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DOI: 10.1542/neo.13-11-e6512012;13;e651 Neoreviews

Alexandria J. Hill and Luis D. PachecoCardiovascular Disease in Pregnancy

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Cardiovascular Disease in PregnancyAlexandria J. Hill, MD,Luis D. Pacheco, MD

Author DisclosureDrs Hill and Pachecohave disclosed nonancial relationshipsrelevant to this article.This commentary doescontain a discussion of an unapproved/investigative use of a commercial product/device.

Educational GapsFetuses and newborns of mothers with cardiovascular disease face a range of risks relatedto the type of maternal disease, the drugs used to manage it, and the inheritability of thedisease.

Abstract Although cardiac lesions in pregnancy are often well tolerated, those that are not war-rant a cardiac evaluation as well as careful management in the antepartum and peripar-tum periods. Congenital heart disease cases comprise the majority of pregnant cardiacpatients, and the lesions can require careful monitoring. Women who have valvulardisease often tolerate pregnancy well, but there are speci c lesions that require closemonitoring throughout the pregnancy. Finally, peripartum cardiomyopathy, althoughrare, is of great concern and must be managed quickly and appropriately. We will review concerns and treatment for pregnant women who have congenital heart disease, valvular lesions, and peripartum cardiomyopathy, as well as provide guidance for drugtherapy in the pregnant patient who has cardiac disease.

Objectives After completing this article, readers should be able to:1. Identify common congenital heart lesions seen in the pregnant patient and

understand basic management for each lesion.2. Understand medical management for valvular cardiac disease in pregnancy.3. Classify heart lesions according to patient symptoms.

4. List medications that should not be used for cardiac patients in pregnancy.

IntroductionCardiac disease in the pregnantpatient is encountered more andmore often because of womensurviving prior cardiac surgeries as well as the advances in assisted reproductive medicine. Infact, more than one half of cardiac patients managed obstetrically have congenital heart disease(CHD). Currently, the incidence of cardiac disease in pregnancy is w 4% but notably the mor-bidity can be much higher (34%). The leading causes for maternal mortality consist of cardio-myopathy, pulmonary hypertension, aortic dissection, and myocardial infarction.

Many physiologic changes occur in the pregnant patient (Table 1). Although total body volume increases, red bloodcell volume increases at a lower rate, causing a dilutional ane-

mia. This anemia allows the pregnant woman to have less viscous blood to better perfuse her placenta to nurturethe fetus. The heart compensates for the overall increased volume during pregnancy with decreased blood pressure(nadir at the late second to early third trimester) and de-creased systemic vascular resistance (SVR). Moreover,the cardiac output is greatly increased, starting as early as8 weeks gestation.

Patients who have cardiac disease in pregnancy shouldbe classi ed according to any limitations in their physical

AbbreviationsAS: aortic stenosisASD: atrial septal defect CHD: congenital heart diseaseNYHA: New York Heart AssociationPDA: patent ductus arteriosusPVR: pulmonary vascular resistanceSVR: systemic vascular resistanceUFH: unfractionated heparin VSD: ventricular septal defect

Department of MaternalFetal Medicine, University of Texas Medical Branch, Galveston, TX.

Article maternal-fetal medicine

NeoReviews Vol.13 No.11 November 2012 e651

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activity as well as symptoms they experience at rest or with physical activity. The basic criteria for the New York

Heart Association (NYHA) classi cation system can befound in Fig1. This classi cation system may beused in pre-conceptional counseling for patients who have known car-diac disease. We will address patients who have cardiacdisease encountered in theobstetric world, including those who have CHD, valvular disease, and cardiomyopathy, as well as discuss medications used in pregnancy.

Congenital Heart DiseaseCHD is the most common form of heart disease man-aged in pregnancy. Generally, the pregnant patient who has CHD should avoid uid overload and be placedin the left lateral decubitus position when laboring. Thepatient should be provided oxygen during labor, and theuse of epidural anesthesia should be evaluated by the an-esthesiology service. In general, narcotic epidurals arepermissible for these patients. Management principlesfor CHD are listed in Table 2. Routine thromboembo-lism prophylaxis is not administered for any of the

CHD lesions but should be strongly considered for pa-tients who have Eisenmenger syndrome because they have a higher rate of thromboembolism. Each lesion isdiscussed brie y in the following text.

Patent Ductus Arteriosus Although patent ductus arteriosus (PDA) is common inthe neonate, surgery is often performed early in age; thus,this lesion is not often encountered in pregnancy. A re-paired PDA is well tolerated in pregnancy. However, if a large PDA is present, pulmonary hypertension and ulti-mately Eisenmenger syndrome are possible complications.

Atrial Septal Defect An atrial septal defect (ASD) is the most common lesionencountered in the pregnant patient. These defectsare generally well tolerated in pregnancy and, even if un-repaired, rarely cause complications. If the defect islarge, shunt reversal and/or cardiac arrhythmias may oc-cur. Any reversal to a right-to-left shunt should causeconcern for pulmonary hypertension and Eisenmengersyndrome.

