Abstract
Background
Obesity is becoming an epidemic threat for the individual and society. The increasing prevalence of overweight children and adolescents is likely to have a great impact on the future cardiovascular health of these subjects. Obesity is a strong risk factor for cardiovascular morbidity and mortality. Cardiac abnormalities of obese children and adolescents include the echocardiographically revealed early and preclinical LV or septal hypertrophy, and left or right ventricular dysfunction. Most of these abnormalities, which are usually more pronounced in patients with morbid obesity, can be partially reversed after weight reduction.
Aim of the study
Evaluate early echocardiography changes in obese children and whether these cardiac abnormalities reverse with significant weight reduction in children and adolescents or not.
Methods
We started this study by 50 obese children and adolescents and 30 non obese controls matched for age and sex. BMI was calculated. Complete echocardiographic study was performed on each patient and control subject. Hematological and biochemical variables were determined in the obese subjects from fasting blood samples and included glucose, total cholesterol, triglycerides (TG), HDL cholesterol and LDL cholesterol. All our patients’ strict dietetic regime with exercises for 6 months. After 6 months full examination, including all measurements and echocardiography and laboratory investigations were done again.
Results
Obese children has abnormalities of left ventricle structure and function (consisting of increased left ventricular wall dimensions and mass and alteration of diastolic function) that can be detected by echocardiography. Furthermore, (parameters of lipid metabolism) were found to be independent predictors of adverse LV remodeling and of diastolic dysfunction. As well as this study provides evidence that abnormalities of left ventricular wall dimension and mass in obese children and adolescents can improve with significant weight reduction.
Conclusion
This study has demonstrated that young, obese children and adolescents have early significant changes in left ventricular wall dimensions and early diastolic filling compared with non obese and this changes are reversible with weight reduction.
Keywords: Obesity, Overweight, Echocardiography, Diet, Exercise, Children, Adolescent
1. Introduction
Obesity in childhood one of the most major clinical and public health problem in most developed countries and is rapidly becoming so in developing countries. Over the past several decades, there is a 3-fold increase in the prevalence of obesity in childhood (Mokdad et al., 1999; de Simone et al., 1992). In the United States, approximately 31.2% of children (aged 6–11) are overweight of which 15.8% are obese. For adolescents (aged 12–19), 30.9% are overweight of which 16.1% are obese (Hedley et al., 2004).
The definition of obesity in children involves BMIs greater than the 85th (commonly used to define overweight) or the 95th (commonly used to define obesity) percentile, respectively, for age-matched and sex-matched control subjects (Xanthaxos and Inge, 2007).
It is well established that obesity is a strong risk factor for cardiovascular morbidity and mortality. Cardiac abnormalities of obese children and adolescents include the echocardiographically revealed early and preclinical LV or septal hypertrophy, and left or right ventricular dysfunction. (Goran and Gower, 1998; Caprio, 2002; Steinberger and Daniels, 2003). Most of these abnormalities, which are usually more pronounced in patients with morbid obesity, can be partially reversed after weight reduction. (Hennekens et al., 2007; Aggoun, 2007) regardless of a concomitant change in blood pressure (Weiss et al., 2004).
In addition, obesity is associated with a heterogeneity of metabolic abnormalities (e.g., dyslipidemia Goran and Gower, 1998, insulin resistance (Caprio, 2002), hyperglycaemia and hypertension (Steinberger and Daniels, 2003).
Little is known about the reversibility of early cardiac abnormalities in obese children and adolescents after weight reduction by diet and exercise.
Purpose of this study was to evaluate early echocardiography changes in obese children and whether these cardiac abnormalities reverse with significant weight reduction children and adolescents or not.
2. Methods
We started this study be 50 obese children and adolescents and 30 non-obese controls matched for age and sex from the outpatient clinic Al Jedaani Hospital in the period from April 2006 to 2008 according to the criteria below:
Inclusion criteria:
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Age > 6 and <18 years.
