heart disease, might have offered the unique clinical opportunity to exclude the influence of possible comorbidities on the evaluation of ventricular function.

In our study of univariate analysis there was a significant correlation between SR and duration of overweight. This finding is in agreement with Nakajima et al.47 demonstrating that LV stroke index was significantly lower in those who had been obese for ≥15 years. Alpert et al.48 showed that in obese patients, with a duration of morbid obesity from 5 to 28 years, duration of morbid obesity is an important determinant of LV mass, systolic function, and diastolic filling. Of note, in our study, LVEF was not correlated with the duration of obesity, probably for the shorter duration of obesity in our sample than in previous studies, and for the lower sensitivity of LVEF (compared with SR imaging) in assessing early systolic abnormalities. The correlation between SR and duration of obesity may suggest that even few years of obesity are able to significantly impair myocardial regional systolic function. This study provides observational findings that may link obesity, insulinaemia, insulin resistance, and abnormal longitudinal myocardial function.


   Limitations
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
Conclusions
 References
 
This study carries some limitations: the ‘gold standard’ for screening of obstructive sleep apnoea in children is sleep polysomnography. Thus, we cannot exclude that undiagnosed obstructive sleep apnoea may have been present in some children, but overnight polysomnography was regarded as impractical in our study. Nonetheless, habitual snoring and observed apnoea were shown to be important symptoms of obstructive sleep apnoea and children with these two symptoms were excluded from the present study. Usual limitations about S, SR, and the angle dependence should be considered.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
References
 
Our study demonstrated that obesity, in the absence of hypertension, is associated with significant changes in myocardial deformation properties already in childhood involving both RV and LV. Thus, childhood obesity is not only a risk factor for later cardiovascular disease, but is also associated with contemporaneous and significant impairment of longitudinal myocardial deformation properties. Our data support the prevention of obesity in paediatric age, because already in childhood, obesity is responsible for significant changes in systolic myocardial function.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 

  1. Sorof J and Daniels S. (2002) Obesity hypertension in children: a problem of epidemic proportions. Hypertension 40:441–447.[Abstract/Free Full Text]
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  4. Pascual M, Pascual DA, Soria F, Vicente T, Hernandez AM, Tebar FJ, Valdes M. (2003) Effects of isolated obesity on systolic and diastolic left ventricular function. Heart 89:1152–1156.[Abstract/Free Full Text]
  5. Scaglione R, Dichiara MA, Indovina A, Lipari R, Ganguzza A, Parrinello G, Capuana G, Merlino G, Licata G. (1992) Left ventricular diastolic and systolic function in normotensive obese subjects: influence of degree and duration of obesity. Eur Heart J 13:738–742.[Abstract/Free Full Text]
  6. Chakko S. (1998) In Alpert MAAJ (Ed.). Obesity and Ventricular Function in Man: Diastolic Function(Armonk, New York, NY, USA) pp. 57–76.
  7. Zarich SW, Kowalchuk GJ, McGuire MP, Benotti PN, Mascioli EA, Nesto RW. (1991) Left ventricular filling abnormalities in asymptomatic morbid obesity. Am J Cardiol 68:377–381.[CrossRef][Web of Science][Medline]
  8. Wong CY, O'Moore-Sullivan T, Leano R, Byrne N, Beller E, Marwick TH. (2004) Alterations of left ventricular myocardial characteristics associated with obesity. Circulation 110:3081–3087.[Abstract/Free Full Text]
  9. Sutherland GR, Di Salvo G, Claus P, D'hooge J, Bijnens B. (2004) Strain and strain rate imaging: a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr 17:788–802.[CrossRef][Web of Science][Medline]
  10. Urheim S, Edvardsen T, Torp H, Angelsen B, Smiseth OA. (2000) Myocardial strain by Doppler echocardiography: validation of a new method to quantify regional myocardial function. Circulation 102:1158–1164.[Abstract/Free Full Text]
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