congenital heart disease

1. Review Cardiac disease in
pregnancy.Part 1: congenital
heart disease
Authors Emily Gelson / Mark Johnson / Michael Gatzoulis / Anselm Uebing
Key content:
• Heart disease is now the most common indirect cause of maternal death in the
United Kingdom.
• Neonatal morbidity and mortality from fetal growth restriction and prematurity
are markedly increased in women with heart disease.
• Women with congenital heart disease should ideally have a planned pregnancy
managed by a multidisciplinary team which includes obstetricians,cardiologists,
anaesthetists,neonatologists and midwives.
Learning objectives:
• To understand the changes to cardiovascular physiology during pregnancy.
• To recognise the risk factors for poor pregnancy outcome in cardiac disease.
• To understand the general management principles for women with cardiac disease
in pregnancy.
Ethical issues:
• Should we be recommending termination of pregnancy in women with high risk
cardiac lesions?
• How do we manage women who become pregnant against medical advice?
• What is the role of surrogacy in women with high risk cardiac lesions?
Keywords acquired heart disease / congenital heart disease / neonatal outcome /
pregnancy / prepregnancy counselling / risk assessment
Please cite this article as: Gelson E, Johnson M, Gatzoulis M, Uebing A. Cardiac disease in pregnancy. Part 1: congenital heart disease. The Obstetrician & Gynaecologist 2007;9:15–20.
Author details
15
Review
2007;9:15–20
10.1576/toag.9.1.015.27291 www.rcog.org.uk/togonline
The Obstetrician & Gynaecologist
© 2007Royal College of Obstetricians and Gynaecologists
Emily Gelson BS MB BCh
Clinical Fellow in Pregnancy and Heart
Disease
Chelsea and Westminster Hospital,
369 Fulham Road, London SW10 9NH, UK
Email: e.gelson@imperial.ac.uk
(corresponding author)
Mark Johnson PhD MRCP MRCOG
Reader in Obstetrics and Obstetric
Medicine
Chelsea and Westminster Hospital,
London, UK
Michael Gatzoulis MD PhD MRCP
Professor of Cardiology, Congenital Heart
Disease
Adult Congenital Heart Disease Unit,
Royal Brompton and Harefield NHS Trust and;
National Heart and Lung Institute,
Imperial College,
London SW3 6NP, UK
Anselm Uebing MD
Fellow in Adult Congenital Heart Disease
Adult Congenital Heart Disease Unit,
Royal Brompton and Harefield NHS Trust and;
National Heart and Lung Institute,
Imperial College,
London, UK
TOG9_1_15-20 1/9/07 12:48 AM Page 15

2. Introduction
The incidence of heart disease during pregnancy in
the UK has remained constant at 0.9% over several
decades.1
However,the severity and the risk it poses
during pregnancy appears to be increasing.Heart
disease has re-emerged as one of the leading causes
of maternal mortality (2.2 per 100 000) and is now
the most common indirect cause of maternal death
in the UK.2
Pregnancy not only poses a risk of
maternal mortality but also of serious morbidity
such as heart failure,stroke and cardiac arrhythmia.
The fetus is not spared: neonatal morbidity and
mortality from fetal growth retardation and
prematurity are markedly increased.3
In Part 1 of
this article we review congenital heart disease in
pregnancy and in Part 2 we look at acquired heart
disease.
