Ultrasound Obstet Gynecol 2017; 50: 58–62
Published online 6 June 2017 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/uog.15998
Fetal cardiac axis in tetralogy of Fallot: associations with
prenatal findings, genetic anomalies and postnatal outcome
Y. ZHAO1 , S. EDINGTON2 , J. FLEENOR2 , E. SINKOVSKAYA1 , L. PORCHE1 and A. ABUHAMAD1
1
Department of Obstetrics and Gynecology, Eastern Virginia Medical School, Norfolk, VA, USA; 2 Department of Pediatrics, Eastern
Virginia Medical School, Norfolk, VA, USA
K E Y W O R D S: 22q11 deletion; fetal cardiac axis; fetal echocardiogram; postnatal outcome; pulmonary atresia; right aortic
arch; tetralogy of Fallot
ABSTRACT
Objective To compare prenatal findings, associated
genetic anomalies and postnatal outcome in fetuses with
tetralogy of Fallot (TOF) with normal cardiac axis (CAx)
and those with abnormal CAx.
Methods In this retrospective cohort study, 85 cases
diagnosed with TOF by prenatal ultrasound at our
clinic between 2005 and 2015 were reviewed. Follow-up
ultrasound and postnatal outcome were available for
68 cases. One case complicated with absent pulmonary
valve syndrome and a further seven cases diagnosed
postnatally with anomalies other than TOF were excluded
from the study. The remaining 60 cases of postnatally
confirmed TOF were divided according to CAx into
two groups: those with normal CAx (n = 33) and those
with abnormal CAx (n = 27). CAx was defined as the
angle between the interventricular septum and midline of
the fetal thorax at the level of the four-chamber view.
CAx > 65◦ or < 25◦ was considered abnormal. Prenatal
sonographic findings, associated genetic anomalies and
postnatal outcome were compared between the two
groups.
Results Fetuses with TOF and abnormal CAx were more
likely to have pulmonary atresia (40.7% vs 15.2%;
P = 0.026) and right-sided aortic arch (48.1% vs 21.2%;
P = 0.028) than those with normal CAx. Postnatal death
occurred in 30.4% of infants with abnormal CAx vs 6.5%
with normal CAx (P = 0.028). Incidence of tested genetic
anomalies was similar between the two groups.
Conclusion In fetuses with TOF, abnormal CAx is
associated with the presence of pulmonary atresia,
right-sided aortic arch and a higher risk of postnatal
death. Copyright © 2016 ISUOG. Published by John
Wiley & Sons Ltd.
Correspondence to: Dr Y. Zhao, Department of Obstetrics and Gynecology, Eastern Virginia Medical School, 825 Fairfax Avenue, Norfolk,
VA 23507, USA (e-mail: zhao001@evms.edu)
Accepted: 10 June 2016
Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.
INTRODUCTION
Tetralogy of Fallot (TOF) represents a common form of
congenital heart defect (CHD), with the following four
components: obstructed right-ventricular outflow tract
(RVOT), malalignment ventricular septal defect (VSD),
overriding aorta and right ventricular hypertrophy. Due
to the presence of the fetal shunts, right ventricular
pressures are not increased in the fetus; right ventricular
hypertrophy develops only postnatally. The reported
prenatal detection rate of TOF is 15–43.1% with
cardiac screening1–3 . Outflow tract and three-vessels and
trachea (3VT) views are important in diagnosis. Typical
ultrasound findings of TOF include discrepancy in great
vessel size in the 3VT view and the presence of a ‘Y’
sign in the five-chamber view. Fetuses with TOF can
have a deviated cardiac axis (CAx), but otherwise normal
appearance in the four-chamber view (4CV).
Abnormal CAx is associated with many CHDs,
especially conotruncal anomalies, of which TOF is an
example4,5 . In a previous study, abnormal CAx was
present in about one-quarter of all CHD cases and in
one-third of cases with conotruncal anomalies6 . CAx
was also found to be more prevalent in cases of fetal
conotruncal anomalies with 22q11.2 deletion7 . The etiol-
ogy of an abnormal CAx is still unclear and its association
with prenatal findings, genetic anomalies and postnatal
