From the Medical College of Virginia/Virginia Commonwealth University,
Richmond (R.M.S., P.F.S.), and Michigan State University, East Lansing
(M.M.G.).
Correspondence to Richard M. Schieken, MD, Division of Pediatric Cardiology, Medical College of Virginia/Virginia Commonwealth University, PO Box 980026, 1200 E Broad St, Room 5–112, Richmond, VA 23298-0026. E-mail schieken{at}gems.vcu.edu
Methods and Results—We repeatedly studied a biracial sample of
children from ages 11 through 17 years. At visits 1 through 5, height,
weight, and pubertal stage were determined. Blood pressure and heart
rate were measured. M-mode and two-dimensional echocardiograms were
performed with a 3.5-MHz transducer with the subject in the supine
position. LV mass was calculated. Repeated-measures analysis
using a mixed modeling approach was performed for LV mass. At all ages,
boys had greater LV mass than girls. For the population as a whole, we
found significant tracking correlations for LV mass between each
interval of measurement and throughout the entire period of
examination. The tracking correlation for the entire sample from visit
1 through visit 5 was r=.41. The LV mass in white
children tracked from the youngest to the oldest. Black children
tracked similarly from ages 1 to 15 years, but tracking was not
significant across the widest interval, visit 1 through visit 5. Racial
differences were found in the interactions of systolic blood
pressure and heart rate, which magnified the differences in LV mass.
During adolescence, LV mass tracks significantly in both black and
white children.
Conclusions—Interactive effects such as weight, blood pressure,
and heart rate magnify sex and race differences in LV mass.
Many of the coronary heart disease risk factors, such as
blood pressure and cholesterol levels, track, ie, remain in
a given rank order relative to peers, over time. In children, such
tracking occurs most dramatically for height and weight, followed to a
lesser extent by total cholesterol, LDL
cholesterol,5 and blood
pressure.6 The tracking coefficients depend on
both the interval between measurements and the age at the initial
measurement. For instance, the lowest correlation coefficients for
height occur between ages 11 and 14 years, reflecting the wide
variations that occur during pubertal growth spurts and the different
patterns of growth between boys and girls.7
To determine whether tracking occurs for LV mass and how it may differ
between boys and girls and between black and white children, we
repeatedly studied a biracial sample of children from ages 11 through
17 years. We asked the following questions: (1) Does LV mass track
during adolescence? (2) Is tracking consistent within age
intervals despite differing rates of pubertal development? (3) Do
tracking patterns differ by sex or race?
Height and weight were obtained twice with a stadiometer and a
calibrated electronic scale and averaged. Pubertal stage was determined
by a self-report form that included drawings based on the pubic hair
and breast-development phases depicted in Tanner's five-stage
scale.5 The self-report stage was validated by
the technicians during the examination procedures. We obtained resting
blood pressures in the sitting position with a mercury sphygmomanometer
according to standard measurement criteria.8
Diastolic blood pressures were measured at the fifth
Korotkoff sound. We used a cardiotachometer to record heart rates.
We obtained the blood pressures and heart rates
M-mode and two-dimensional echocardiograms were performed with a
3.5-MHz transducer with the subject in the supine position. LV
dimensions were measured in the short-axis view with two-dimensional
guided M-mode echocardiograms that were digitized and measured
according to standard criteria.9 Three cycles
were measured, and the average was used in subsequent analyses.
LV mass was calculated by use of the anatomically validated Penn
convention10: LV mass
(g)=1.04[(LVDD+IVS+LVPW)3-
LVDD3]-13.6, where LVDD is the LV
end-diastolic dimension, IVS is the
interventricular septal dimension, and LVPW is the LV
posterior wall thickness.
Test-retest reliability with repeated measures of subjects and repeated
digitizing of LV dimensions demonstrated that the reproducibility for
the IVS (r=.88), LVDD (r=.97), and LVPW
(r=.86) was high (all P<.01).