Congenital heart disease
In the developed world,congenital heart disease is
now more common in pregnant women than
acquired heart disease. Among pregnant women
with heart disease,the proportion with heart disease
of congenital origin has risen in two decades from
5% to almost 80%.4
This reflects advances in cardiac
surgery and medication,meaning that 85% of the 7
in 1 000 infants with congenital heart disease now
survive to adulthood and reproductive maturity.5
Physiological changes in
normal pregnancy
During normal pregnancy there are dramatic
alterations in cardiovascular physiology initiated by
a fall in systemic vascular resistance to 30–70% of
its preconception value by 8 weeks of gestation.6
The mechanism responsible for triggering such
widespread vasodilatation is unclear,but increased
circulating levels of estrogens,vasodilatory
peptides or factors such as nitric oxide and
calcitonin-gene related peptide (CGRP) have all
been suggested as possible causes.The fall in
systemic vascular resistance results in fluid
retention and an increased blood volume.Since
there is a relatively greater expansion in plasma
volume this results in a fall in haematocrit and
plasma osmolality. The increase in cardiac output is
secondary to a greater stroke volume and higher
heart rate.It rises to a peak between 20–24 weeks of
gestation and remains stable until term. Arterial
blood pressure falls until mid pregnancy,gradually
returning to prepregnancy levels late in the second
trimester.Prolonged volume overload results in
progressive physiological left ventricular
hypertrophy.
Labour,particularly the second stage,is associated
with a further increase in cardiac output.Pain
induces a sympathetic response,causing an
increase in heart rate.Stroke volume is augmented
by auto-transfusion during contractions.Following
delivery the return of uterine blood into the
systemic circulation results in a further increase in
cardiac output.Stroke volume,heart rate and
cardiac output remain high for 24 hours post
delivery,with rapid intravascular volume shifts in
the first 2 weeks postpartum. Thus,the later stages
of labour and early postpartum period are periods
of high risk of pulmonary oedema.7
Management principles
Women with congenital heart disease should
ideally have a planned pregnancy managed by a
multidisciplinary team which includes
obstetricians,cardiologists,anaesthetists,
neonatologists and midwives.This requires close
collaboration between tertiary cardiac and high-
risk obstetric services.Effective management
involves prepregnancy counselling and risk
assessment,close fetal and maternal monitoring
during pregnancy,a detailed management plan for
labour and delivery and close surveillance in the
immediate postpartum period.
Prepregnancy counselling
Prepregnancy counselling enables the impact of
pregnancy on pre-existing heart disease to be
explained to the woman and her family to allow
them to make informed choices.The risks to the
mother and fetus should be discussed and the
likelihood of congenital heart disease in the fetus
outlined (Box 1). Any medical,interventional or
surgical treatments that can improve pregnancy
outcome should be considered.
Labour and delivery
The appropriate timing for delivery is crucial to
balance maternal and neonatal morbidity and
mortality. A clear plan of management for labour
and delivery should be established in advance,
clearly documented and widely disseminated.
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Review 2007;9:15–20 The Obstetrician & Gynaecologist
© 2007Royal College of Obstetricians and Gynaecologists
Box 2
Cardiac indications for caesarean
section26
• Aortopathy with aortic root 4cm
• Aortic dissection or aneurysm
• Warfarin treatment within 2weeks
Box 1
Predictors for adverse pregnancy-
related cardiac events3
Predictors for a maternal cardiac event
• Prior cardiac event (heart failure, transient ischaemic attack
or stroke) or arrhythmia
• Baseline NYHA class II or cyanosis
• Left heart obstruction (mitral valve area 2cm2
, aortic valve
area 1.5cm2
, or peak ventricular outflow tract gradient
30mmHg by echocardiography)
• Reduced systemic left ventricular function (ejection fraction
40%)
Predictors for adverse neonatal events
• NYHA class II or cyanosis during the baseline prenatal visit
• Maternal left ventricular obstruction
• Maternal smoking
• Multiple gestation
• Anticoagulation during pregnancy
NYHA NewYork Heart Association
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3. In general,vaginal delivery with low dose epidural
anaesthesia is the mode of choice (Box 2 shows
cardiac indications for caesarean section).Labour
requires careful monitoring of both mother and
fetus.Preload and blood pressure should be
monitored carefully and blood loss minimised.
Women should be nursed in the left lateral position.
Forceps or ventouse delivery can be used to shorten
maternal expulsive effort in the second stage.
Antibiotic prophylaxis should be given during
labour and delivery for all women except those with
repaired patent ductus arteriosus (PDA),isolated
ostium secundum atrial septal defects and mitral
valve prolapse without regurgitation.