outcome in fetuses with TOF has not been evaluated fully.
The aim of this study was to investigate prenatal
findings, associated genetic anomalies and postnatal
outcome in fetuses with TOF and normal CAx and those
with abnormal CAx.
METHODS
This retrospective cohort study enrolled cases diagnosed
with TOF by prenatal ultrasound at Eastern Virginia
ORIGINAL PAPER
Fetal cardiac axis in tetralogy of Fallot
Medical School, Division of Maternal-Fetal Medicine,
Fetal Cardiovascular Center, between January 2005
and January 2015. Fetuses with absent pulmonary
valve syndrome or other cardiac abnormalities were
excluded from the study. Sonographic findings, genetic
testing results and postnatal outcome data were retrieved
retrospectively and reviewed. Prenatal diagnosis of TOF
was confirmed by postnatal echocardiography, surgery
or autopsy. This study was approved by the Human
Investigation Review Board at Eastern Virginia Medical
School.
Postnatally confirmed cases of TOF were divided
into two groups: those with normal CAx and those
with abnormal CAx. CAx was defined as the angle
between the interventricular septum and the midline of
the fetal thorax at the level of the 4CV. CAx > 65◦
or < 25◦ was considered abnormal (Figure 1). Measure-
ments were obtained retrospectively at end-systole on
stored 4CV images by one author (Y.Z.). Inter- and
intraobserver variability of CAx measurements were
assessed in a previous study6 . Sidedness of the aor-
tic arch and ductus arteriosus were determined in the
3VT view.
All genetic testing results were obtained either prena-
tally or postnatally. Prenatal screening for aneuploidy
was performed by first- or second-trimester screening
methods and/or by non-invasive prenatal testing. To diag-
nose chromosomal aneuploidy, prenatal karyotyping on
samples obtained by amniocentesis or postnatal kary-
otyping on peripheral blood samples was performed.
Deletion of 22q11.2 was diagnosed by fluorescence in-situ
hybridization.
Information regarding postnatal outcome was retrieved
from postnatal records.
Figure 1 Ultrasound images in four-chamber view showing: (a) normal cardiac axis (49◦ ) in a breech fetus with left aortic arch; and
(b) abnormal cardiac axis (89◦ ) in a breech fetus with right aortic arch. Cardiac axis > 65◦ was defined as abnormal.
Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.
59
Statistical analysis
All continuous or ordinal variables were documented
as median (interquartile range) and compared between
groups using the Mann–Whitney U-test. All categorical
variables were documented as percentages and compared
using the chi-square test or Fisher’s exact test, depending
on the expected cell frequencies. Odds ratios and 95%
CIs were calculated when the difference between groups
was found to be significant. All statistical analysis
was performed using SPSS Statistics 22.0 (IBM Corp.,
Armonk, NY, USA). A P-value of < 0.05 was considered
significant.
RESULTS
During the 10-year study period, 85 fetuses were
diagnosed with TOF. In 17 cases, diagnosis was not
confirmed because patients either delivered elsewhere or
were transferred to another facility for a second opinion.
Of the 68 cases with postnatally confirmed TOF, one case
was complicated by absent pulmonary valve syndrome
and was not included in the study. Seven further cases
had diagnoses other than TOF (atrioventricular septal
defect (n = 1), tricuspid atresia with L-transposition of
the great arteries (L-TGA) and coarctation of the aorta
(n = 1), polyvalvular abnormality (n = 1), L-TGA
with ventricular septal defect (VSD) (n = 1), pulmonary
atresia (PA) with intact ventricular septum (n = 1) and
perimembranous VSD (n = 2)) confirmed postnatally;
these were also excluded from the study. Ultimately,
60 cases with postnatally confirmed TOF, including one
case with double-outlet right ventricle (TOF type), were
included in the study (Figure 2).
Ultrasound Obstet Gynecol 2017; 50: 58–62.
60 Zhao et al.