Statistical Analyses
Repeated-measures ANOVA using a mixed modeling
approach11 12 was performed for LV mass. The
analysis was performed in the SAS System using PROC
MIXED13 (SAS Institute, 1992). The mixed modeling
approach allows for missing information over visits and allows for
modeling of the variance as well as the mean. The general form of the
mixed model is given by
y=Xß+Z
Of all the children studied at 11 years of age, black children
represented 19% of the sample. During the subsequent study
periods, they continued to represent 18% to 21% of the sample
population.
At all ages, boys had greater LV mass than girls (Table 1
We compared these variables across race (Table 2
No heart rate or diastolic blood pressure differences were
noted between the races.
We next examined differences between the races by sex. In the youngest
children, black boys weighed more, had higher systolic blood
pressures, and had greater LV masses than the white boys at comparable
ages (Table 3
For the population as a whole, we found significant tracking
correlations for LV mass between each interval of measurement and
throughout the entire period of examination (Table 5
The repeated-measures analysis (Table 7
The genetic control of growth that regulates both weight and LV mass is
probably responsible for a major portion of tracking variability in LV
mass during adolescence.14 These increases in LV
mass are developmental and are the consequences of normal
growth.15 In adults, increased LV mass may be a
more important predictor of subsequent hypertension than resting blood
pressure.16 In childhood, however, the blood
pressure contribution to the variability of LV mass is quite
small.17 Nonetheless, some interactions of blood
pressure and LV mass affect the tracking of LV mass during childhood.
In children who participated in the Muscatine School Study,
echocardiograms performed earlier were excellent predictors of resting
blood pressure 3 years later.18 Although we have
demonstrated significant tracking during puberty, the degree of
tracking between adolescence and adulthood is largely unknown. At our
state of knowledge, we do not know whether or not the degree of LV mass
in adolescence predicts premature atherosclerosis in
the adult.
Race and genetic factors contribute to LV mass. Black adults with mild
hypertension have an up to twofold greater prevalence of LV
hypertrophy than white adults with similar blood pressure
levels.19 In our study of randomly selected
subjects, we did not find differences in the level of LV mass between
black and white children. However, LV wall thickness and mass are
consistently greater in children and adolescents with a
positive family history of hypertension, and this appears to be
independent of slight blood pressure
elevations.20 Our findings of the interactions of
LV mass with weight, blood pressure, and heart rate may subsequently
prove to be useful predictors of future cardiovascular
disease.
In summary, during adolescence, LV mass tracks significantly in both
black and white children. There are interactive effects, such as
weight, blood pressure, and heart rate, that magnify sex and race
differences in LV mass. The importance of this tracking to predict
premature cardiovascular disease is not yet known.
Received August 25, 1997;
revision received January 29, 1998;
accepted February 4, 1998.
2.
Brandao AA, Pozzan R, Albanesi Filho FM, Brandao AP.
Role of anthropometric indexes and blood pressure as determinants of
left ventricular mass and geometry in adolescents: the Rio
de Janeiro Study. Hypertension. 1995;6:1190–1194.
3.
Gutgesell HP, Rembold CM. Growth of the human heart
relative to body surface area. Am J Cardiol. 1990;65:662–668.[Medline]
[Order article via Infotrieve]
4.
Daniels SR, Meyer RA, Liang T, Bove KE.
Echocardiographically determined left
ventricular mass index in normal children, adolescents and
young adults. J Am Coll Cardiol. 1988;12:703–708.[Abstract]
5.
Freedman DS, Shear CL, Srinivasan SR, Webber LS,
Berenson GS. Tracking of serum lipids and lipoproteins in children over
an 8-year period: the Bogalusa Heart Study. Prev Med. 1985;14:203–216.[Medline]
[Order article via Infotrieve]
6.
Clarke WR, Schrott HG, Leaverton PE, Connor WE, Lauer
RM. Tracking of blood lipids and blood pressures in school age
children: the Muscatine Study. Circulation. 1978;58:626–634.
