SHA24/025003

Azza M. Ahmed1, Shadia H. Ragab2, Nagwa A. Ismail1, Mona A.M. Awad2 and Manal E. Kandil1 1

Pediatrics, 2 Clinical Pathology NRC. Egypt.

The prevalence of overweight and obesity in children is increasing worldwide at an alarming rate in both developing and developed countries. It is well established that obesity is a strong risk factor for cardiovascular morbidity and mortality.

Studies in adults using echocardiography, catheterization, and necropsy examinations have shown relations between morbid obesity, structural alterations of the heart and systolic function.

However, the relation between obesity and cardiac function in children is less well documented and conflicting results have been reported.

Visceral fat is a far better indicator of left ventricular mass (LVM) than body mass index (BMI). Epicardial adipose tissue (EAT), a part of the visceral fat, it is situated on the free wall of right ventricle, left ventricular apex, atrium and coronary vessels.

Epicardial adipose tissue, an index of cardiac visceral adiposity might function as a lipid storage depot, and as an inflammatory tissue secreting cytokines , so it could play roles in the pathogenesis of cardiomyopathy and coronary atherosclerosis.

Obesity is associated with a heterogeneity of metabolic abnormalities e.g. dyslipidemia, insulin resistance, hyperglycemia and hypertension. The clustering of these risk factors is referred to as metabolic syndrome. Epicardial adipose tissue is closely related to insulin resistance and dyslipidemia and producing a much greater risk for metabolic syndrome and cardiovascular disease.

The aim of this study was to evaluate cardiac function and EAT of obese children with echocardiography and to study the relationship of EAT to clinical parameters of metabolic syndrome in children.

This study included 74 obese children and adolescents (29 males and 45 females) from the patient population attending the obesity clinic of the National Research Centre (NRC).

Exclusion criteria: • A significant concomitant illness.

• Medication known to modify cardiac function.

• Antihypertensive drugs.

• Hormone replacement therapy.

• Obvious clinical signs of cardiac disease.

Metabolic syndrome was determined according to International Obesity Task Force (IOTF) 2007 criteria.

Forty age and sex matched lean children (16 males and 24 females) were included in the study as a control group.

Parental consent for all children was obtained according to the form approved by the Ethics Committee of the National Research Center.

Clinical assessment: • Standing height (cm).

• Body weight (kg).

• BMI was calculated using the formula (body weight in kilograms)/ (body height in meters2).

• BMI values were converted to SD scores (BMI-SDS) using the standard growth curves for Egyptian Children and Adolescents 2008.

• Waist circumference (WC), Hip circumference (HC).

• Systolic (SBP) and diastolic blood pressure (DBP).

Echocardiography examination: Echocardiographic studies were performed with a Vivid3 Expert- Norway using 3 and 7 MHz transducers.

Triplicate measurements of all variables were made off line by one observer who was blinded to the patient's clinical details.

Echocardiography examination: • Chamber dimensions.

• Wall thickness. (According to the recommendation of the American Society of Echocardiography).

• LV systolic functions (EF% and FS%) .

• The LV mass and relative posterior wall thickness (RWT) were calculated according to the formulae of Devereux et al (1984).

• The LV diastolic functions (E wave, A wave, E/A ratio and Deceleration time “DT”).

Echocardiography examination: Epicardial adipose tissue was measured in two-dimensional echocardiography as an echo free space over the pericardial layers and its thickness was measured on the free wall of the right ventricle, perpendicular to the wall from LT parasternal long axis view at enddiastole.

Biochemical parameters: - Fasting serum glucose.

- Fasting serum insulin.

- insulin resistance was calculated by a homeostasis model assessment (HOMA) index.

- Total cholesterol and triglyceride.

- HDL-cholesterol.

- LDL-cholesterol.

Table 1: Clinical characteristics of obese and non obese children Characteristic

Obese (n=74)

Non obese (n=40)

P-value

Age (yr)

11.28 ± 3.71

11.45 ± 3.44

0.81

BMI (kg/m2)

29.68 ± 5.76

18.83 ± 4.34

0.001*

SDS BMI

2.17 ± 1.35

0.87± 0.53

0.001*

WC (cm)

88.28 ± 14.12

66.36 ± 15.34

0.001*

HC (cm)

100.55 ± 16.7

80.03 ± 16.85

0.001*

WC/HC

0.871 ± 0.069

0.825 ± 0.076

0.006*

SBP (mmHg)

104.64 ± 11.78

105.0 ± 8.51

0.88

DBP (mmHg)

68.35 ± 9.29

69.67 ± 6.01

0.48

Table 1: Clinical characteristics of obese and non obese children Characteristic

Obese (n=74)

Non obese (n=40)

P-value

Fasting glucose (mg/dl)

