Valvular Heart Disease in Pregnancy

Feb 12, 2018 | Kathryn Lindley, MD, FACC; Dominique Williams, MD

Expert Analysis

Introduction

Cardiovascular disease has emerged as one of the leading causes of maternal

morbidity and mortality in the United States. 1 With advancements in medicine and
surgery, more women with acquired and congenital heart disease (CHD) are
reaching child bearing age and desiring pregnancy. 2,3 There is a vast array of
congenital and acquired valvular disease that may be present in pregnant women.
Valvular heart disease due to rheumatic heart disease has declined, but it remains
a prevalent cause of maternal cardiovascular morbidity and mortality in non-
industrialized nations and in immigrant populations. 4-8 Mechanical prosthetic
valves pose unique challenges in management of the pregnant patient given the
requirement for anticoagulation. Given the complexity of valvular heart disease in
pregnancy, women with congenital and acquired heart disease should be managed
with a multidisciplinary approach before and throughout pregnancy. 9-11 This
article will focus on the management of valvular heart disease during pregnancy.

Hemodynamics in Pregnancy
Significant hemodynamic changes occur during pregnancy, which can lead to
decompensation in the setting of severe valvular disease. Cardiac output increases
by 30-50% due to increased stroke volume and, to a lesser extent, increased heart
rate later in pregnancy. Cardiac output rises early in pregnancy and plateaus
between the second and third trimesters. 12-14 Additionally, systemic vascular
resistance decreases by the end of the second trimester and then slowly begins to
increase until term. 15 Pregnancy is accompanied by physiologic anemia due to
greater expansion in plasma volume than in red blood cell mass. 16 Together, these
changes lead to increased flow, and thus increased gradients, across pre-existing
valvular lesions. 17 Lastly, the hypercoagulable state of pregnancy predisposes to
thrombosis, which prompts concern, especially in the patient with prosthetic
valves. 18
During labor and delivery, maternal hemodynamics are influenced by an array of
factors, including response to pain, method of delivery, and analgesia. Cardiac
output increases up to 30% in the first stage of labor and up to 80% in the
immediate post-partum period. 19,20 The increase in cardiac output is driven by
increased stroke volume, which remains elevated up to 24 hours post-partum. 19
With each uterine contraction, 300-500 ml of blood is "auto-transfused" from the
placental to systemic circulation. 13,21 Similarly, systolic and diastolic blood pressure
increase with each uterine contraction. 19 Epidural and spinal analgesia may result
in transient hypotension related to systemic vasodilation. Alterations in maternal
hemodynamics change dramatically in the first 24 hours post-partum. Preload
increases with relief of inferior vena compression by the uterus; however, blood
loss can also be significant. 19 Although blood loss is expected with both vaginal
and cesarean deliveries, it is generally more profound with cesarean delivery. 22
Shifts in maternal hemodynamics peak within 24-72 hours after delivery. Thus, it
is within this period that women are at increased risk for symptomatic heart
failure (HF) due to underlying valvular disease or ventricular dysfunction. Lastly,
pregnancy creates a hypercoagulable state. The risk of thrombosis peaks during
the post-partum period. It is highest within the first 6 weeks post-partum, but
increased risk persists up to 12 weeks after delivery. 23 Meticulous management of
anticoagulation in women with a prosthetic valve is required during this period
given the high risk of thrombosis.
Risk Stratification

Preconceptual counseling and risk stratification of women with valvular heart

disease is ideal and recommended based on current guidelines. 24 Preconceptual
imaging with echocardiogram and/or myocardial resonance imaging can assist with
risk assessment for both maternal and fetal adverse outcomes and allow for
preconceptual interventions if indicated. There are three well-known models to
assist with maternal cardiac risk stratification. The Cardiac Disease in Pregnancy
(CARPREG) risk score was derived from a prospective multicenter study of
pregnant women with congenital and acquired heart disease. This risk score
stratifies women based on four predictors, one of which includes left-sided heart
obstruction. 25 The Zwangerschap bij Aangeboren HARtAfwijkingen I (ZAHARA) risk
score was derived from a study of pregnant woman with CHD. In contrast to the
CARPREG score, valvular heart and mechanical prosthesis are used in the risk
prediction model. 26 The World Health Organization (WHO) classification divides
women with congenital and acquired heart disease into four classes, ranging from
low to high risk. Women who fall into WHO Class IV are at the highest risk, and
thus pregnancy is contraindicated due to the risk of mortality. 10 A recent
prospective validated study compared the ZAHARA score, CARPREG score, and WHO
classification in pregnant women with CHD. Although none of these are ideal, the
WHO risk assessment model performed the best in estimating cardiovascular risk
in pregnant women with CHD. 27
Left-Sided Obstructive Lesions