7.
Voors AW, Harsha DW, Webber LS, Berenson GS. Obesity
and external sexual maturation: the Bogalusa Heart Study. Prev
Med. 1981;10:50–61.[Medline]
[Order article via Infotrieve]
8.
Report of the Second Task Force on Blood Pressure
Control in Children. Pediatrics. 1987;79:1–25.
9.
Schieken RM, Mahoney L, Clarke W, Lauer R. Measurement
criteria for group echocardiographic studies.
Am J Epidemiol. 1979;110:504–514.
10.
Devereux RB, Reichek N.
Echocardiographic determination of left
ventricular mass in man: anatomic validation of the method.
Circulation. 1977;55:613–618.
11.
Jennrich RI, Schluchter MD. Unbalanced repeated
measures models with structured covariance matrices.
Biometrics. 1986;42:805–820.[Medline]
[Order article via Infotrieve]
12.
Searle SR. Linear Models. New York, NY: John
Wiley & Sons; 1971.
13.
SAS Institute Inc.
SAS® Technical Report P-229,
SAS/STAT® Software Changes and Enhancements,
Release 6.07. Cary, NC: SAS Institute Inc; 1992.
14.
Verhaaren HA, Schieken RM, Mosteller M, Hewitt JK,
Eaves LJ, Nance WE. Bivariate genetic analysis of left
ventricular mass and weight in pubertal twins: the Medical
College of Virginia Twin Study. Am J Cardiol. 1991;68:661–668.[Medline]
[Order article via Infotrieve]
15.
Schieken RM. Large hearts in children: biology or
disease? Circulation. 1995;92:3156–3157.
16.
Casale PN, Devereux RB, Milner M, Zullo G, Harshfield
GA, Pickering TG, Laragh JH. Value of echocardiographic
measurement of left ventricular mass in predicting
cardiovascular morbid events in hypertensive men.
Ann Intern Med. 1986;105:173–178.
17.
Goble MM, Mosteller M, Moskowitz WB, Schieken RM. Sex
differences in the determinants of left ventricular mass in
childhood: the Medical College of Virginia Twin Study.
Circulation. 1992;85:1661–1665.
18.
Mahoney LT, Schieken RM, Clarke WR, Lauer RM. Left
ventricular mass and exercise responses predict future
blood pressure: the Muscatine Study. Hypertension. 1988;12:206–213.
19.
Hypertension prevalence and the status of awareness,
treatment, and control in the United States: final report of the
Subcommittee on Definition and Prevalence of the 1984 Joint National
Committee. Hypertension. 1985;7:457–468.
20.
Malcolm DD, Burns TL, Mahoney LT, Lauer RM. Factors
affecting left ventricular mass in childhood: the Muscatine
Study. Pediatrics. 1993;92:703–709.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Tracking of Left Ventricular Mass in Children: Race and Sex Comparisons
The MCV Twin Study
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Increased left
ventricular (LV) mass is a predictor of
cardiovascular disease in adults. The mechanism(s) for
these observations are not fully understood.
Key Words: mass, left ventricular • race • sex
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Increased left
ventricular (LV) mass is an accepted, independent predictor
of cardiovascular morbidity and mortality in
adults.1 The mechanisms for these observations
are not fully understood. Although blood pressure contributes to the
variability of LV mass in all age groups, there is only a weak
association between the level of blood pressure in children and the
amount of LV mass.2 Body size, and in particular
lean body mass, explains the major portion of the variability of LV
mass.3 4
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
The Medical College of Virginia (MCV) Twin Study was approved by
the Human Studies Institutional Review Board. Parents and children all
gave informed consent before the study. From the participants in the
MCV Twin Study, a twin was selected randomly from each of the pairs of
twins. Measurements including echocardiographic
determinants of LV mass were performed in each child at 18-month
intervals from age 11 until 17 years (visit 1 through visit 5). Each
twin was studied as close as possible to his or her birth date. Each
cohort, therefore, had large groups of children all of whom were the
same age. 