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BMI > 95 percentile for age and sex (BMI = weight/height2, where weight is in kilograms and height is in meters.
Exclusion criteria:
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Congenital heart disease.
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Significant concomitant illness.
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Medication known to modify cardiac function.
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Obvious clinical signs of cardiac disease.
Patient weight, height, gender, and age, were recorded at the time of the first echocardiogram. Weights were obtained without shoes, in light clothing, with a digital scale. Systolic (SBP) and diastolic blood pressure (DPB) was measured by the cuff method (Dinamap automated vital signs monitor, Criticon, Norderstedt, Germany). BMI was calculated using the formula (body weight in kilograms)/(body height in meters) (Hedley et al., 2004). Hematological and biochemical variables were determined in the obese subjects from fasting blood samples and included glucose, total cholesterol, triglycerides (TG), HDL cholesterol and LDL cholesterol.
2.1. Echocardiographic measurements
Complete echocardiographic study was performed on each patient and control subject. Guided by two-dimensional echocardiography, standard M-mode recordings of the left ventricle (LV) dimensions and function were obtained. The LV mass (LVM) and relative posterior wall thickness were calculated according to the formulae of Devereux et al. (1984). Conventional Doppler tracings of the mitral and the tricuspid valve and pulmonary venous return flow were obtained from an apical 4-chamber view (Tei et al., 1995).
All our patients’ strict dietetic regime with exercises for 6 months.
2.2. Dietary intervention
Both groups (children and parents) participated in the same diet education program and were interviewed by the same dietitian, who was blinded to the exercise program. The diet prescribed was a balanced hypocaloric diet that provided 900–1200 kcal daily. The menu varied according to the child’s age and eating habits. It was low in fat (20–25%), high in complex carbohydrate (50–60%), and sufficient in protein (25–30%) to support growth. A 3-day dietary recording was done by the children with the help of their parents at baseline and before each scheduled follow-up. Compliance for follow-up attendance was 85% and for dietary advice 80%.
2.3. Exercise training
A fitness assessment test was carried out before the commencement of the program. Each child’s exercise ability was measured, and customized training was prescribed by trained physiotherapists. The exercise sessions were all carried out in the hospital and supervised by the same physiotherapist team and was of circuit style, with a preset sequence of 18 workout stations; each child had to go through 9 stations in each session, twice per week for 6 weeks and then once weekly for one year. Each training session lasted 75 min, including 10 min of warm up, 30 min of resistance training, 10 min of aerobic exercise, 10 min of agility training, 5 min of cool-down, and short rest periods between stations. Participation in the exercise training program averaged 83% of scheduled visits during the first 6 weeks and 80% for subsequent visits.
After 6 months full examination, including all measurements and echocardiography and laboratory investigations were done again.
Only 40 patients from previously examined patients were continue the dietetic and exercise intervention from those 40 patients 30 patients BMI became <85% percentile and the remaining 10 patients BMI became >85% percentile excluded from the study.
2.4. Statistical analysis
Data are summarized using means and standard deviations, unless indicated otherwise. Means of obese and nonobese subjects were compared using an unpaired t test. A p value of ⩽0.05 was considered statistically significant.
3. Results
See Tables 1–6.
Table 1.
Clinical characteristics of the studied cases.
| Non-obese (n = 50) | Obese (n = 30) | p value | |
|---|---|---|---|
| Age | 11.5 ± 3.4 | 11.2 ± 2.9 | >0.5⁎ |
| Sex (boys/girls) | 24/26 | 13/17 | >0.5⁎ |
| weight | 33.8 ± 8.4 | 57.9 ± 14.8 | <0.001⁎⁎ |
| BMI (kg/m2) | 17.3 ± 2.8 | 28.4 ± 8.3 | <0.001⁎⁎ |
| Systolic blood pressure (mm Hg) | 112 ± 15 | 130 ± 14 | <0.001⁎⁎ |
| Diastolic blood pressure (mm Hg) | 60 ± 10 | 71 ± 12 | <0.001⁎⁎ |
| Heart rate | 80 ± 12 | 84 ± 11 | >0.5⁎ |
BMI, body mass index; BMI-SDS, BMI standard deviation scores; BSA, body surface area.