Left-sided obstructive lesions include aortic stenosis (AS) (subvalvular or valvular),

coarctation of the aorta and mitral valve stenosis (Shone's complex and rheumatic
heart disease). Left-sided obstructive lesions are preload dependent, yet patients
are prone to pulmonary venous congestion. Gradients across fixed valvular lesions
increase with the physiologic increase in cardiac output, which can lead to
pulmonary venous congestion. 17 Maintenance of euvolemia with judicious use of
diuretics may be required during pregnancy and the peripartum period.
Aortic Stenosis

In women of childbearing age, AS is most commonly due to a congenital bicuspid

aortic valve, which may be associated with an aortopathy or coarctation of the
aorta. 28,29 Adverse maternal and fetal outcomes increase with the severity of AS.
The risk of hemodynamic compromise and HF is highest during the second to third
trimester, during labor and delivery, and 24-72 hours after delivery as the cardiac
output peaks. 13,19-21 Although pregnancy-related mortality is low, and reported at
zero in some studies, women with severe AS are more likely to develop HF and
atrial arrhythmias and have adverse fetal outcomes such as preterm birth and low
birth weight. 28-31

Mitral Stenosis

Moderate to severe mitral stenosis (MS) is poorly tolerated in pregnancy. As the

heart rate increases, diastolic filling time is decreased, which leads to increased
pulmonary hypertension and pulmonary venous congestion. As a result, women
with moderate to severe MS who were asymptomatic prior to pregnancy may
become symptomatic during pregnancy. Arrhythmias, specifically atrial fibrillation
(AF) and supraventricular tachycardia, are increased and occur in as many as 11%
in one study of women with rheumatic mitral valve disease. Poor fetal outcomes
including fetal growth restriction, low birth weight and preterm birth increase
with increasing severity of MS. 30,32

Management

We recommend serial imaging with echocardiography in addition to close clinical

monitoring. Echocardiography once per trimester is sufficient, with the third
trimester echocardiogram performed around 32 weeks gestation, at the time of
peak hemodynamic load. Women with a congenital bicuspid valve should have
imaging of the ascending and proximal aorta, given the association of coarctation
of the aorta and aortopathy. 24,33 The data obtained will assist with
multidisciplinary delivery planning.

Medical management for HF related to increased valvular gradients included

uptitration of nodal blocking agents, which may improve valvular gradients via
reduction in heart rate. Metoprolol, propranolol, and diltiazem are safe to use for
nodal blockade during pregnancy. 34 Diuretics such as furosemide may be used to
decrease pulmonary venous congestion, but care should be given to avoid over-
diuresis. Aortic or mitral valvuloplasty can also be considered in severely
symptomatic patients who are refractory to medical management and with
favorable anatomy. This is not recommended as a prophylactic measure. If surgical
intervention is required during pregnancy, intervention during the second
trimester, after organogenesis is complete and prior to fetal viability around 20-22
weeks, is generally recommended to maximize fetal outcomes. 35-39

Right-Sided Obstructive Lesions

Right-sided obstructive lesions, such as pulmonic stenosis, are typically well
tolerated, even when severe. 40 An increase in measured valve gradients should be
expected as cardiac output increases during pregnancy. 17 Serial clinical and
echocardiographic monitoring is appropriate in patients with severe lesions to
assess for development of right-sided HF. Women with isolated pulmonic stenosis
may be at increased risk for hypertensive disorder of pregnancy, although data
regarding this are scarce. 41 Balloon valvuloplasty may be considered in patients
who remain symptomatic despite medical management. 42

Regurgitant Lesions
During pregnancy, cardiac output increases and systemic vascular resistance
decreases. Pregnancy is a volume-overload state, with physiologic four-chamber
dilatation. As annular dilatation occurs with the increased volume load of
pregnancy, severity of regurgitation may increase. However, in the setting of
normal left ventricular systolic function, valvular regurgitant lesions are well
tolerated. 13,19,43 In patients with moderate to severe regurgitant lesions,
symptomatic volume overload may occur during the second and third trimester
and during the first 24-72 hours after delivery as cardiac output peaks. Diuretics
can be administered, and afterload reduction can be initiated with hydralazine and
nitrates during pregnancy or enalapril post-partum. Patients with significant
valvular regurgitation may also be prone to atrial arrhythmias.
Mechanical Heart Valves

