Growth in Children With Congenital Heart Disease
WHAT’S KNOWN ON THIS SUBJECT: Children with congenital AUTHORS: Carrie Daymont, MD, MSCE,a,b Ashley Neal, MD,c
heart disease (CHD) are at increased risk for poor growth.
Several factors may play a role in poor growth, including feeding
difficulties, increased caloric requirements, and the effects of
cardiac lesions on growth regulation.
WHAT THIS STUDY ADDS: In children with CHD, impaired growth
as measured by weight, length, and head circumference occurs
simultaneously rather than sequentially, supporting the theory
that altered growth regulation likely plays an important role in
the poor growth of children with CHD.
abstract
OBJECTIVE: We sought to describe growth in young children with
congenital heart disease (CHD) over time.
METHODS: We performed a retrospective matched cohort study, iden-
tifying children with CHD in a large primary care network in Pennsyl-
vania, New Jersey, and Delaware and matching them 10:1 with control
subjects. The primary endpoint was the difference in mean World
Health Organization z score for cases and controls for weight-for-
age (WFAZ), length-for-age (LFAZ), weight-for-length (WFLZ), and head
circumference-for-age (HCFAZ) at traditional ages for preventive visits,
stratified by CHD category.
RESULTS: We evaluated 856 cases: 37 with single ventricle (SV) phys-
iology, 52 requiring complex repair (CR), 159 requiring simple repair
(SR), and 608 requiring no repair. For children in the SV, CR, and SR
categories, large, simultaneous, and statistically significant (Student’s
t test P , .05) decreases in WFAZ and LFAZ appeared within the first
month of life, peaked near 4 months, and persisted through 24 or 36
months. There were fewer and smaller decreases in the no-repair
group between 2 and 18 months. HC data were available between 1
week and 24 months; at those ages, decreases in mean HCFAZ
generally paralleled decreases in WFAZ and LFAZ in the SV, CR, and
SR groups.
CONCLUSIONS: Children with CHD experience early, simultaneous
decreases in growth trajectory across weight, length, and head circum-
ference. The simultaneous decrease suggests a role for altered growth
regulation in children with CHD. Pediatrics 2013;131:e236–e242
e236 DAYMONT et al
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Aaron Prosnitz, MD,d and Meryl S. Cohen, MDe
aDepartment of Pediatrics and Child Health, University of
Manitoba, Winnipeg, Canada; bThe Manitoba Institute of Child
Health, Winnipeg, Canada; cBoston Children’s Hospital, Boston,
Massachusetts; dYale-New Haven Children’s Hospital, New Haven,
Connecticut; and eDivision of Cardiology, Department of
Pediatrics, The Children’s Hospital of Philadelphia, The Perelman
School of Medicine at the University of Pennsylvania,
Philadelphia, Pennsylvania
KEY WORDS
congenital heart disease, growth, nutrition, failure to thrive
ABBREVIATIONS
CHD—congenital heart disease
CR—complex repair
HC—head circumference
HCFAZ—head circumference-for-age z score
ICD-9—International Classification of Diseases, Ninth Revision
IGF-1—Insulin-like growth factor 1
LFAZ—length-for-age z score
NR—no repair
R-C—repair-combined
SR—simple repair
SV—single ventricle
WFLZ—weight-for-length z score
WHO—World Health Organization
WFAZ—weight-for-age z score
Dr Daymont participated in the conception and design of the
study, analyzed the data, drafted the manuscript, and approved
the final manuscript as submitted; Dr Neal participated in the
acquisition of data, critically revised the manuscript for
important intellectual content, and approved the final
manuscript as submitted; Dr Prosnitz participated in the
acquisition of data, critically revised the manuscript for
important intellectual content, and approved the final
manuscript as submitted; and Dr Cohen participated in the
conception and design of the study, contributed to the
interpretation of results, critically revised the manuscript for
important intellectual content, and approved the final
manuscript as submitted.
www.pediatrics.org/cgi/doi/10.1542/peds.2012-1157
doi:10.1542/peds.2012-1157
Accepted for publication Aug 20, 2012
Address correspondence to Carrie Daymont, MD MSCE, The
Manitoba Institute of Child Health, 655A-715 McDermot Ave,
Winnipeg, Manitoba, R3E 3P4, Canada. E-mail: cdaymont@mich.ca
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright © 2013 by the American Academy of Pediatrics
FINANCIAL DISCLOSURE: The authors have indicated they have
no financial relationships relevant to this article to disclose.