In the management of the third stage,bolus doses
of oxytocin should be avoided as they can cause
severe hypotension.Low dose oxytocin infusions
are safer.Ergometrine should also be avoided in
most cases as it can cause acute hypertension.
Uterine compression sutures can be helpful in the
management of uterine atony at caesarean section.
The safety of misoprostol is yet to be determined.
Careful haemodynamic monitoring postpartum is
typically required for 24–72 hours,but this should
be extended to 10–14 days in women with
pulmonary hypertension.Multidisciplinary follow-
up should take place 6 weeks after delivery.
Specific lesions and maternal
and fetal risk
Risk to the mother from congenital heart disease
appears to be determined by the ability of her
cardiovascular system to adapt to pregnancy.
Different congenital cardiac lesions carry specific
mortality risks,7
dependent on current
haemodynamic status,previous operations and
anatomical features.8
Pregnancy also poses the risk
of serious maternal morbidity.In 2001,a large
prospective study of pregnancy outcomes in
women with congenital heart disease reported a
13–23.5% rate of primary cardiac events.3
Pulmonary oedema and/or cardiac arrhythmia
account for the majority of events,with
thromboembolism,angina,hypoxaemia and
infective endocarditis also reported.Predictors of
primary maternal cardiac events are:9
• prior cardiac event
• prior arrhythmia
• NewYork Heart Association (NYHA) functional
class II
• left heart obstruction
• myocardial dysfunction.
Low risk lesions
Small left-to-right shunts
In pregnancy,increased cardiac output and blood
volume are counterbalanced by a decrease in
peripheral vascular resistance.Left-to-right
shunting in women with atrial septal defects
(ASDs),ventricular septal defects and PDA is,
therefore,reduced.In the absence of pulmonary
hypertension,pregnancy,labour and delivery are
well tolerated.10
Women with ASDs are at risk of
atrial arrhythmias and paradoxical emboli. As such,
there is a low threshold for heparin prophylaxis.
Labour needs to be managed carefully as acute
blood loss or vasodilatation (from regional
anaesthesia) can affect the degree and direction of
intracardiac shunting acutely,reducing left
ventricular output.
Coarctation of the aorta
Coarctation of the aorta (Figures 1and 2) occurs in
6–8% of patients with congenital heart disease.The
majority of cases are diagnosed in infancy or
childhood and are either surgically corrected or
treated by balloon dilatation or stent implantation.
Women with repaired coarctation of the aorta are
expected to reach childbearing age.In contrast,
native coarctation is encountered much less
frequently.Pregnancy is usually well tolerated in
women with adequately repaired coarctation.11
It is
essential to assess cardiac status before conception,
excluding and appropriately managing
complications such as re-coarctation,aneurysm at
the site of repair,an associated bicuspid aortic valve
or systemic hypertension.In both corrected and
native coarctation,pregnancy poses the risk of
aortic dissection and rupture and resistant
hypertension.Poorly controlled hypertension can
lead to adverse neonatal outcomes (such as growth
restriction,placental abruption and premature
delivery) and maternal outcomes (including pre-
eclampsia,hypertensive crisis and rupture of an
intracranial aneurysm). As such,it needs to be
tightly controlled with beta-blockers as the first line
agent.There is a small risk of intrauterine growth
restriction with beta-blockers and fetal growth
should be monitored regularly and assessed by
ultrasound.
Tetralogy of Fallot
Tetralogy of Fallot (ToF) is the most common form
of cyanotic congenital heart disease.It is
characterised by a non-restrictive ventricular septal
defect,aortic override,pulmonary stenosis and
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Review
2007;9:15–20
The Obstetrician Gynaecologist
© 2007Royal College of Obstetricians and Gynaecologists
Figure 1
Magnetic resonance imaging of
severe aortic coarctation before
(left) and after (right) primary stent
implantation in an adult patient.