Management of anticoagulation in women with mechanical heart valves poses a

unique challenge given the risk of valve thrombosis and risk of adverse fetal
outcomes. Warfarin is associated with fetal birth defects, and studies have shown
this effect may be pronounced when used during weeks 6-12. 44-46 The fetal risk
appears to be dose dependent, with observed fetal risk similar to low molecular
weight heparin (LMWH) when the daily dose is ≤5 mg of warfarin. 47-49 Although
maternal risk of valve thrombosis is lowest with continued warfarin use
throughout all three trimesters of pregnancy, fetal risk is optimized with the use
of LMWH or low dose (≤5 mg daily) of warfarin. Thus, weighing risks and benefits
of both maternal and fetal health, warfarin continuation is generally
recommended when daily maternal dose is ≤5mg daily, whereas switching to
therapeutic LMWH should be considered in patients who require higher warfarin
dosing. 24,47,49 Low-dose aspirin is recommended in mechanical and bioprosthetic
valves in the second and third trimester. 24 When LMWH is used for
anticoagulation, meticulous monitoring of anti-Xa levels is required. Anti-Xa levels
should be measured 4-6 hours after a dose with a goal range of 0.8–1.2 U/ml. 24,50
Arrhythmias

Arrhythmias may be poorly tolerated in the setting of valvular heart disease

during pregnancy. These can be managed with nodal blockade using calcium
channel or beta-blockers or anti-arrhythmic agents such as flecainide or sotalol
when needed. Adenosine use is safe in pregnancy and unlikely to reach the fetal
circulation given the short half-life. Synchronized electrical cardioversion is
generally safe. 51-53 Anticoagulation should be given to pregnant women with MS
and AF given the increased risk of stroke. 52,54-56

Labor and Delivery

Multidisciplinary delivery planning is important for women with valvular disease.
Valvular regurgitant lesions are usually well-tolerated in contrast to stenotic
lesions. Early use of epidural anesthesia is recommended for regional anesthesia
with slow uptitration in dosage to achieve adequate analgesia. Intravenous fluids
should be used to maintain euvolemia. In women with mild symptoms and good
functional status, vaginal delivery with consideration of an assisted second stage
of labor to reduce the need for prolonged Valsalva is appropriate. In highly
symptomatic patients, planned cesarean section with the assistance of a cardiac
anesthesiologist may be required. 57 Antibiotics for endocarditis prophylaxis are not
recommended at the time of delivery. 10
Anticoagulation should be held prior to delivery because therapeutic
anticoagulation increases the risk for hemorrhagic complications with regional
anesthesia, and warfarin (which crosses the placenta) increases the risk for fetal
intraventricular hemorrhage. 45 Warfarin should be held after 36 weeks gestation
and replaced with LMWH or unfractionated heparin. Anticoagulation should be
discontinued 24 hours prior to the induction of labor or cesarean section. 56
Intravenous unfractionated heparin can then be resumed 6 hours after a vaginal
delivery or 12 hours after a cesarean delivery, if adequate hemostasis is
achieved. 10,58 Warfarin may be resumed post-partum and is safe for use during
breastfeeding.

Family Planning

Preconceptual counseling for women with congenital and acquired heart disease is
important given the risk of hemodynamic deterioration with pregnancy, risk of
congenital heart defects in the offspring of women with CHD, and the potential
teratogenicity of cardiac medications. Combined hormonal methods of
contraception that contain estrogen, including the patch, the pill, and the vaginal
ring, should generally be avoided by women with mechanical valves or AF or
flutter. These methods are associated with increased risk of thrombosis. Long-
acting, reversible methods of contraception, such as the hormonal or copper
intrauterine device or etonogestrel subcutaneous implant, offer highly effective (1-
year failure rate <1%) and safe protection against unintended pregnancy for all
cardiac patients. 59-62

CARPREG RISK SCORE

Risk Factor Score and Risk of Cardiac Complications

Prior cardiac event or 0: 5% risk
arrhythmia 1: 27% risk
New York Heart Association >2: 75% risk
(NYHA) Class >II or cyanosis
Left heart obstruction
Systemic ventricular
dysfunction (ejection fraction
<40%)

ZAHARA RISK SCORE

Risk Factor and Weight Points Score and Risk of Cardiac Complications

0-0.5: 2.9% risk

History of arrhythmia 1.5 0.51-1.5: 7.5% risk
1.51-2.5: 17.5% risk
2.51-3.5: 43.1% risk
Cardiac medication prior 1.5 >3.51: 70% risk
to pregnancy

NYHA Class ≥II 0.75

Left heart obstruction 2.5

Systemic atrioventricular 0.75

valve regurgitation
(moderate or severe)