FUNDING: Dr Daymont’s time was supported by the Manitoba
Health Research Council and The Manitoba Institute of Child
Health.

Congenital heart disease (CHD) is the
most common congenital anomaly, af-
fecting ∼8 in 1000 children.1 In addition
to the management of the specific heart
defect, practitioners are often chal-
lenged by issues related to the facilita-
tion of normal growth and development
in this population. Growth status in
these vulnerable children may be asso-
ciated with neurodevelopmental out-
comes in addition to adult height and
weight.2–4 Risk factors for poor growth
are multifactorial and may include the
increased metabolic demands of con-
gestive heart failure, poor oral-motor
skills, the physiologic impact of the
primary cardiac defect, and associated
genetic and noncardiac disease.5–7
The timing of growth differences may
provide insight into both the causes of
poor growth and critical periods for
possible intervention. Therefore, we
sought to evaluate longitudinal growth
in young children with CHD of variable
severity compared with the growth of
healthy peers.
METHODS
We performed a retrospective cohort
study comparing attained growth in
children with CHD to matched controls
without CHD as well as published ref-
erences. We used electronic medical
record data from a large primary care
network. The records included data
from 33 practices in urban, suburban,
and semirural locations in Pennsylva-
nia, New Jersey, and Delaware. Practi-
ces in the network started using the
electronic record between August 2001
and June 2006.
Patient Selection
We identified children born after Janu-
ary 1, 2000, and before January 31, 2009,
with International Classification of Dis-
eases, Ninth Revision (ICD-9) codes for
structural CHD who had been seen in
a primary care practice and had at least
2 weight measurements before age 3
PEDIATRICS Volume 131, Number 1, January 2013
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years in the electronic record. Each
chart was reviewed individually by at
least 1 author to confirm a true diag-
nosis of CHD. Children born prematurely
(before 37 weeks of gestation) and
those with ICD-9 codes for noncardiac
complex chronic conditions (as defined
by Feudtner et al,8 including “malignancy,
neuromuscular, respiratory, renal, gas-
trointestinal, immunodeficiency, and
metabolic, genetic, and other congen-
ital anomalies”8), were excluded from
the analysis.
Cases were categorized into 1 of 4 cat-
egories of CHD: single-ventricle (SV)
physiology; 2-ventricle heart disease
requiring complex repair (CR), defined
as Risk Adjustment for Congenital Heart
Surgery 1 class 3 or higher; 2-ventricle
heart disease requiring simple repair
(SR), defined as Risk Adjustment for
Congenital Heart Surgery class 1 or 2;
and 2-ventricle heart disease requiring
no repair (NR).9 Cases were classified on
the basis of indicated or planned repair
at the last evaluable visit rather than
whether repair had occurred at the time
of the last evaluated visit. Chart review
was used to determine the age at repair.
Measures
All measurements for weight, length or
height, and head circumference (HC)
recorded before January 31, 2010, were
obtained from the electronic medical
record. Attained growth z scores for
each parameter (as well as weight-for-
length were determined for the World
Health Organization (WHO) 2006 growth
standard by using data from the WHO
Anthro macro.10 Growth parameters
that were determined likely to be non-
representative of actual growth based
on the deviation of the recorded value
from inverse distance-weighted means
of the subject’s growth parameters
were excluded from analysis; values
that were extreme but consistent with
a subjects’ other growth parameters
were included.11–13
ARTICLE
Evaluation of growth parameters in
a different cohort from the same pri-
mary care network indicated that the
distribution of growth parameters in
this regional population was not well-
described by the WHO growth curves
or by the Centers of Disease Control
growth reference, as has been shown
in other populations.15–17 To identify a
population against which to compare
growth, each case was matched to 10
control subjects in the primary care
network database by year of birth (61
year), gender, race, and primary care
site. Site group (urban versus all oth-
ers) was used to match when there
were insufficient controls in a site.