Insignificant.
Significant.
Table 2.
Laboratory results of the studied cases.
| Non-obese (n = 50) | Obese (n = 30) | p value | |
|---|---|---|---|
| Total cholesterol (mg/dl) | 154 ± 28.2 | 188 ± 32.4 | <0.01⁎⁎ |
| HDL cholesterol (mg/dl) | 50.4 ± 5.5 | 46.7 ± 6.2 | <0.01⁎⁎ |
| Triglycerides (mg/dl) | 108.4 ± 25.1 | 125.4 ± 30.6 | <0.01⁎⁎ |
| LDL cholesterol (mg/dl) | 92.8 ± 22.7 | 115.3 ± 26 | <0.01⁎⁎ |
| Fasting glucose (mg/dl) | 80.6 ± 4.5 | 84.4 ± 5.8 | >0.5⁎ |
HDL, high density lipoprotein. LDL, low density lipoprotein.
Insignificant.
Significant.
Table 3.
Comparison of left ventricular dimensions, diastolic function, and time intervals between obese and nonobese patients.
| Non-obese (n = 50) | Obese (n = 30) | p value | |
|---|---|---|---|
| LV dimension | |||
| IVSd (cm) | 0.63 ± 0.15 | 0.69 ± 0.14 | 0.013⁎⁎ |
| IVSs (cm) | 0.98 ± 0.22 | 1.09 ± 0.18 | 0.005⁎⁎ |
| LVIDd (cm) | 4.48 ± 0.56 | 4.67 ± 0.48 | 0.042⁎⁎ |
| LVIDs (cm) | 2.84 ± 0.32 | 2.91 ± 0.35 | 0.218⁎ |
| LVPWd (cm) | 0.47 ± 0.11 | 0.55 ± 0.04 | <0.001⁎⁎⁎ |
| LVPWs (cm) | 0.95 ± 0.18 | 1.17 ± 0.27 | <0.001⁎⁎⁎ |
| LVM (gm) | 77.6 ± 38.8 | 98.5 ± 36.4 | 0.008⁎⁎ |
| LVMI | 25.6 ± 7.1 | 34.3 ± 10.3 | <0.001⁎⁎⁎ |
| Diastolic function Mitral valve | |||
| E/A max | 2.32 ± 0.58 | 2.43 ± 0.46 | 0.336⁎ |
| E/A mean | 2.15 ± 0.45 | 2.23 ± 0.47 | 0.438⁎ |
| Pulmonary venous flow | |||
| PVS (m/s) | 0.48 ± 0.08 | 0.52 ± 0.11 | 0.056⁎ |
| PVD (m/s) | 0.57 ± 0.09 | 0.57 ± 0.10 | 0.949⁎ |
| D/S | 1.21 ± 018 | 1.09 ± 024 | 0.124⁎ |
IVSd, ventricular septum in diastole; IVSs, ventricular septum in systole.
LVIDd, internal left ventricular diameter in diastole.
LVIDs, internal left ventricular diameter in systole.
LVPWd, LV posterior wall in diastole.
LVPWs, LV posterior wall in systole.
LVM, left ventricular mass.
LVMI, left ventricular mass index.
E, velocity of passive mitral filling.
A max, maximum velocity of active mitral filling.
A mean, mean velocity of active mitral filling.
PVS, pulmonary v velocity venous follow during systole.
PVD, pulmonary v velocity venous follow during diastole.
Insignificant.
Significant.
High significant.
Table 4.