Note the aneurysmal dilatation in
the ascending aorta. (With kind
permission from Dr SV
Babu-Narayan and Dr R Mohiaddin,
CMR Unit, Royal Brompton and
Harefield NHSTrust, London, UK.)
TOG9_1_15-20 1/9/07 12:48 AM Page 17

4. right ventricular hypertrophy.In developed
countries,ToF is usually corrected surgically in
infancy,well before pregnancy is contemplated,and
it is generally accepted that pregnancy in women
with repaired ToF is well tolerated in this context.12
However,complications such as arrhythmias and
right ventricular failure do occur,particularly in the
presence of residual shunts,right ventricular
outflow obstruction and pulmonary hypertension.
Careful assessment,including echocardiography,is
advisable before pregnancy.Many women with ToF
will have significant pulmonary regurgitation and,
therefore,can become symptomatic during
pregnancy,occasionally needing diuretic treatment
or admission for bed rest.Regular cardiac review
throughout pregnancy for all women with repaired
or unrepaired ToF is advised.
Moderate risk lesions
Transposition of the great arteries
Complete transposition of the great arteries (TGA)
(Figure 3) can be repaired using Mustard rerouting,
in which the tricuspid valve and the right ventricle
support the systemic circulation.Although survival
rates for this procedure are favourable,a number of
potential long term complications exist.These
include systemic right ventricle failure,tricuspid
regurgitation,sinus node dysfunction,arrhythmias
and baffle obstruction (venous pathway
obstruction).Pregnancy is well tolerated following
an uncomplicated repair; right ventricular
dysfunction and/or atrial arrhythmia,may
however,still occur.13
In women with long term
complications,pregnancy is poorly tolerated with
an increased risk of cardiac complications.14
Many
women with corrected TGA are on ACE inhibitors,
which should ideally be stopped before conception
as they are associated with fetal nephrotoxicity and
congenital malformations.15
Since 1975,complete
repair has been carried out using the Jatene
procedure,in which the left ventricle remains the
systemic ventricle.The outcome of pregnancy in
these women remains to be seen but recent case
reports are promising.16
Cyanotic heart disease without pulmonary
hypertension
Cyanotic heart disease without pulmonary
hypertension is caused by uncorrected
transposition of the great arteries,truncus
arteriosus,uncorrected ToF with pulmonary
stenosis/atresia,univentricular heart,tricuspid
atresia and Ebstein’s anomaly with ASD.During
pregnancy the fall in systemic vascular resistance
and rise in cardiac output exacerbates any right-to-
left shunting,worsening pre-existing cyanosis and
hypoxia.Maternal complications depend mainly
on ventricular function and include haemorrhage,
paradoxical embolism and heart failure.The effects
on the fetus are marked,with a high incidence of
spontaneous miscarriage and a 30–50% risk of
premature delivery and low birthweight.The
degree of maternal hypoxaemia is the most
important predictor of neonatal outcome.17
Admission for bed rest and oxygen therapy is an
effective method of maintaining maternal oxygen
saturation and fetal oxygenation and growth.
Fontan procedure
Fontan-type procedures have become recognised as
the definitive palliative procedure available for
complex cyanotic heart defects characterised by a
single functional ventricle. Atrial separation divides
the systemic and pulmonary circulations and with
the construction of atriopulmonary connections
blood enters the pulmonary circulation without
pulsatile ventricular flow.Increasing numbers of
women with a Fontan circulation are reaching
childbearing age.The main concern regarding
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Review 2007;9:15–20 The Obstetrician Gynaecologist
© 2007Royal College of Obstetricians and Gynaecologists
Figure 2
Magnetic resonance imaging of
woman with mild residual
coarctation and aneurysm at the
site of previous coarctation repair.
The maximum diameter of the
aneurysm was 33 mm. (With kind
permission from Dr PJ Kilner and
Dr R Mohiaddin, CMR Unit, Royal
Brompton and Harefield NHSTrust,
London UK.)