Some controls were excluded during
analysis because of insufficient growth
measurements at the evaluated ages.
Primary Analysis
The ages at which growth data were
available for each patient varied widely.
Therefore, we were unable to evaluate
each case’s growth compared with its
own controls at each age. Instead, we
evaluated growth at the ages of typical
preventive visits, comparing the mean
attained z score for cases and controls
for each of the four CHD classes sepa-
rately. The birth age group consisted
only of measurements on the first day of
life, and the other age groups included
visits at the ages at which children were
most commonly seen for preventive vis-
its in the network. We used a 1-week
range of ages for the 1- and 2-week visits;
a 2-week range for the 1-, 2-, and 4-month
visits; a 1-month range for the 6-, 9-, 12-,
15-, and 18-month visits, and a 2-month
range for the 24- and 36-month visits.
The analyses were limited to the first 36
months of life because of the relative
scarcity of measurements after that
age. When $1 value was available for
a subject in an age group, 1 value per
subject per age group was selected.
Visits designated as preventive visits
were retained preferentially, otherwise
selection was random.
e237
The primary endpoint was the differ-
ence in mean growth WHO z score for
weight-for-age (WFAZ), length-for-age
(LFAZ), weight-for-length (WFLZ), and
HC-for-age (HCFAZ) between cases and
controls in each group at each time
point. We evaluated the statistical sig-
nificance of the differences by using
the Student’s t test with a threshold of
P = .05. Differences between CHD cat-
egories were evaluated by using linear
regression.
The proportion of subjects with a z score
#1.88 (corresponding to the third per-
centile) was also compared for cases
and controls. For this analysis, the SV,
CR, and SR groups were analyzed to-
gether as the repair-combined (R-C)
group to have sufficient sample size.
Statistical significance of the differ-
ence between cases and controls was
evaluated by using Fisher’s exact test
with a threshold of P = .05. Differences
between CHD categories were evalu-
ated by using logistic regression.
Exploratory Analysis of Age and
Repair Status
Across CHD severity and growth para-
meters, the greatest difference between
cases and controls was seen near 4
months of age. An exploratory post hoc
analysis was designed to compare the
association of improvement in WFAZ
with age and with repair status in the R-C
group. All available measurements, in-
cluding those taken at ages not tradi-
tionallyassociated withpreventivevisits,
were included in this analysis. Mixed
effects models were designed by using
the “xtmixed” command in Stata 11.2
to compare the change in slopes (Dz
score/time in years) of WFAZ before and
after a certain time point for cases and
controls clustered at the level of subject
nested within case group (a case and its
matched controls). We compared the
change in WFAZ slopes before and after
4 months of age for cases and controls
and then compared the change in WFAZ
slopes before and after the age at the
e238 DAYMONT et al
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cases’ second surgery (or first surgery
if only 1 surgery was done). Cases with
the first or second repair done after 365
days of life were excluded from this
analysis.
All analyses were performed by using
Stata 11.2. This project was approved by
the Institutional Review Board at the
Children’s Hospital of Philadelphia.
RESULTS
Identified Cases
There were 1862 potential cases initially
identified based on ICD-9 codes for CHD
(Fig 1). Three hundred twenty potential
cases were excluded because the sub-
ject did not have CHD; in most of these
cases, the ICD-9 code had been used to
indicate potential CHD that was not
confirmed with diagnostic testing. Ul-
timately, 64 116 visits from 856 cases
and 7674 controls were included in the
primary analysis (Supplemental Table
3). Characteristics of included cases
are described in Table 1 with primary
diagnostic categories in Table 2.
During data cleaning, 0.8% of weight,
2.5% of length, and 1.2% of HC meas-
urements were excluded because they
FIGURE 1
Flow sheet describing exclusion of ineligible cases.
were likely to be nonrepresentative of
the subjects’ growth. A sensitivity ana-
lysis was performed including inter-
polated data to replace excluded values;
results were almost identical to that of
the primary analysis.