Clinical characteristics of the studied cases before and after weight reduction.
| After weight reduction (n = 30) | Before weight reduction (n = 50) | p value | |
|---|---|---|---|
| Age | 12.1 ± 2.6 | 11.2 ± 2.9 | >0.5⁎ |
| Sex (boys/girls) | 12/18 | 23/27 | >0.5⁎ |
| Weight | 38.5 ± 6.3 | 57.9 ± 14.8 | <0.001⁎⁎ |
| BMI (kg/m2) | 19.2 ± 2.8 | 28.4 ± 8.3 | <0.001⁎⁎ |
| Systolic blood pressure (mm Hg) | 116 ± 18 | 130 ± 14 | <0.001⁎⁎ |
| Diastolic blood pressure (mm Hg) | 63 ± 15 | 71 ± 12 | <0.001⁎⁎ |
| Heart rate | 82 ± 14 | 84 ± 11 | >0.5⁎ |
BMI, body mass index; BMI-SDS, BMI, standard deviation scores; BSA, body surface area.
Insignificant.
Significant.
Table 5.
Laboratory results of the studied cases before and after weight reduction.
| After weight reduction (n = 30) | Before weight reduction (n = 50) | p value | |
|---|---|---|---|
| Total cholesterol (mg/dl) | 157 ± 42.6 | 188 ± 32.4 | <0.01⁎⁎ |
| HDL cholesterol (mg/dl) | 49.7 ± 6.3 | 46.7 ± 6.2 | <0.01⁎⁎ |
| Triglycerides (mg/dl) | 110.6 ± 28.2 | 125.4 ± 30.6 | <0.01⁎⁎ |
| LDL cholesterol (mg/dl) | 93.6 ± 24.1 | 115.3 ± 26 | <0.01⁎⁎ |
| Fasting glucose (mg/dl) | 82. 2 ± 5.2 | 84.4 ± 5.8 | >0.5⁎ |
HDL, high density lipoprotein; LDL, low density lipoprotein.
Insignificant.
Significant.
Table 6.
Comparison of left ventricular dimensions, diastolic function, and time intervals between obese and nonobese patients before and after weight reduction.
| After weight reduction (n = 30) | Before weight reduction (n = 50) | p value | |
|---|---|---|---|
| LV dimension | |||
| IVSd (cm) | 0.64 ± 0.18 | 0.69 ± 0.14 | 0.016⁎⁎ |
| IVSs (cm) | 0.99 ± 0.27 | 1.09 ± 0.18 | 0.005⁎⁎ |
| LVIDd (cm) | 4.51 ± 0.46 | 4.67 ± 0.48 | 0.047⁎⁎ |
| LVIDs (cm) | 2.88 ± 0.21 | 2.91 ± 0.35 | 0.224⁎ |
| LVPWd (cm) | 0.48 ± 0.09 | 0.55 ± 0.04 | <0.001⁎⁎⁎ |
| LVPWs (cm) | 0.96 ± 0.24 | 1.17 ± 0.27 | <0.001⁎⁎⁎ |
| LVM (gm) | 79.3 ± 34.2 | 98.5 ± 36.4 | 0.009⁎⁎ |
| LVMI | 27.4 ± 6.2 | 34.3 ± 10.3 | <0.001⁎⁎⁎ |
| Diastolic function Mitral valve | |||
| E/A max | 2.45 ± 0.47 | 2.43 ± 0.46 | 0.338⁎ |
| E/A mean | 2.24 ± 0.42 | 2.23 ± 0.47 | 0.440⁎ |
| Pulmonary venous flow | |||
| PVS (m/s) | 0.50 ± 0.02 | 0.52 ± 0.11 | 0.058⁎ |
| PVD (m/s) | 0.57 ± 0.09 | 0.57 ± 0.10 | 0.966⁎ |
| D/S | 1.14 ± 016 | 1.09 ± 024 | 0.134⁎ |
IVSd, vetricular septum in diastole.
IVSs, ventricular septum in systole.
LVIDd, internal left ventricular diameter in diastole.
LVIDs, internal left ventricular diameter in systole.
LVPWd, LV posterior wall in diastole.
LVPWs, LV posterior wall in systole.
LVM, left ventricular mass.
LVMI, left ventricular mass index.
E, velocity of passive mitral filling.
