Valvular Heart Disease in Pregnancy

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

Expert Analysis

Font Size
A
A
A

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

  • 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

ZAHARA RISK SCORE

Risk Factor and Weight

Points

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

1.5

Cardiac medication prior to pregnancy

1.5

NYHA Class ≥II

0.75

Left heart obstruction

2.5

Systemic atrioventricular valve regurgitation (moderate or severe)

0.75

Pulmonic atrioventricular valve regurgitation (moderate or severe)

0.75

Mechanical valve prosthesis

4.25

Cyanotic heart disease (corrected or uncorrected)

1.0

WHO CLASSIFICATION FOR PREGNANCY

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

References

  1. Creanga AA, Berg CJ, Ko JY, et al. Maternal mortality and morbidity in the United States: where are we now? J Womens Health (Larchmt) 2014;23:3-9.
  2. van der Bom T, Bouma BJ, Meijboom FJ, Zwinderman AH, Mulder BJ. The prevalence of adult congenital heart disease, results from a systematic review and evidence based calculation. Am Heart J 2012;164:568-75.
  3. Ntiloudi D, Giannakoulas G, Parcharidou D, Panagiotidis T, Gatzoulis MA, Karvounis H. Adult congenital heart disease: A paradigm of epidemiological change. Int J Cardiol 2016;218:269-74.
  4. Zühlke L, Engel ME, Karthikeyan G, et al. Characteristics, complications, and gaps in evidence-based interventions in rheumatic heart disease: the Global Rheumatic Heart Disease Registry (the REMEDY study). Eur Heart J 2015;36:1115-22a.
  5. Diao M, Kane A, Ndiaye MB, et al. Pregnancy in women with heart disease in sub-Saharan Africa. Arch Cardiovasc Dis 2011;104:370-4.
  6. Mocumbi AO, Sliwa K. Women's cardiovascular health in Africa. Heart 2012;98:450-5.
  7. Soler-Soler J, Galve E. Worldwide perspective of valve disease. Heart 2000;83:721-5.
  8. Doukky R, Abusin SA, Bayissa YA, Kelly RF, Ansari AH. Rheumatic heart disease in modern urban America: a cohort study of immigrant and indigenous patients in Chicago. Int J Cardiol 2014;175:178-80.
  9. Canobbio MM, Warnes CA, Aboulhosn J, et al. Management of Pregnancy in Patients With Complex Congenital Heart Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation 2017;135:e50-e87.
  10. European Society of Gynecology (ESG); Association for European Paediatric Cardiology (AEPC); German Society for Gender Medicine (DGesGM), et al. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). Eur Heart J 2011;32:3147-97.
  11. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;129:2440-92.
  12. Sanghavi M, Rutherford JD. Cardiovascular physiology of pregnancy. Circulation 2014;130:1003-8.
  13. Ouzounian JG, Elkayam U. Physiologic changes during normal pregnancy and delivery. Cardiol Clin 2012;30:317-29.
  14. van Oppen AC, van der Tweel I, Alsbach GP, Heethaar RM, Bruinse HW. A longitudinal study of maternal hemodynamics during normal pregnancy. Obstet Gynecol 1996;88:40-6.
  15. Hunter S, Robson SC. Adaptation of the maternal heart in pregnancy. Br Heart J 1992;68:540-3.
  16. Sifakis S, Pharmakides G. Anemia in pregnancy. Ann N Y Acad Sci 2000;900:125-36.
  17. Samiei N, Amirsardari M, Rezaei Y, et al. Echocardiographic Evaluation of Hemodynamic Changes in Left-Sided Heart Valves in Pregnant Women With Valvular Heart Disease. Am J Cardiol 2016;118:1046-52.
  18. James AH. Pregnancy and thrombotic risk. Crit Care Med 2010;38:S57-63.