Growth in Controls
The means and SDs for WFAZ, LFAZ, LFAZ,
and HCAZ for controls were significantly
different from zero (P , .05) at many
ages for all 4 growth parameters (Fig
2). Z scores using Centers for Disease
Control growth curves were also sig-
nificantly different from zero at many
ages.18 Therefore, our primary analysis
was performed as planned by using the
difference between case and control
mean WHO z scores at the various time
points as the primary endpoint.
Comparison of Means
At birth, WFA and LFA z scores for cases
in the SV, CR, and SR groups were all
lower than control z scores at birth, but
differences were relatively small and
were statistically significant (P , .05)
only for LFA in the SR group (Fig 2 and
Fig 3). For children with CHD requiring
repair, larger and statistically significant
 ARTICLE

TABLE 1 Characteristics of Cases the combined repair group, cases were

Characteristic SV CR SR NR significantly more likely than controls
n (cases) 37 52 159 608 to be less than the third percentile for
n (controls) 344 464 1377 5489 all growth parameters starting at 1
Median age (d) at first repair 4 5 126 NA
month of age and persisting through 24
Male 23 (62%) 31 (60%) 85 (53%) 260 (43%)
Race months (WFAZ), 36 months (LFAZ), and 9
Asian 0 (0%) 2 (4%) 12 (8%) 15 (2%) months (HCFAZ). In the NR group, dif-
Black/African American 12 (32%) 11 (21%) 43 (27%) 150 (25%) ferences in proportions for cases and
Native American 0 (0%) 0 (0%) 2 (1%) 1 (,1%)
White 24 (65%) 32 (62%) 92 (58%) 367 (60%) controls were statistically significant at
Other 1 (3%) 7 (13%) 10 (6%) 75 (12%) fewer ages. For WFAZ, differences in the
Because gender and race were used as matching criteria, the proportions are the same in controls as for cases. NA, not R-C group were significantly larger than
applicable.
for the NR group at 1, 2, 4, and 6 months.
The odds ratios for being less than the
differences appeared by 1 week of age. cept WFAZ in the SR group. The de-
third percentile for cases versus con-
Peak differences for WFAZ occurred at creases in mean WFAZ between cases
trols were generally large in the post-
4 months of age in each category: 21.6 in the NR group and matched controls
natal period. At 2 months, the odds
(SV), 21.5 (CR), 20.6 (SR), 20.2 (NR). were small compared with the de-
ratios for the R-C group were 12.1
Peak differences for LFAZ were 21.4 at creases for children requiring repair
(WFAZ), 3.8 (LFAZ), and 20.9 (HCFAZ) and
4 months (SV), 21.3 at 2 months (CR), but were significant between 2 and 18
for the NR group were 3.9 (WFAZ), 2.1
20.6 at 2 months (SR), and 20.3 at 0.5 months.
(LFAZ), and 2.5 (HCFAZ).
months (NR). Differences in growth There were substantial differences
were smaller after 4 months of age but between controls and cases requiring Exploratory Analysis of Age and
persisted through age 36 months, ex- repair in length as well as weight. Ac- Repair Status
cordingly, decreases in WFLZ were There were 25 973 visits from 180 cases
generally smaller than for WFAZ. and 1643 controls included in the fol-
TABLE 2 Diagnostic Categories of Cases lowing analyses. The median age at
with CHD by Repair Category Few HC measurements were available
at birth and 36 months in the electronic second repair (or first if only 1 was
CHD Diagnostic SV CR SR NR
Categories record, so only measurements between performed) was 130 days (interquartile
Hypoplastic left heart 14 1 week and 24 months were evaluated. range 46–213). Among cases in the R-C
syndrome Even at those ages, HC was measured group, increasing z scores were, tem-
Tricuspid atresia 5 less often than weight and length. Be- porally, more strongly associated with
Unspecified single ventricle 13
tween 2 weeks and 24 months, the pat- age than with repair status. There was
abnormality
Double-outlet right ventricle 1 4 tern of differences in HCFAZ between a large, significant increase in slopes
Pulmonary valve abnormalities 4 2 13 84 cases and controlswas generally similar (Dz score/time in years) for WHO weight
Transposition of the great 21 z score before and after 4 months (b =
arteries
to the pattern seen for weight and length
Truncus arteriosus 3 with a few important exceptions. There 4.2, 95% confidence interval 3.6–4.9).
