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Research Article
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Left Ventricular Mass and Geometry in Obese Children
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A. Khositseth,
U. Suthutvoravut
and
N. Chongviriyaphan
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ABSTRACT
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This study was to evaluate the left ventricular mass
index (LVMI) and geometry in obese children. Forty-nine obese children,
median age of 9.7 (range 3.4-15.4 years), underwent echocardiography to
assess LVMI and Relative Wall Thickness (RWT). LV geometry was categorized
as normal, concentric remodeling, eccentric hypertrophy and concentric
hypertrophy. Mean weight was 61.8 ±22.0 kg, BMI 29.9 ±5.8 kg m-2, LVMI 38.3 ±8.9 g m-2.7 and percentage
of actual weight to ideal body weight-for-height (IBW %) 172.4 ±28.3%. Twenty-one children had mild to moderate obesity (group 1) and
28 had severe obesity (group 2). Twenty-six children had normal LV geometry,
2 had concentric remodeling, 15 had eccentric hypertrophy and 6 had concentric
hypertrophy. LVMI and abnormal geometry in group 2 were significantly
greater than in group 1 (40.7 ±8.8 vs 35.1 ±8.1 g m-2.7,
60.7 vs 28.6%, p = 0.03). Thirty-seven children (75.5%) had normotensive
whereas 12 (24.5%) had systemic hypertension. The LVMI and abnormal geometry
were not significantly different in both groups (37.6 ±9.7 vs
40.4 ±5.7 g m-2.7, 40.5 vs 60.7%). Left ventricular
mass and abnormal LV geometry were increased in obese children especially
in severe obesity. These may increase cardiovascular risk in the future.
Weight control to decrease the severity of obesity should be recommended.
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INTRODUCTION
The prevalence of obesity in children and adolescents is increasing (Freedman
et al., 1997; Ogden et al., 2006).
In 2003-2004, 17.1% of US children and adolescents (age 2-19 years) were overweight.
The prevalence of overweight female and male children and adolescents increased
from 13.8 and 14.0% in 1999-2000 to 16.0 and 18.2% in 2003-2004, respectively
(Ogden et al., 2006). Overweight and obese adolescents
often maintain overweight and obesity in adulthood (Guo et
al., 1994; Guo et al., 2002). Obesity
in children has affected many systems causing diseases such as systemic hypertension,
diabetes mellitus, hyperlipidemeia and obstructive sleep apnea. Increased left
ventricular mass (LVM) has been reported in overweight children and adolescents
and strongly associated with lean body mass and systolic blood pressure (Daniels
et al., 1995a). Earlier report revealed that obese children had increased
LVM and cardiac output (Humphries et al., 2002).
The left ventricular hypertrophy (LVH) and geometry can predict an increased
incidence of cardiovascular events especially concentric LVH which is consistently
associated with markedly increased cardiovascular risk (Koren
et al., 1991). De Simone et al. (1997)
demonstrated that the risk of LVH was significantly higher in children with
a high casual blood pressure, compared with children with normal blood pressures,
independent of the effect of obesity and they recommended an aggressive approach
to prevention and treatment of obesity in pediatric patients with hypertension
to reduce the future cardiovascular morbidity in these children. The aim of
this study was to evaluate left ventricular mass index (LVMI) and left ventricular
(LV) geometry in young obese children.
MATERIALS AND METHODS
Study Population
Between August 2004 and April 2006, 49 obese children attending at
Nutrition Clinic, Division of Nutrition, Department of Pediatrics, Faculty
of Medicine, Ramathibodi Hospital with median age of 9.7 years (range
3.4-15.4 years) underwent history and physical examination, anthropometric
assessment (body weight, height, waist and hip circumference and body
mass index) and echocardiography. Blood pressure greater than 95th percentile
for age was considered to have systemic hypertension. The Body Mass Index
(BMI) was calculated by using the formula:
BMI = weight (kg)/height (m)2 |
The percentage of actual weight to ideal body weight for height (IBW %) was
calculated as the actual weight divided by the ideal body weight for height
at the 50th percentile of reference and times 100. Obesity is defined as a BMI>age-and
sex-specific cut off points (Cole et al., 2000).
The degree of obesity is defined as followings: IBW% <140%, mild; 141-160%,
moderate and >160%, severe obesity. The parents of the patients were informed
about the risk and benefit of the study.
Echocardiography Study
Echocardiography was performed in all children using Hewlett Packard Sonos
4500. Left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic
dimension (LVESD), interventricular septal thickness and posterior wall thickness
were measured through 2-dimensional guided M-mode echocardiography using parasternal
short axis view at the level of papillary muscles. Left ventricular mass (LVM)
was calculated by the formula described by Devereux and Reichek
(1977). LVM index (LVMI) was obtained by dividing LV mass by height2.7
to normalize and linearize the relations between LVM and height (De
Simone et al., 1992). The percentile of LVMI was obtained, based
on normal value (De Simone et al., 1992). LVMI
was used to evaluate left ventricular hypertrophy (LVH) adjusted to body size
as described elsewhere (De Simone et al., 1992).