  19. Robson SC, Dunlop W, Boys RJ, Hunter S. Cardiac output during labour. Br Med J (Clin Res Ed) 1987;295:1169-72.
  20. Robson SC, Dunlop W, Moore M, Hunter S. Combined Doppler and echocardiographic measurement of cardiac output: theory and application in pregnancy. Br J Obstet Gynaecol 1987;94:1014-27.
  21. Lee W, Rokey R, Miller J, Cotton DB. Maternal hemodynamic effects of uterine contractions by M-mode and pulsed-Doppler echocardiography. Am J Obstet Gynecol 1989;161:974-7.
  22. Stones RW, Paterson CM, Saunders NJ. Risk factors for major obstetric haemorrhage. Eur J Obstet Gynecol Reprod Biol 1993;48:15-8.
  23. Kamel H, Navi BB, Sriram N, Hovsepian DA, Devereux RB, Elkind MS. Risk of a thrombotic event after the 6-week postpartum period. N Engl J Med 2014;370:1307-15.
  24. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:2438-88.
  25. Siu SC, Sermer M, Colman JM, et al. Prospective multicenter study of pregnancy outcomes in women with heart disease. Circulation 2001;104:515-21.
  26. Drenthen W, Boersma E, Balci A, et al. Predictors of pregnancy complications in women with congenital heart disease. Eur Heart J 2010;31:2124-32.
  27. Balci A, Sollie-Szarynska KM, van der Bijl AG, et al. Prospective validation and assessment of cardiovascular and offspring risk models for pregnant women with congenital heart disease. Heart 2014;100:1373-81.
  28. Silversides CK, Colman JM, Sermer M, Farine D, Siu SC. Early and intermediate-term outcomes of pregnancy with congenital aortic stenosis. Am J Cardiol 2003;91:1386-9.
  29. Orwat S, Diller GP, van Hagen IM, et al. Risk of Pregnancy in Moderate and Severe Aortic Stenosis: From the Multinational ROPAC Registry. J Am Coll Cardiol 2016;68:1727-37.
  30. Hameed A, Karaalp IS, Tummala PP, et al. The effect of valvular heart disease on maternal and fetal outcome of pregnancy. J Am Coll Cardiol 2001;37:893-9.
  31. Yap SC, Drenthen W, Pieper PG, et al. Risk of complications during pregnancy in women with congenital aortic stenosis. Int J Cardiol 2008;126:240-6.
  32. Silversides CK, Colman JM, Sermer M, Siu SC. Cardiac risk in pregnant women with rheumatic mitral stenosis. Am J Cardiol 2003;91:1382-5.
  33. Nanna M, Stergiopoulos K. Pregnancy complicated by valvular heart disease: an update. J Am Heart Assoc 2014;3:e000712.
  34. Frishman WH, Elkayam U, Aronow WS. Cardiovascular drugs in pregnancy. Cardiol Clin 2012;30:463-91.
  35. Ben Farhat M, Gamra H, Betbout F, et al. Percutaneous balloon mitral commissurotomy during pregnancy. Heart 1997;77:564-7.
  36. de Souza JA, Martinez EE Jr, Ambrose JA, et al. Percutaneous balloon mitral valvuloplasty in comparison with open mitral valve commissurotomy for mitral stenosis during pregnancy. J Am Coll Cardiol 2001;37:900-3.
  37. McIvor RA. Percutaneous balloon aortic valvuloplasty during pregnancy. Int J Cardiol 1991;32:1-3.
  38. Dawson J, Rodriguez Y, De Marchena E, Alfonso CE. Aortic balloon valvuloplasty in pregnancy for symptomatic severe aortic stenosis. Int J Cardiol 2012;162:e12-13.
  39. Savas V, Grines CL, O'Neill WW. Percutaneous triple-valve balloon valvuloplasty in a pregnant woman. Cathet Cardiovasc Diagn 1991;24:288-94.
  40. Hameed AB, Goodwin TM, Elkayam U. Effect of pulmonary stenosis on pregnancy outcomes--a case-control study. Am Heart J 2007;154:852-4.
  41. Drenthen W, Pieper PG, Roos-Hesselink JW, et al. Non-cardiac complications during pregnancy in women with isolated congenital pulmonary valvar stenosis. Heart 2006;92:1838-43.