88.8 ±12.06

79.8 ± 9.3

0.001*

Fasting insulin (mcIu/ml)

7.16 ±3.83

4.02 ± 2.13

0.001*

HOMA index

1.41 ± 0.76

0.93 ± 0.5

0.003*

Triglycerides (mg/dl)

106.59±42.8

86.07±18.78

0.01*

Total cholesterol (mg/dl)

170.3 ±34.4

167.13± 20.04

0.64

HDL- cholesterol (mg/dl)

41.61±8.9

41.13± 6.12

0.79

LDL- cholesterol (mg/dl)

110.83±29.4

105.87±17.5

0.39

Table 2: Comparisons of echocardiographic findings between obese and non obese children Characteristic

Obese (n=74)

Non obese (n=40)

P-value

LA diameter (mm)

25.34 ± 4.84

20.75 ± 3.24

0.001*

IVSd (mm)

8.88 ± 2.28

7.3 ± 0.98

0.001*

LVEdD (mm)

44.0 ± 7.9

39.56 ± 5.16

0.002*

LVPW d (mm)

9.0 ± 1.9

7.1 ± 1.16

0.001*

IVSs (mm)

10.92 ± 2.57

9.46 ± 1.34

0.001*

LVEsD (mm)

28.86 ± 5.78

24.73 ± 3.65

0.001*

LVPWs (mm)

11.95 ± 3.13

9.69 ± 1.88

0.001*

RWT (mm)

0.41 ± 0.1

0.36 ± 0.05

0.008*

LVM (g)

122.55 ± 55.38

77.34 ± 22.04

0.001*

Table 2: Comparisons of echocardiographic findings between obese and non obese children Characteristic

Obese (n=74)

Non obese (n=40)

EAT thickness (mm)

7.17 ± 2.72

2.04 ± 0.63

0.001*

EF (%)

67.89 ± 2.38

66.89 ± 3.93

0.09

FS (%)

34.5 ± 4.4

35.96 ± 3.74

0.07

Mitral E wave (m/s)

0.94 ± 0.17

0.9 ± 0.12

0.1

Mitral A ware (m/s)

0.58 ± 0.12

0.61 ± 0.16

0.4

Mitral E/A

1.63 ± 0.31

1.63 ± 0.27

0.9

Deceleration time (ms)

187.82 ± 43.29

188.58 ± 38.39

0.9

P-value

Fig. 1: Transthoracic echocardiography showing a large area of epicardial adipose tissue (EAT) on free wall of right ventricle (arrows)

Table 3: Correlation between epicardial adipose tissue (EAT) and other findings in obese children.

Variable

EAT thickness R

P

BMI (kg/m2)

0.77

0.001*

WC (cm)

0.55

0.001*

HC (cm)

0.62

0.001*

LA diameter (mm)

0.66

0.001*

RWT (mm)

0.22

0.08

LVM (g)

0.43

0.001*

Mitral E/A

0.03

0.77

Table 3: Correlation between epicardial adipose tissue (EAT) and other findings in obese children.

Variable

EAT thickness R

P

Fasting glucose (mg/dl)

0.01

0.9

Fasting insulin (mcIu/ml)

0.28

0.05*

HOMA index

0.34

0.02*

TC (mg/dl)

0.26

0.06

Triglyceride (mg/dl)

0.32

0.02*

HDL-C (mg/dl)

0.11

0.4

LDL-C (mg/dl)

0.29

0.04*

r=o.55, p=0.001 18

Epicardial adipose tissue (mm)

16 14 12 10 8 6 4 2 0 40

60

80

100

120

140

Waist circumference (cm)

Fig. (2): Relation of epicardial adipose tissue thickness to waist circumference

The International Diabetes Federation (IDF) Definition 2006: Person who have Ms must have: - Central obesity Pluse any 2 of the following 4 factors:

Raised triglyceride

≥ 150 mg/dl

Reduced HDL cholesterol

< 40 mg/dl

Raised blood pressure

Systolic ≥ 130, diastolic ≥ 85

Raised fasting plasma glucose

≥ 100 mg/dl

18

Epicardial adipose tissue (mm)

16 14 12 10 8 6 4 2 0

1

Metabolic syndrome

Fig 3: Epicardial adipose tissue thickness in obese children with (1) and without (0) metabolic syndrome (p>0.05).

Assessment of EAT thickness in routine echocardiographic examinations might be a feasible and reliable method for the evaluation of obesity and its related cardiovascular risks during childhood.

Although there is a significant correlation between EAT thickness with WC, insulin resistance, triglyceride and LDL-C there is lake of relationship of EAT thickness with MS in obese children.

Longitudinal studies on the role of EAT in stimulation of different metabolic parameters in adolescents and increasing the risk of coronary artery disease in adults may unravel the mechanisms which

promote

complications.

the

development

of

these

common

obesity