A max, maximum velocity of active mitral filling.
A mean, mean velocity of active mitral filling.
PVS, pulmonary v velocity venous follow during systole.
PVD, pulmonary v velocity venous follow during diastole.
Insignificant.
Significant.
High significant.
4. Discussion
This study provides evidence that asymptomatic obese children exhibit abnormalities of left ventricle structure and function (consisting of increased left ventricular wall dimensions, mass and alteration of diastolic function) that can be detected by echocardiography. Furthermore, (parameters of lipid metabolism) were found to be independent predictors of adverse LV remodeling and of diastolic dysfunction. As well as this study provides evidence that abnormalities of left ventricular wall dimension and mass in obese children and adolescents can improve with significant weight reduction. These results are important, because reversals of these abnormalities are predictors of future cardiovascular morbidity.
The association of LV remodeling and obesity in the present study is supported by previous studies in adults and children (Li et al., 2004; Chinali et al., 2006). The Bogulosa Heart Study showed a strong association between LVM in childhood and the degree of obesity (Li et al., 2004). Additionally, they found a significant increase in stroke volume in obese children and adolescents, indicating increased cardiac workload (Chinali et al., 2006; Pascual et al., 2003). This study shows the posterior wall and septal thicknesses in children and adolescents can significantly improve after weight loss, demonstrating remodeling of the myocardium. This might be an argument for intervention at an earlier age (Table 6). Although likely related to age and duration of obesity, these differences between adults, children & adolescents.
For our knowledge this are the first study measure reversibility of cardiac abnormalities after significant weight reduction by diet and exercises. However many studies were measured reversibility of these abnormalities after weight reduction by surgery and detect elevated LVM index, concentric LVH, altered diastolic function, and cardiac workload significantly improve following surgically induced weight loss in morbidly obese adolescents and adults (Ippisch et al., 2008; Inge et al., 2004; Sjostrom et al., 2007; Leichman et al., 2006; Ikonomidis et al., 2007).
One hypothesis to explain these observations is that weight loss translates into a reduction in cardiac workload that thereby decreases LVM (Steinberger and Daniels, 2003). This possibility is supported by the reduction in heart rate, decrease in systolic blood pressure (Aggoun, 2007) (Tables 3 and 4).
Few studies have investigated diastolic function in obese children and adolescents. Harada et al. (2001) found altered transmitral and pulmonary venous velocities in 21 obese children using pulse-wave Doppler, suggesting a reduction in early diastolic filling. In the present study, no abnormalities can be detected (Tables 3 and 6). Only one recent study investigated diastolic function in 25 obese and overweight children (Mehta et al., 2004) providing unique insights into the effects obesity on LV diastolic function. They observed impaired early diastolic function (E′) in the overweight and obese group. The E′/A′ ratio was found to be inversely related to BMI. In this analysis, there were also several measures of diastolic function that improved after weight loss, Again, the improvements seen in this children and adolescent population might reflect advantages to earlier age at intervention.
Obesity is associated with a group of metabolic abnormalities e.g., dyslipidemia, insulin resistance and hyperglycaemia could be involved in the modulation of left ventricular structure. In the present study, weight reduction is effective in lowering total cholesterol, triglyceride, LDL and rising of HDL levels in obese children, which might result in an increased cardiovascular protective effect that can predict a significant portion of adverse LV remodeling (Tables 2 and 5). Several studies have investigated the relation between dyslipidemia and left ventricular mass on obese subjects with varying results. Some studies found a relation between dyslipidemia and left ventricular mass, whereas others found no relation (Sasson et al., 1993; Urbina et al., 1999; Steinberger et al., 2009; Meyer et al., 2006). Additional studies are needed to determine the effect of other confounding factors, including: sample size, length of follow-up, and magnitude of weight loss.
5. Conclusion
This study has demonstrated that young, obese children and adolescents have early significant changes in left ventricular wall dimensions and early diastolic filling compared with non obese and this changes are reversible with weight reduction.
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