Figure 3
Cardiac magnetic resonance
imaging of a patient with
transposition of the great arteries
and atrial switch operation. A baffle
(small arrows) is created in the
atria to redirect blood from the left
atrium (LA) into the systemic right
ventricle (RV). Systemic venous
blood returns to the subpulmonary
left ventricle (LV).The systemic
right ventricle (RV) is markedly
enlarged, squashing the left
ventricle. (With kind permission
from Dr Philip Kilner, CMR Unit,
Royal Brompton and Harefield NHS
Trust, London UK.)
TOG9_1_15-20 1/9/07 12:48 AM Page 18

5. pregnancy is the ability to augment,maintain and
adjust cardiac output and heart rate.There is also a
tendency towards atrial arrhythmias,which are
poorly tolerated.However,recent studies suggest
that the maternal risks of pregnancy are low in
NYHA class I–II women,provided ventricular
function is good.18
High risk lesions
Marfan syndrome
Marfan syndrome is an inherited disorder of
connective tissue. The risk of thoracic aortic
aneurysm leading to aortic dissection, rupture or
both is increased in pregnancy. This is the result
of haemodynamic stress and is dependent on
aortic root diameter. With an aortic root smaller
than 4 cm, the overall maternal mortality during
pregnancy is 1%. This increases to as much as
25% as the aortic root diameter expands beyond
4 cm.19
In this situation, pregnancy should be
postponed until aortic arch replacement.20
In the
event of an unplanned pregnancy the option of
termination should be discussed. Aortic root
diameter should be monitored throughout
pregnancy with serial echocardiograms and if
aortic root dilatation occurs, prophylactic beta
blockade is advised and hypertension should be
treated aggressively.
Pulmonary vascular disease
Pregnancy in the presence of pulmonary
hypertension of any cause remains high risk. Fixed
pulmonary vascular resistance prevents any
increase in pulmonary blood flow matching the
increased cardiac output. Pregnancy is poorly
tolerated, with a risk of worsening cyanosis and
hypoxia, arrhythmias, heart failure and death. The
majority of complications occur at term or during
the first postpartum week. Maternal mortality
depends on the underlying cause, with a 36%
maternal mortality in Eisenmenger syndrome,
30% in primary pulmonary hypertension and 56%
in secondary pulmonary hypertension.21
Women
should be advised of these risks when
contemplating pregnancy. In the event of an
unplanned pregnancy a termination should be
offered. Those who elect to continue require close
cardiovascular monitoring and bed rest from the
third trimester with monitoring for up to 14 days
postpartum. Fetal morbidity and mortality are
considerable, with premature delivery and
restricted fetal growth occurring in 50% of cases
and only 15–25% of pregnancies reaching term.
Anticoagulation, oxygen therapy and pulmonary
vasodilators (nitric oxide or prostacyclin) may
improve outcome.22
Neonatal outcome
The rate of neonatal complications is significantly
increased in women with heart disease.They include
preterm birth,being small for gestational age,
respiratory distress syndrome,intraventricular
haemorrhage and death.Maternal predictors of
adverse neonatal outcome are obstetric risk factors,
multiple gestation,smoking and anticoagulation.23
The children of a mother with congenital heart
disease are also at increased risk of inheriting a
congenital heart disease.The overall risk of
inheriting polygenic cardiac disease is quoted at
3–5%,compared with a 1% risk in the general
population.24
The risk is,in fact,dependent on the
parent’s condition,being 3% in common conditions
such as ToF and as high as 10% withASD,
coarctation of the aorta and aortic stenosis.25
Marfan syndrome is an autosomal dominant
condition and,therefore,has a 50% recurrence rate
in offspring.
Conclusion
Cardiac disease in pregnancy is a leading cause of
maternal and neonatal morbidity and mortality.
Congenital heart disease now accounts for the
majority of disease.Effective management is based
upon prepregnancy counselling and risk
assessment,close fetal and maternal monitoring
during pregnancy,a detailed management plan for
labour and delivery and close surveillance in the
immediate postpartum period.
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