LVH is diagnosed when LVMI is over the 95th percentile for healthy children
and adolescents (38.6 g m-2.7) (Daniels et
al., 1995). Relative Wall Thickness (RWT) was measured at end diastole
as the ratio of the sum of posterior wall thickness and septal thickness over
LVEDD. The sex-specific 95th percentile for LVMI from normal children and adolescents
was used as one cut-point. A RWT of 0.41 was used, which represents the 95th
percentile for relative wall thickness for normal children and adolescents.
This value was also used by Ganau et al. (1992)
for partitioning by relative wall thickness in adults. Cutoff levels for LV
mass and RWT were created to evaluate LV geometry. From these values LV can
be categorized into four categories: normal, concentric remodeling, eccentric
hypertrophy and concentric hypertrophy. Children with normal geometry had LV
mass and RWT below the 95th percentile. Concentric remodeling was defined as
normal LVMI but elevated RWT; eccentric hypertrophy was defined as elevated
LVMI with normal RWT and concentric LV hypertrophy was defined as both LVMI
and RWT greater than the 95th percentile.
The cutoff level used to define the most severe LVH was a LVMI of 51
g m-2.7. This value represents approximately the 97.5th percentile
for LVMI in adults.
Left Ventricular Systolic Function
Left ventricular ejection fraction (LVEF) and left ventricular fractional
shortening (LVFS) were calculated by Wilson et al.
(1981) formula. The normal values for LVEF and LVFS are >55% and >25%, respectively.
Left Ventricular Dimension
The predicted LVEDD was calculated using equation by Henry
et al. (1980):
Predicted LVEDD = [45.3x{body surface area (m2)}0.3]-[0.03xage(years)]-7.2. |
The ratio of left ventricular diastolic dimension to predicted LVEDD
expressed in percentage (LVEDD %) was calculated using the following formula:
LVEDD % = [(Measured LVEDD)/(Predicted LVEDD)]x100. |
The normal value for LVEDD% is < 112%. When the% LVEDD is >117%,
there is left ventricular enlargement.
Statistical Analysis
Statistical analyses were performed using SPSS 13.0 for window soft
ware. Data were presented as Mean ±Standard Deviation (SD) for
continuous variables and as proportions for categorical variables. The
unpaired Student t-test was used to compare numeric variables between
groups. Mann-Whitney U-test was used to compare nonparametric variables
between groups. Correlations between numeric variables were determined
by Spearman correlation analysis. A p-value <0.05 was considered to
be statistically significant.
RESULTS AND DISCUSSION
Forty-nine children had mean weight 61.8 ±22.0 kg, BMI 29.9 ±5.8 kg m-2 and percentage of actual weight to ideal body weight
for height (IBW%) 172.4 ±28.3%. According to grading severity
using IBW%; 3, 18 and 28 children had mild, moderate and severe obesity,
respectively. Cardiac dimension determined by LVEDD% was 98.4 ±7.8%. None had LVEDD% >117%. LV systolic function determined by the
LVFS and LVEF were 37.5 ±4.8 and 67.7 ±5.9%, respectively.
Hence, all children had normal LV dimension and systolic function. Overall,
mean LVM, LVMI and RWT were 100.4 ±37.7 g, 38.3 ±8.9 g
m-2.7 and 0.34 ±0.06, respectively. Twenty children
(40.8%) had LVH (LVMI >38.6 g m-2.7). Three of these children
had LVMI >51 g m-2.7. Of these 3 children, two of them had
severe obesity (IBW % = 169 and 215%) and one had moderate obesity (IBW%
= 156%), however, none of these 3 children had systemic hypertension.
Eight children (16.3%) had RWT >0.41. By LVMI and RWT, LV geometry
was categorized into four groups: normal (n = 26), concentric remodeling
(n = 2), eccentric hypertrophy (n = 15) and concentric hypertrophy (n
= 6). Figure 1a demonstrated LV geometry according to
severity of obesity, mild to moderate vs severe obesity. Thirty-seven
children (75.5%) had normotension whereas 12 (24.5%) had systemic hypertension.
Figure 1b demonstrated LV geometry according to systemic
blood pressure, normotension vs systemic hypertension. Characteristics
including age, sex, body weight, BMI, IBW%, blood pressure, LVMI and LV
geometry were compared in normotensive and hypertensive obese children
(Table 1). Mean age in hypertensive group was significantly
greater than in normotensive group (11.5 ±2.4 vs 9.0 ±2.4 years). Body weight, BMI and IBW% were significantly higher in hypertensive
group than in normotensive group (Table 1). LVMI and
abnormal LV geometry were not significantly different in both groups.
However, there were 8 of 12 (66.7%) in hypertensive group had LVMI >38.6
g m-2.7 compared to 13 of 37 (35.1%) in normotensive group.
We also performed the subgroup analysis by severity into group 1: mild
to moderate obesity (n = 21) and group 2: severe obesity (n = 28).