30 minutes after the
child's arrival at the testing site. Blood pressures and heart rates
were taken twice and averaged.
We performed pooled t tests, taking into account
whether or not different variances were present, and Pearson
product-moment correlations using the SAS (Cary, NC) computer
package. 
+e, where
y is the observed response vector, X is a known
design matrix for the fixed effects, ß is a vector of unknown
parameters for the fixed effects, Z is a known
design matrix for the random effects, is a vector of unknown
parameters for the random effects, and e is a
vector of unknown random errors. The variance of y is
modeled by an unstructured variance matrix, and for the mixed model,
E(y) =Xß, and thus, the mean LV mass is modeled
as
where y=LV mass,
x1=weight,
x2=sex (female or male),
x3=race (black or white),
x4=heart rate,
x5=systolic blood
pressure, x6=diastolic
blood pressure, ßi=unknown main fixed-effect
parameters (I=1, 2, 3, 4, 5, 6), and
ßij=unknown interaction parameters
(I=1, 2, 3, 4, 5, 6; j=2, 3, 4, 5, 6; I
j).
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
The sample sizes for each of the 5 study periods
(Table 1
) ranged from 231 subjects studied on
at least 3 occasions, 203 subjects on 4 occasions, and 87 subjects on 5
occasions. Because of the number of technically acceptable
echocardiograms, a larger number of subjects were studied during visit
3 than during visit 2. The small number of subjects at visit 5 reflects
the number of subjects returning at age 17 years for restudy at the
conclusion of the funding period. During visit 5, of the 81 subjects
returning for measurement, 74 had acceptable
echocardiographic tracings for analysis. We
achieved an overall rate of acceptable echocardiograms during the
entire study of 96%. The dropout rate of subjects between visits 1 and
4 was 8.5%.
View this table:
[in a new window]
Table 1. Mean±SD and t Test for Boys Versus
Girls 
).
Although not shown in the table, these differences persisted after
adjustment for body mass index. Prepubertal boys and girls weighed the
same, but by visit 4 boys weighed more. Beginning at visit 2, boys had
consistently lower heart rates than girls. During early
puberty, boys had lower diastolic blood pressures than
girls. In contrast, from mid to late puberty, the systolic
blood pressures in boys were higher than in girls. ). In the youngest children, the LV
mass of the black children exceeded that of the white children, but
this difference disappeared by visit 2. Until late puberty, black
children weighed more than white children. In the youngest children
(visits 1 and 2) and at visit 4, the black children had higher
systolic blood pressures. These differences were not found in
the oldest subjects.
View this table:
[in a new window]
Table 2. Mean±SD and t Test for Blacks Versus
Whites ). At older ages, we did
not observe differences for any of these variables among the boys.
Only weight and systolic blood pressure were greater in the
youngest black girls compared with white girls of the same age (Table 4). In older girls, we did not find
differences between white and black adolescents for body size, blood
pressure, or LV mass.
View this table:
[in a new window]
Table 3. Mean±SD and t Test for Black Boys
Versus White Boys
View this table:
[in a new window]
Table 4. Mean±SD and t Test for Black Girls
Versus White Girls ). The tracking correlation for the
entire sample from visit 1 through visit 5 was r=.41.
Similar tracking correlations persisted after the sample was subdivided
by race and sex. The LV mass of white children tracked from the
youngest to the oldest (Table 6). Black
children tracked similarly from age 11 to 15.5 years, but the tracking
was not significant across the widest interval (visit 1 through visit
5). The small sample size (n=13) for 17-year-old black children was
most likely responsible for this change. Of particular interest, the
oldest black children tracked highly in the interval from visit 4 to
visit 5.