TOF suspected prenatally

Normal CAx was observed in 33 (55%) fetuses and
(n = 85) abnormal CAx (all > 65◦ ) in 27 (45%) fetuses. There
was no significant difference regarding the demographic
Lost to follow-up data between the two groups (Table 1). Prevalence of
(n = 17) chromosomal aneuploidy and 22q11.2 deletion were not
statistically different between the two groups (Table 2).
Not TOF
Both PA (40.7% vs 15.2%; P = 0.026) and right-sided
(n = 7)
aortic arch (RAA) (48.1% vs 21.2%; P = 0.028) were
TOF with APVS present more frequently in fetuses with abnormal CAx
(n = 1) than in those with normal CAx. After consideration of
TOF subtypes, among fetuses with pulmonary stenosis
TOF cases enrolled (PS), a significantly higher rate of RAA was observed in
(n = 60) those with abnormal CAx (50.0% vs 17.9%, P = 0.040).
However, this was not the case for fetuses with PA
(Table 2).
Normal cardiac axis Abnormal cardiac axis Gestational age at delivery and neonatal Apgar scores
(n = 33) (n = 27) were similar between the two groups. Postnatal mortality
was significantly higher in fetuses with abnormal CAx
Figure 2 Flowchart of inclusion in the study of fetuses with than in those with normal CAx (30.4% vs 6.5%;
tetralogy of Fallot (TOF). APVS, absent pulmonary valve P = 0.028) (Table 3). There were no significant differences
syndrome. between groups regarding admission to the neonatal

Table 1 Maternal characteristics for 60 pregnancies in which tetralogy of Fallot with normal or abnormal cardiac axis (CAx) was confirmed
postnatally

Characteristic Normal CAx (n = 33) Abnormal CAx (n = 27) P

Maternal age (years) 30 (23–35) 28 (24–30) 0.349

Gestational age at diagnosis (weeks) 22.2 (20.0–26.3) 23.0 (21.7–27.1) 0.311
Gravidity 2 (1–3) 3 (1–4) 0.482
Parity 0 (0–1) 0 (0–2) 0.756
Race 0.427
White 11 (33.3) 13 (48.1)
Black 16 (48.5) 10 (37.0)
Latino 1 (3.0) 1 (3.7)
Asian 2 (6.1) 1 (3.7)
Multiracial 3 (9.1) 0 (0)
Unknown 0 (0) 2 (7.4)

Data are given as median (interquartile range) or n (%).

Table 2 Prenatal ultrasound findings and genetic results in 60 fetuses with tetralogy of Fallot with normal or abnormal cardiac axis (CAx)
confirmed postnatally

Finding Normal CAx (n = 33) Abnormal CAx (n = 27) P Odds ratio (95% CI)

Pulmonary atresia 5/33 (15.2) 11/27 (40.7) 0.026 3.85 (1.13–13.08)

MAPCA 1/21 (4.8) 5/21 (23.8) 0.184
Cardiac axis (◦ ) 52 (46–58) 71 (69–75) < 0.001
Sidedness of aortic arch 0.028 3.45 (1.12–10.63)
Left 26/33 (78.8) 14/27 (51.9)
Right 7/33 (21.2) 13/27 (48.1)
In cases with pulmonary stenosis 0.040 4.60 (1.16–18.23)
Left 23/28 (82.1) 8/16 (50.0)
Right 5/28 (17.9) 8/16 (50.0)
In cases with pulmonary atresia 1
Left 3/5 (60.0) 6/11 (54.5)
Right 2/5 (40.0) 5/11 (45.5)
Sidedness of DA in cases with RAA 0.234
Right 1/4 (25.0) 9/12 (75.0)
Left 3/4 (75.0) 3/12 (25.0)
Chromosomal aneuploidy* 10/22 (45.5) 9/20 (45.0) 1
22q11.2 deletion 2/16 (12.5) 3/14 (21.4) 0.642

Data are given as median (interquartile range) or n/N (%). Denominators represent number of cases with data available. *Including 22q11.2
deletion. DA, ductus arteriosus; MAPCA, major aortopulmonary collateral artery; RAA, right-sided aortic arch.

Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd. Ultrasound Obstet Gynecol 2017; 50: 58–62.
Fetal cardiac axis in tetralogy of Fallot
Table 3 Postnatal outcome in 60 fetuses with tetralogy of Fallot with normal or abnormal cardiac axis (CAx) confirmed postnatally
Outcome Normal CAx (n = 33)
Gestational age at delivery (weeks) 38 (35.9–39.1)
Apgar score at 1 min (n = 51) 8 (6–8)
Apgar score at 5 min (n = 51) 8 (8–9)
PGE infusion 6/27 (22.2)
Admission to NICU 16/26 (61.5)
Procedure
None 3/26 (11.5)*
Palliative surgery 1/26 (3.8)
Multistage repair 4/26 (15.4)
One-stage complete repair 18/26 (69.2)
Postnatal death 2/31 (6.5)
In cases with pulmonary stenosis 1/26 (3.8)
In cases with pulmonary atresia 1/5 (20.0)
Data are given as median (interquartile range) or n/N (%). Denominators represent number of cases with data available. *One case died
before operation. †Both cases died before operation. NICU, neonatal intensive care unit; PGE, prostaglandin E.
intensive care unit (61.5% vs 75.0%, P = 0.335) or the
type of procedure performed after delivery (P = 0.323). In
total, 11 infants received prostaglandin E (PGE) infusion
after birth. Among those, 10 had PA and one had PS. Of
the 39 infants that received postnatal surgical treatment,
1/23 with normal CAx and 4/16 with abnormal CAx
had palliative surgery only (P > 0.05). No perioperative
mortality was noted in the 34 infants that underwent
complete repair. Early complete repair < 3 months after
delivery was performed in four infants, all of whom had
PA with normal CAx. They required a prolonged hospital
stay compared with those who received complete repair
≥ 3 months after delivery (median (interquartile range),
31.3 (25.8–36.3) vs 7 (3–17) days; P = 0.048).
DISCUSSION
The 4CV is one of the standard planes used in cardiac
screening. Normal CAx measured in the 4CV is typically
at 45 ± 20◦ 8 . Fetuses with TOF can have either a normal
or an abnormal CAx. In this study, we investigated the
association of abnormal CAx with prenatal findings,
genetic anomalies and pregnancy outcome in fetuses
with TOF.
Association with prenatal findings
CAx represents the orientation of the heart within
the chest. Abnormal CAx is usually the consequence
of intracardiac and extracardiac anomalies, some of
which are well understood, such as a disproportion of
cardiac chambers and compression from intrathoracic
or abdominal masses4,5,9,10 . Abnormal CAx can be
observed in the presence of conotruncal anomalies,
with an otherwise normal-appearing 4CV. In this study,
45% of all TOF cases had an abnormal CAx, similar
to that reported previously4,5 . Over-rotation of the
bulboventricular loop is believed to be the cause of
abnormal CAx. Vigneswaran et al. found a negative
association between CAx and thymic–thoracic ratio in
Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.
61
Abnormal CAx (n = 27) P Odds ratio (95% CI)
38.6 (34.3–39.1) 0.714
8 (6–8) 0.896
8 (8–9) 0.833
5/17 (29.4) 0.724
15/20 (75.0) 0.335
0.323
2/18 (11.1)†
4/18 (22.2)
3/18 (16.7)
9/18 (50.0)
7/23 (30.4) 0.028 4.72 (1.18–34.24)
3/13 (23.1) 0.099
4/10 (40.0) 0.600
fetuses with 22q11.2 deletion, but not in fetuses with
a normal karyotype7 . They speculated that the lack
of thymic tissue may allow for greater rotation of
the developing heart and increase the CAx. Our study
included only five cases with 22q11.2 deletion and thus is
not sufficiently powered to confirm this finding. However,
not all fetuses with TOF and an abnormal CAx had
22q11.2 deletion or abnormal thymus. This indicates that
there may be other mechanisms contributing to abnormal
CAx in fetuses with TOF.
Based on studies in chick embryos, after initial dextral
looping (c-looping) and ventral bending of the heart tube,
the ‘c-shaped’ heart tube continues to bend and rotate
(s-looping), causing leftward and caudal displacement of
embryonic ventricles. Meanwhile, the distance between
the arterial and venous ends of the heart tube is shortened
due to the pressure from the splanchnopleure, forcing
rotation of the cardiac tube along the cranial–caudal
axis11–13 . In a physical simulation model, subtle
left- and rightward displacements of the caudal end
could determine the direction of cardiac looping. Left
displacement usually leads to D-looping12,14,15 . The major
momentum of rotation is from the venous end, but it