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Fig. 1: |
Distribution of left ventricular geometry according severity
of obesity in this cohort study (a) and according to systemic blood pressure
in this cohort study (b) |
Table 1: |
Demonstration of characteristics, blood pressure, left ventricular
mass index, and abnormal left ventricular geometry in normotensive and hypertensive
obese children |
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BMI: Body mass index, BP: Blood pressure, LV: Left ventricle,
IBW%: Percentage of actual weight to ideal body weight for height
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Table 2: |
Demonstration of characteristics, blood pressure, left ventricular
mass index and abnormal left ventricular geometry in different severity
of obese children |
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BMI: Body mass index, BP: Blood pressure, LV: Left Ventricle,
IBW%, Percentage of actual weight to ideal body weight for height |
Characteristics including age, sex, body weight, BMI, IBW% , blood pressure,
LVMI and LV geometry were compared in both groups (Table
2). LVMI, blood pressure and abnormal LV geometry were significantly
higher in group 2 than in group 1 (Table 2).
There was fair correlation between LVMI and IBW% (r = 0.31, p = 0.01)
but no correlation between LVMI and systemic hypertension (r = 0.17, p
= 0.1).
Obesity in adolescents has been associated with increased values of LVM and
high prevalence of left ventricular hypertrophy (Chinali
et al., 2006). Echocardiography performed on asymptomatic severely
obese adult patients can detect alterations in the cardiac structure including
enlarged left chambers (42.9%), diastolic dysfunction (54.6%) and left ventricular
hypertrophy (82.1%), leading to obesity cardiomyopathy, the development of heart
failure, arrhythmias and sudden death (Rocha et al.,
2007). One study reported the autopsies of 210 children aged 5-15 years
who suffered a violent death in Finland and found that the ponderous index was
a significant predictor for heart weight and the presence of coronary intimal
fatty streaks (Kortelainen et al., 1997). Interestingly,
coronary fatty streaks were not found at all in the leanest individuals (Kortelainen
et al., 1997). The cardiac adaptation to obesity in adults consists
of left ventricular dilatation and hypertrophy regardless of the level of blood
pressure (Messerli, 1983). In present study there was
left ventricular hypertrophy in obese children but no dilatation associated
with obesity. This may be explained by the early onset of detection in children
which dilatation may not develop yet.
The present study has been studied in younger children with median age of 9.7
years, range from 3.4 to 15.4 years. LV dimension and systolic function were
normal in all of these obese children. Present findings demonstrated that, even
in the younger age group, there was the high prevalence of LVH (40.8%). Interestingly,
3 of 49 (6.1%) with normotension had severe LVH (LVMI of 51 g m-2.7)
which has previously been shown to be associated with a fourfold increase in
risk for cardiovascular morbidity in adults (De Simone et
al., 1995). Abnormal LV geometry has been demonstrated in 23 obese children
(46.9%). Moreover, concentric LV hypertrophy with associated with increased
cardiovascular morbidity in adults 11 has been demonstrated in 6 children. The
LVH has been shown to be an independent risk factor for cardiovascular morbidity
and mortality in adult population (Levy et al., 1990).
Importantly, LVH may start early even in the younger age group as shown in this
study. Factors associated with LVH include obesity, high blood pressure and
dietary sodium intake (Daniels et al., 1995b). In this study, the severity
of obesity was an important factor in developing LVH and abnormal LV geometry
in obese children. Mean LVMI in severe obese children was significantly greater
than in mild to moderate obese children (40.7 ±8.8 vs 35.1 ±8.1 g m-2.7,
p = 0.03) and abnormal LV geometry was demonstrated more in severe obese children
than in mild to moderate obese children (60.7b vs 28.6%). There also was fair
correlation between %IBW (which indicated severity of obesity) and LVMI (which
indicated LVH).
Only 12 obese children had high blood pressure. Although, mean LVMI in
hypertensive group and abnormal LV geometry were not significantly different
compared to normotensive group (40.4 ±5.6 vs 37.6 ±9.7
g m-2.7, p = 0.23 and 66.7 vs 40.5%) and no correlation between
systolic blood pressure and LVMI (r = 0.17) but systemic hypertension
may be a factor in developing LVH in obese children according to 8 of
12 hypertensive obese children had LVH (LVMI >38.5 g m-2.7)
compared to 13 of 37 in normotensive obese children. This may be explained
by the small number of hypertensive obese children in our study.
Both LVH and abnormal LV geometry may therefore be affected not only
by severity of obesity, but also by other factors such as systemic hypertension,
hypercholesterolemia and obesity itself. Whether the findings of LVH and
abnormal LV geometry especially LV concentric hypertrophy in younger obese
children have any effect on cardiovascular morbidity and mortality when
these children grow up to be adult or not is interesting and needed to
have a long-term follow-up. However, there was evidence that cardiac adaptation
change can occur even in these younger obese children.
CONCLUSION
The left ventricular mass and abnormal LV geometry were increased in
obese children especially in severe obesity. These may increase cardiovascular
risk in the future. Weight control to decrease the severity of obesity
should be recommended.
ACKNOWLEDGMENTS
We are indebted to the patients and their parents for their participation
in this study. This study was approved and financially supported by Committee
on Human Rights Related to Researches Involving Human Subjects, Faculty
of Medicine, Ramathibodi Hospital, Mahidol University and had informed
consent from parents of all children.
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