  42. Galal MO, Jadoon S, Momenah TS. Pulmonary valvuloplasty in a pregnant woman using sole transthoracic echo guidance: technical considerations. Can J Cardiol 2015;31:103.e5-7.
  43. Vered Z, Poler SM, Gibson P, Wlody D, Pérez JE. Noninvasive detection of the morphologic and hemodynamic changes during normal pregnancy. Clin Cardiol 1991;14:327-34.
  44. Walfisch A, Koren G. The "warfarin window" in pregnancy: the importance of half-life. J Obstet Gynaecol Can 2010;32:988-9.
  45. Hall JG, Pauli RM, Wilson KM. Maternal and fetal sequelae of anticoagulation during pregnancy. Am J Med 1980;68:122-40.
  46. Barbour LA. Current concepts of anticoagulant therapy in pregnancy. Obstet Gynecol Clin North Am 1997;24:499-521.
  47. Steinberg ZL, Dominguez-Islas CP, Otto CM, Stout KK, Krieger EV. Maternal and Fetal Outcomes of Anticoagulation in Pregnant Women With Mechanical Heart Valves. J Am Coll Cardiol 2017;69:2681-91.
  48. Hassouna A, Allam H. Limited dose warfarin throughout pregnancy in patients with mechanical heart valve prosthesis: a meta-analysis. Interact Cardiovasc Thorac Surg 2014;18:797-806.
  49. Xu Z, Fan J, Luo X, et al. Anticoagulation Regimens During Pregnancy in Patients With Mechanical Heart Valves: A Systematic Review and Meta-analysis. Can J Cardiol 2016;32:1248.e1-1248.e9.
  50. Saeed CR, Frank JB, Pravin M, Aziz RH, Serasheini M, Dominique TG. A prospective trial showing the safety of adjusted-dose enoxaparin for thromboprophylaxis of pregnant women with mechanical prosthetic heart valves. Clin Appl Thromb Hemost 2011;17:313-9.
  51. Wright JM, Page RL, Field ME. Antiarrhythmic drugs in pregnancy. Expert Rev Cardiovasc Ther 2015;13:1433-44.
  52. Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J 2016;37:2893-962.
  53. Tromp CH, Nanne AC, Pernet PJ, Tukkie R, Bolte AC. Electrical cardioversion during pregnancy: safe or not? Neth Heart J 2011;19:134-6.
  54. Norrad RS, Salehian O. Management of severe mitral stenosis during pregnancy. Circulation 2011;124:2756-60.
  55. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:e57-185.
  56. Bates SM, Greer IA, Middeldorp S, Veenstra DL, Prabulos AM, Vandvik PO. VTE, thrombophilia, antithrombotic therapy, and pregnancy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141:e691S-e736S.
  57. Kela M, Buddhi M. Combined mitral and aortic stenosis in parturient: Anesthesia management for labor and delivery. J Anaesthesiol Clin Pharmacol 2017;33:114-6.
  58. James A, Committee on Practice Bulletins—Obstetrics. Practice bulletin no. 123: thromboembolism in pregnancy. Obstet Gynecol 2011;118:718-29.
  59. Silversides CK, Sermer M, Siu SC. Choosing the best contraceptive method for the adult with congenital heart disease. Curr Cardiol Rep 2009;11:298-305.
  60. Sable C, Foster E, Uzark K, et al. Best practices in managing transition to adulthood for adolescents with congenital heart disease: the transition process and medical and psychosocial issues: a scientific statement from the American Heart Association. Circulation 2011;123:1454-85.
  61. Trussell J. Contraceptive failure in the United States. Contraception 2011;83:397-404.
  62. Bahamondes L, Brache V, Meirik O, et al. A 3-year multicentre randomized controlled trial of etonogestrel- and levonorgestrel-releasing contraceptive implants, with non-randomized matched copper-intrauterine device controls. Hum Reprod 2015;30:2527-38.

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


< Back to Listings