is not unreasonable to presume that changes on the
arterial end may also have an impact. Based on our
data, RAA is more common in fetuses with abnormal
CAx. Sidedness of the aortic arch is determined at the
end of cardiac looping, and thus should not impact the
direction of looping. However, an anteriorly displaced
and enlarged aorta in TOF combined with RAA may
cause anterior and rightward displacement on the arterial
end and consequently exaggerate the rotation process.
However, association between RAA and abnormal CAx
was not observed in TOF cases with PA.
Association with genetic anomalies
Chromosomal anomalies are detected frequently in
fetuses with TOF. The reported prenatal incidence is
approximately 29% if 22q11.2 deletion is included16,17 . A
recent systematic review concluded that 22q11.2 deletion
is three times more common in TOF with PA than in TOF
Ultrasound Obstet Gynecol 2017; 50: 58–62.
62
with PS, while major trisomies are more often noted in
TOF with PS18 .
No statistically significant difference was identified
between the two groups in our study in terms of prevalence
of 22q11.2 deletion. Nevertheless, 22q11.2 deletion is
a relatively common finding in fetuses with TOF, and
prenatal diagnostic testing should be offered.
Association with postnatal outcome
Reversed blood flow in the ductus arteriosus is a sign of
ductal-dependent circulation and a predictor of adverse
postnatal outcome. PGE infusion is required to maintain
patency of the ductus arteriosus after birth in those
patients. Approximately 90% of all cases that required
PGE infusion in this study had PA.
Surgical repair of TOF is performed commonly around
6 months after birth. Early operation can also achieve
excellent outcome19 . In our cohort, all 34 infants
who received complete repair survived the operation.
Estimated long-term survival (> 20 years) is more than
90% for patients with corrective surgery20 . However,
patients undergoing open heart surgery are at risk of
neurodevelopmental deficiencies16 . Complete repair of
TOF includes closure of the VSD and widening of the
RVOT. Pulmonary valve-sparing surgery (PVSS) and
transannular patch (TAP) repair are the two major
approaches. PVSS can better preserve the functional
pulmonary valve and causes fewer complications. TAP is
adopted in cases with a severely stenotic pulmonary valve.
Infants with TAP repair are at a higher risk of developing
pulmonary regurgitation and a later need for pulmonary
valve replacement17 . A pulmonary annulus Z-score of –4
or higher was reported to be a good marker for successful
PVSS repair21 . Prenatally, a pulmonary valve Z-score ≤
–3.5 in the second trimester and increased pulmonary
valve peak systolic velocity ≥ 87.5 cm/s were found to
be useful in predicting need for TAP repair and earlier
intervention22,23 .
Outcome prediction should be performed on an
individual basis. Our results suggest that fetuses with TOF
with an abnormal CAx have higher postnatal mortality.
Interestingly, this is different from the findings in cases
of diaphragmatic hernia, in which abnormal CAx did
not affect survival rate10,24 . One possible explanation
is that fetal TOF with abnormal CAx has a higher
association with PA, and PA was reported previously
as an independent risk factor for death and need for
reoperation19,25 . RVOT that fails to grow or actually
decreases in size is also associated with a poor prognosis.
We acknowledge that our study has some limitations.
Its retrospective nature limits the ability to collect
more comprehensive data. An important component of
consultation with the parents is the long-term physical
and mental outcome of fetuses with TOF, which cannot
be gained from this study. In addition, the sample size is
relatively small.
In conclusion, fetuses with TOF and abnormal CAx are
more likely to have PA and RAA and postnatal mortality
rate is higher than for those with normal CAx. However,
Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.
Zhao et al.
the likelihood of aneuploidy is similar between the two
groups. Therefore, in the presence of abnormal CAx in
fetuses with TOF, further counseling should be provided,
especially concerning the risks for genetic anomalies and
unfavorable postnatal outcome.
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