View this table:
[in a new window]
Table 5. Tracking Correlations for Left Ventricular Mass for
Visits 1 Through 5, Overall
View this table:
[in a new window]
Table 6. Tracking Correlations by Race for Left Ventricular
Mass for Visits 1 Through 5 ) documented that for the entire group,
as weight increased, LV mass increased (Figure). Race
was found to interact with weight, systolic blood pressure, and
heart rate. In each case, the differences in LV mass in blacks and
whites were magnified as either weight, systolic blood
pressure, or heart rate increased. Heart rate was the only significant
interaction that occurred between boys and girls. As the heart rate
increased, the LV mass differences between boys and girls
increased.
View this table:
[in a new window]
Table 7. Repeated-Measures Analysis for Visits 1 Through 5
View larger version (10K):
[in a new window]
Figure 1. Weight-by-race interaction. Plot shows fitted LV mass across
weight for black and white boys. Fitted lines are shown for fixed
levels of all other independent variables. In other words, fitted
lines are shown for boys at average diastolic blood
pressure, average systolic blood pressure, and average heart
rate. 
Black subjects; 
white subjects.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
In this longitudinal study of 231 normotensive subjects examined
at ages 11 through 17 years, we that found persistence of peer rank
order, or tracking, occurs for LV mass. Throughout adolescence, LV mass
was consistently larger in boys than girls. Increases in
weight, systolic blood pressure, and heart rate all increased
the differences in LV mass between boys and girls. We did not observe
sex differences in the degree of tracking. The tracking correlations
remained constant throughout early puberty and increased in the later
stages of puberty. Repeated-measures analysis showed sex and
race differences in the tracking of LV mass.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
Levy D, Garrison RJ, Savage DD, Kannel WB,
Castelli WP. Prognostic implications of
echocardiographically determined left
ventricular mass in the Framingham Heart Study.
N Engl J Med. 1990;322:1561–1566.[Abstract]
This article has been cited by other articles:
 |
|
 |
|
  W. Lieb, V. Xanthakis, L. M. Sullivan, J. Aragam, M. J. Pencina, M. G. Larson, E. J. Benjamin, and R. S. Vasan Longitudinal Tracking of Left Ventricular Mass Over the Adult Life Course: Clinical Correlates of Short- and Long-Term Change in the Framingham Offspring Study Circulation, June 23, 2009; 119(24): 3085 - 3092. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Gardin, D. Brunner, P. J. Schreiner, X. Xie, C. L. Reid, K. Ruth, D. E. Bild, and S. S. Gidding Demographics and correlates of five-year change in echocardiographic left ventricular mass in young black and white adult men and women: the Coronary Artery Risk Development in Young Adults (CARDIA) Study J. Am. Coll. Cardiol., August 7, 2002; 40(3): 529 - 535. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Dekkers, F. A. Treiber, G. Kapuku, E. J.C.G. van den Oord, and H. Snieder Growth of Left Ventricular Mass in African American and European American Youth Hypertension, May 1, 2002; 39(5): 943 - 951. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Montgomery, S. Dhamrait, J. R. Payne, A. Jones, D. Woods, L. A. Sonna, C. M. Lilly, M. A. Sharp, J. J. Knapik, and J. F. Patton ACE Genotype and Performance J Appl Physiol, April 1, 2002; 92(4): 1774 - 1777. [Full Text] [PDF]
|
|
|
|
 |
|
 K. F. Janz, J. D. Dawson, and L. T. Mahoney Predicting Heart Growth During Puberty: The Muscatine Study Pediatrics, May 1, 2000; 105(5): 63e - 63. [Abstract] [Full Text]
|
|
|
|
|
|
G. K. Kapuku, F. A. Treiber, H. C. Davis, G. A. Harshfield, B. B. Cook, and G. A. Mensah Hemodynamic Function at Rest, During Acute Stress, and in the Field : Predictors of Cardiac Structure and Function 2 Years Later in Youth Hypertension, November 1, 1999; 34(5): 1026 - 1031. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. S. Gidding Clinical and Epidemiological Significance of Left Ventricular Mass Assessed in Children and Adolescents Circulation, May 19, 1998; 97(19): 1893 - 1894. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||