Ventricular Septal DefectEven thoughventricular septal defect (VSD) is a commonlesion in the neonatal population, it is rarely seen in the

pregnant patient because most VSDs close in the rst few years after birth or are repaired in childhood. Regardless if the lesion is repaired or unrepaired, an echocardiogram is warranted in pregnancy. If the VSD is patent, blood most often ows from left to right. If there is concern for right ventricular hypertrophy, reversal of a patent shunt ishighly possible, and the possibility of Eisenmenger syn-drome must be considered.

Coarctation of the AortaPatients who have coarctation may often have co-existingcardiac defects such as septal defects or a bicuspid aortic

valve. Patients undergo repair when there is a signi cant difference in pressure gradients between the upper andlower extremities. These patients are also at a higher risk of intracranial aneurysms. Therefore, rupture of the aortaas well as potential intracranial aneurysms are possibleconcerns. If the coarctation is signi cant, the mother isat higher risk of hypertension; overall, these patientscarry a higher risk of pre-eclampsia. Stable patients canundergo vaginal delivery, but use of the Valsalva maneuver during the second stage of labor should be mini-mized. Patients who have coarctation of the aortashould maintain an adequate preload and avoid hypoten-sion (Table 2).

Table 1. Physiologic Changes inPregnancy

Physiologic Change % Change

Heart rate [ 1020Stroke volume [ 30Cardiac output [ 3050Blood volume [ 2050Systemic vascular resistance Y 20

Figure 1. New York Heart Association (NYHA) functionalclassication.

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Tetralogy of FallotThe tetrad of VSD, overriding aorta, right ventricularhypertrophy, and pulmonary stenosis often has beencorrected surgically by the time a patient reaches child-bearing age and thus is well tolerated in pregnancy. These women should be monitored for pulmonary regurgita-tion because it places them at the greatest risk forcomplications such as arrhythmia and heart failure. Echo-cardiograms should be performed on these women to as-sess for any remaining cardiac shunts that could placethem at increased risk for pulmonary hypertension.

Eisenmenger SyndromeThis syndrome occurs when a left-to-right intracardiacshunt (PDA, ASD, or VSD) shifts to a right-to-left shunt.This happens when the pulmonary vasculature system isoverloaded, resulting in pulmonary hypertension, whichprovides enough pressure to reverse the shunt. In severecases, a heart lung transplant may be the ultimate

treatment for this diagnosis. SVR decreases in pregnancy.If a woman experiences hypertension, she will have an in-crease in SVR, which could then lead to a worsening of a left-to-right shunt. Equally, if the pulmonary vascularresistance (PVR) falls, a left-to-right shunt can worsen.Therefore, increases in SVR and decreases in PVR shouldbe avoided in patients who have a PDA, ASD, or VSD. When a patient has already experienced reversal of a shunt, and thus has a right-to-left shunt with pulmonary hypertension, it is important to avoid increases in PVR (metabolic acidosis, hypoxia, or lung hyperin ation), which could worsen a right-to-left shunt.

Marfan SyndromeMarfan syndrome is an autosomal dominant conditionthat will be accompanied by cardiac complications 80%of the time. The main concern is a dilation of the aorticroot and therefore risk of dissection or rupture. It isrecommended that women undergo repair before

Table 2. Management of Congenital Heart Disease in PregnancyCardiac Lesion Medical Management

Patent ductus arteriosus Avoid: hypertension, a decrease in PVR,a arrhythmias, tachycardia a,b

Atrial septal defect Avoid: hypertension, a decrease in PVR,a arrhythmias, tachycardia a,b

Ventricular septal defect Avoid: hypertension, a decrease in PVR,a arrhythmias, tachycardia a,b

Coarctation Avoid: hypotension, bradycardia, myocardial depressants, excess blood lossTetralogy of Fallotc Avoid: hypotension, bradycardia, myocardial depressants, excess blood lossEisenmenger syndromec Avoid: hypotension, excess blood loss, increase in PVR, myocardial depressants

Treatment: CCB, inotropic agents, diuretics, oxygen, anticoagulationMarfan syndrome Avoid: hypertension, tachycardia, positive inotropic drugs

Treatment: b -blockers (keep HR< 90 beats per minute when at rest)

CCB calcium channel blocker; HR heart rate; PVR pulmonary vascular resistance.a Can lead to increase in left-to-right shunt.b If pulmonary hypertension is present, avoid increase in PVR (ie, hypoxemia, nitrous oxide, hypercarbia, vasoconstrictors) because it can worsen a right-to-left

shunt.c No epidural; may consider with Tetraology of Fallot if no intracardiac shunt is present.

Table 3. Recurrence Risk of Fetal Congenital Heart Defects in FutureFetus (%)

Cardiac Lesion Prior Affected Sibling Father Affected Mother Affected

Tetralogy of Fallot 2.5 1.5 2.6Aortic coarctation 14.1Atrial septal defect 2.5 1.5 4.611 Ventricular septal defect 3 2 9.515.6Pulmonary stenosis 2 2 6.5Aortic stenosis 2 3 1517.9Patent ductus arteriosus 3 2.5 4.1Marfan syndrome 50 50





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pregnancy if the dilation of the aortais more than 4.5 cm. Risk of rupture when the aorta is not dilated is ex-tremely low ( < 1%). In labor, women should be encouraged tominimize the use of the Valsalvamaneuver. Women should be coun-seled strongly regarding the highrisk of having a neonate who hasMarfan syndrome (Table 3).

