Valvular Heart Disease in Pregnancy


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


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 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


Risk Factor

  • Prior cardiac event or arrhythmia
  • New York Heart Association (NYHA) Class >II or cyanosis
  • Left heart obstruction
  • Systemic ventricular dysfunction (ejection fraction <40%)

Score and Risk of Cardiac Complications

0: 5% risk
1: 27% risk
>2: 75% risk


Risk Factor and Weight


Score and Risk of Cardiac Complications

0-0.5: 2.9% risk
0.51-1.5: 7.5% risk
1.51-2.5: 17.5% risk
2.51-3.5: 43.1% risk
>3.51: 70% risk

History of arrhythmia


Cardiac medication prior to pregnancy


NYHA Class ≥II


Left heart obstruction


Systemic atrioventricular valve regurgitation (moderate or severe)


Pulmonic atrioventricular valve regurgitation (moderate or severe)


Mechanical valve prosthesis


Cyanotic heart disease (corrected or uncorrected)



Risk Classification

Cardiac Lesion

I: No detectable increased risk of maternal mortality and no/minimal increase in maternal morbidity

  • 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

II: Small increased risk of maternal mortality or moderate increase in morbidity

Unoperated atrial or ventricular septal defect, repaired tetralogy of Fallot, most arrhythmias

II-III: Depending on patient

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

III: Significantly increased risk of maternal mortality or severe morbidity; expert cardiac and obstetric pre-pregnancy, antenatal, and postnatal care are required

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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