Atrioventricular canal 9 was no difference in mean HCFAZ be- The difference in slopes before and af-
Coronary abnormalities 3 ter repair was smaller (b = 2.1, 95%
tween cases and controls in the NR
Tetralogy of Fallot 5 24
Total anomalous pulmonary 1 1 group. There were also no differences in confidence interval 1.7–2.5). This overall
venous return HCFAZ between cases and controls in the pattern of findings was robust to sen-
Partial anomalous pulmonary 1 SV group at 9 months and older, but sitivity analyses excluding data from the
venous return
a substantial decrease in HCFAZ per- first month after surgery and using the
Aortic abnormalities 1 19
Aortic valve abnormalities 3 6 75 sisted for cases in the CR and SR groups. age at first surgery rather than second
Pulmonic artery abnormalities 2 2 surgery when .1 was performed.
Patent ductus arteriosus 23 24 Comparison of Proportion Below
Atrial septal defect (including 17 54 DISCUSSION
the Third Percentile
patent foramen ovale)
Ventricular septal defect 40 360 There was no difference in the pro- Within weeks of birth, children with
Vascular ring 8 2
portion of cases and controls with CHD show large, early, statistically sig-
Mitral or tricuspid valve 6
abnormalities growth parameters below the third nificant deficits in weight, length, and
Other 5 1 percentile (z score #1.88) at birth in HC trajectory compared with matched
Total 37 52 159 608 either the R-C or NR categories (Fig 4). In controls without CHD from the same

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FIGURE 2
Means and 95% confidence intervals at typical ages for preventive visits for WHO z scores for cases and controls. Means are plotted when data were available for
at least 6 cases. Statistically significant differences (P , .05 using Student’s t test) are marked with a small plus.

primary care network. The largest dif- magnitude of differences in WFAZ at 1 The strengths of our study include
ferences in weight occurred at 4 months year for cases in the CR and SR groups comparison of growth of cases with
of age. Full catch-up growth was not seen was similar to those described by a control population rather than solely
by 36 months for children with CHD re- Knirsch et al.19,20 with published references, the rela-
quiring repair. Children with CHD re- A small increase in the risk of poor tively large sample size, and the con-
quiring repair were much more likely growth is seen even in the population of firmation of diagnoses with chart
to be below the third percentile for patients with CHD that does not require review rather than reliance solely on
weight, length, and HC in early infancy. surgery (NR group). The majority of billing codes. Analysis of cases using z
The magnitude and timing of differences subjects in this group had ventricular scores without comparison with peers
for WFAZ and LFAZ for cases in the SV septal defects, which may be hemody- would have mischaracterized the dif-
group were similar to those published namically significant early in life even if ferences between these children with
by Williams et al in 2011, and the they later self-resolve. CHD and healthy children. For example,
at 6 months of age, 5.8% of cases, and
0.5% of controls in the C-R group had
microcephaly (HC less than third per-
centile). Therefore, cases were 11.6
times as likely as controls to have mi-
crocephaly. If we had compared them
only to the WHO standards, the expec-
ted proportion of microcephaly would
have been 3%, and it would have ap-
peared that cases were only 1.9 times
as likely as healthy children to have
microcephaly, dramatically under-
FIGURE 3 estimating the difference between
Median weight for cases requiring CR and matched controls plotted on WHO growth curve. Values for children with CHD and healthy children
male and female subjects are combined by converting female z scores to the equivalent weight for male
subjects and plotting on the male growth curve. All time points demonstrated statistically significant from the same population. Extensive
(P , .05) differences between case and control groups at $1 month. efforts were also made to identify

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FIGURE 4
Proportion of controls versus cases below the third percentile for weight (WFA), length (LFA), and HC
(HCA) for age. The R-C includes subjects from the SV, CR, and SR categories. Statistically significant
differences (P , .05 using Fisher’s exact test) are marked with a small red plus.