Pulmonic atrioventricular 0.75

valve regurgitation
(moderate or severe)

Mechanical valve 4.25

prosthesis

Cyanotic heart disease 1.0

(corrected or
uncorrected)

WHO CLASSIFICATION FOR PREGNANCY

Risk Classification Cardiac Lesion

I: No detectable increased risk of
maternal mortality and
no/minimal increase in maternal
morbidity
II: Small increased risk of
maternal mortality or moderate
increase in morbidity
II-III: Depending on patient
III: Significantly increased risk of
maternal mortality or severe
morbidity; expert cardiac and
obstetric pre-pregnancy,
antenatal, and postnatal care are
required
Uncomplicated, small or mild pulmonary
stenosis; ventricular septal defect; patent
ductus arteriosus; mitral valve prolapse
with no more than trivial mitral
regurgitation
Successfully repaired simple lesions (atrial
or ventricular septal defect, patent ductus
arteriosus, anomalous pulmonary venous
drainage)
Isolated ventricular extrasystoles and atrial
ectopic beats
Unoperated atrial or ventricular septal defect,
repaired tetralogy of Fallot, most arrhythmias
Mild ventricular impairment, heart
transplantation, hypertrophic cardiomyopathy,
native or tissue valvular heart disease not
considered WHO I or IV, repaired coarctation,
Marfan syndrome without aortic dilatation,
bicuspid valve with aorta <45 mm
Mechanical valve, systemic right ventricle,
Fontan circulation, unrepaired cyanotic heart
disease, other complex CHD, Marfan syndrome
with aorta 40–45 mm, bicuspid aortic valve
with aorta 45–50 mm
IV: Pregnancy is contraindicated Pulmonary hypertension/Eisenmenger
syndrome, systemic ventricular ejection
fraction <30% or systemic ventricular
dysfunction with NYHA class III–IV
Severe MS, severe symptomatic AS, Marfan
syndrome with aorta >45 mm,
bicuspid aortic valve with aorta >50 mm,
native severe coarctation
Prior peripartum cardiomyopathy with any
residual impairment of ventricular function

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Keywords: Adenosine, Analgesia, Anemia, Anesthesia, Conduction, Anesthesia, Epidural,

Anti-Arrhythmia Agents, Anti-Bacterial Agents, Aorta, Aortic Coarctation, Aortic Valve, Aortic
Valve Stenosis, Arrhythmias, Cardiac, Aspirin, Atrial Fibrillation, Atrial Premature Complexes,
Balloon Valvuloplasty, Heart Valve Diseases, Blood Pressure, Breast Feeding, Cardiac Output,
Cardiomyopathies, Cardiomyopathy, Hypertrophic, Cardiovascular Diseases, Cesarean Section,
Child, Contraception, Cyanosis, Desogestrel, Dilatation, Diltiazem, Diuresis, Diuretics, Drainage,
Ductus Arteriosus, Patent, Echocardiography, Eisenmenger Complex, Electric Countershock,
Enalapril, Endocarditis, Erythrocytes, Estrogens, Family Planning Services, Fetal Growth
Retardation, Fetal Viability, Flecainide, Furosemide, Half-Life, Heart Defects, Congenital, Heart
Failure, Heart Rate, Heart Septal Defects, Ventricular, Heart Transplantation, Heart Valve
Diseases, Heart Ventricles, Hemostasis, Heparin, Heparin, Low-Molecular-Weight, Hydralazine,
Hyperemia, Hypertension, Pulmonary, Hypotension, Infant, Low Birth Weight, Infant, Newborn,
Intrauterine Devices, Copper, Labor, Induced, Marfan Syndrome, Maternal Mortality,
Metoprolol, Mitral Valve, Mitral Valve Stenosis, Mitral Valve Prolapse, Mitral Valve
Insufficiency, Nitrates, Organogenesis, Pain, Peripartum Period, Placenta, Plasma Volume,
Postnatal Care, Pregnancy, Pregnancy Trimesters, Pregnancy Trimester, Third, Pregnancy
Trimester, Second, Pregnancy Trimester, First, Premature Birth, Propranolol, Prospective
Studies, Prostheses and Implants, Pulmonary Valve Stenosis, Rheumatic Heart Disease, Risk
Assessment, Risk Factors, Sotalol, Stroke, Stroke Volume, Tachycardia, Supraventricular,
Tetralogy of Fallot, Uterine Contraction, Thrombosis, Uterus, Vascular Resistance, Vasodilation,
Ventricular Dysfunction, Ventricular Function, Ventricular Premature Complexes, World Health
Organization
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Last Updated February 2022