erroneous values without eliminating
values from subjects with growth at the
extremes of the distribution. The limi-
tations of our study include its reliance
on a single network, its retrospective
nature, the lack of HC data at birth and
in the neonatal period, lower case
numbers for specific categories of dis-
ease complexity, and the variability in
timing of growth measurements. We
also did not have sufficient information
to determine whether some patients
were cyanotic before repair, which
likely has a large impact on growth.7,21
A postnatal decrease in HC growth ve-
locity in children with CHD would in-
dicate a restriction of brain growth
during the critical developmental pe-
riod of infancy and may have lifelong
effects on neurodevelopment.2,3 It is
important to determine whether this
decrease in HC growth in children with
CHD is confirmed in other studies and
whether it is modifiable by nutritional
or other treatments. The lack of HC
values at birth and our subsequent
inability to determine more precisely
the time point at which differences in
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HC become apparent, particularly in
the SV and CR groups, is a significant
limitation to our study. Review of 3
published studies evaluating HC at
birth in children with CHD does not
reveal a consistent answer.22–25
One previous study found no associa-
tion between prerepair weight ,10th
percentile and neurodevelopmental out-
comes among children with CHD. How-
ever, the sample size of 101 subjects may
not have been sufficient to identify an
association if one were present, and the
study did not formally assess HC.20
It is important to identify the etiology of
poor growth in CHD in order to guide
attempts to improve growth. Inade-
quate caloric intake certainly plays
a role in poor growth for at least some
children with CHD.19 Children with CHD
frequently have feeding difficulties,6
and many have increased metabolic
demands as a result of their cardiac
defect.26 These higher demands are of-
ten most profound in the first 6 months
of life as pulmonary vascular resistance
decreases. However, decreased growth
in children with CHD may also be related
ARTICLE
to other factors, such as genetic abnor-
malities, decreased growth factors, and
hormonal changes. When caloric intake
is inadequate to meet demands, effects
are generally seen in weight before
length and finally HC. In this population,
no lag was seen between the decreased
growth trajectory for cases in WFAZ, LFAZ,
and HCFAZ. This simultaneous change in
trajectory supports the idea that im-
paired growth in children with CHD re-
quiring repair is mediated at least in
part by factors unrelated to nutrition.
Dinleyici et al identified decreases in
insulin-like growth factor 1 (IGF-1), an
important anabolic hormone affecting
childhood growth, in children with
CHD, particularly those who are cya-
notic.21 Another recent study identified
increases in IGF-1 and its carrier protein
insulin-like growth factor binding
protein-3 after surgical repair in chil-
dren with acyanotic CHD.27 Although
the authors postulate that these
increases are related to improved
postoperative nutrition, the increase in
growth factors may be more directly
related to the repair, which often
results in resolution of congestive
heart failure with improved cardio-
vascular physiology. However, our ex-
ploratory analysis of time at repair did
not suggest a strong independent as-
sociation between repair and growth
velocity in the overall population. Rather,
a consistent improvement of growth ve-
locity at ∼4 months was seen. Pro-
spective evaluation will be crucial to
confirm this finding and to determine if
it is related to diet, such as the addition
of solid foods at ∼4 months of age, or
primarily mediated by growth factors
or other physiologic changes.
CONCLUSIONS
Children with complex CHD have large,
early, and sustained decreases in
growth trajectory compared with their
peers. The simultaneous change in all
3 parameters seen in this analysis
e241
supports the role of factors beyond
calorie balance in the growth of children
with CHD. However, the extent to which
the poor growth seen in children with
CHD is caused by potentially modifiable
factors, such as the amount and type of
nutrition support, medical treatment of
CHD, and timing of surgical repair, is
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 Growth in Children With Congenital Heart Disease
Carrie Daymont, Ashley Neal, Aaron Prosnitz and Meryl S. Cohen
Pediatrics 2013;131;e236
DOI: 10.1542/peds.2012-1157 originally published online December 10, 2012;

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 Growth in Children With Congenital Heart Disease
Carrie Daymont, Ashley Neal, Aaron Prosnitz and Meryl S. Cohen
Pediatrics 2013;131;e236
DOI: 10.1542/peds.2012-1157 originally published online December 10, 2012;

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