Ebstein AnomalyEbstein anomaly is rarely seen in thepregnant population, and reportedcases resulted in no maternal compli-cations and neonatal complicationsof prematurity and congenital car-diac abnormalities. This anomaly isde ned as apical displacement of the tricuspid septal lea et and is al- ways accompanied by tricuspid re-gurgitation, which can lead to right atrial dilation. Onehalf of these patients have a co-existing ASD or PDA.

Transposition of the Great VesselsPatients who have complete transposition of the great ves-sels whoreach childbearing age have undergone correctiveprocedures, most commonly an atrial switch (Mustardprocedure). These women tolerate pregnancy well but can eventually experience irreversible right ventriculardysfunction.

Finally, when counseling a mother who has CHD, sheshould be aware that she has approximately a 5% chance of having a child who has CHD. Also, the mother should be

counseled on the risk of recurrence of CHD in the fetusdepending on the type of maternal CHD (Table 3). Mater-nal mortality risks should also be reviewed and can vary widely, from less than 1% with ASD and VSD up to 25%to 50% in patients who have pulmonary hypertension

(Fig 2).

Valvular Heart Disease Valvular lesions are either congenital or acquired, andmost lesions seen in pregnancy are acquired from rheu-matic fever. Of the valves affected, the mitral valve isthe most common, followed by the aortic, tricuspid,and then pulmonic valves. Women who present with

Figure 2. Maternal mortality associated with cardiac lesions in pregnancy. AS [ aorticstenosis; ASD[ atrial septal defect; PDA[ patent ductus arteriosus; MI [ myocardialinfarction; MS [ mitral stenosis; NYHA[ New York Heart Association; VSD[ ventricularseptal defect.

Table 4. Classication of Valvular Heart Lesions According to Maternal

and Fetal RisksLow Maternal and/or Fetal Risks High Maternal and/or Fetal Risks

Asymptomatic AS with low mean outow gradient andnormal LV systolic function (EF > 50%)

Severe AS with or without symptoms

NYHA I or II AR and normal LV systolic function NYHA IIIIV and AR (or MR)NYHA I or II MR and normal LV systolic function NYHA IIIV and MSMVP with no MR (if mild to moderate MR and normal LV

systolic function)Aortic and/or mitral disease with severe pulmonary

hypertension or LV systolic dysfunction (EF < 40%)Mild MS without pulmonary hypertension Marfan syndrome with or without ARMild to moderate pulmonary stenosis Mechanical prosthetic valve requiring anticoagulation

AR aortic regurgitation; AS aortic stenosis; EF ejection fraction; LV left ventricular; MR mitral regurgitation; MS mitral stenosis; NYHA New York Heart Association.





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a valvular lesion in pregnancy should be counseled regard-ing their risks during the pregnancy. After identifying thelesionand the NYHA classi cation, onecan further classify the patient into low or high maternal and/or fetal risks(Table 4). NYHA I patients fall into the low-risk cat-egory. Conversely, patients who fall into NYHA III orIV carry higher risks during pregnancy.

Patients who have tricuspid lesions usually have an iso-lated lesion, which is well tolerated during pregnancy. Re-gurgitant lesions in the mitral and aortic valves, mitralvalveprolapse, and pulmonary stenosis also cause minimal con-cern in thepregnant patient. Moreover, these lesions rarely require treatment throughout pregnancy or during labor.Stenotic lesions of the mitral and aortic valveare most con-cerning in pregnancy and will be addressed speci cally inthis section. General management criteria for patients whohave valvular disease in pregnancy can be found in Table 5.

Mitral StenosisMitral stenosis is the most common valvular lesion foundin pregnancy. The stenotic mitral valve causes decreasedleft ventricle lling and can ultimately lead to pulmonary hypertension and right ventricle failure. Individuals whohave mitral stenosis warrant an echocardiogram and anelectrocardiogram. Patients must be carefully monitoredfor pulmonary edema and can experience atrial brillation

and arrhythmias. Anticoagulation should be considered,especially if the patient experiences atrial brillation. Med-ications that cause tachycardia (eg, terbutaline) should beavoided, and an assisted second stage of labor to decreaseuse of Valsalva maneuvers should be strongly considered.

Aortic StenosisPregnant patients who have aortic stenosis (AS) generally tolerate pregnancy well if their disease is mild (valvulararea > 1.5 cm 2 ). If the valve becomes more stenotic

and is decreased to one fourth the normal 3 to 4 cm 2

in diameter, then the disease is considered severe, andsurgical repair is recommended. The cardiac output forthese patients is xed, due to the stenotic aortic valve,making proper perfusion of the mother, as well as the fe-tus, dif cult. For this reason, patients who have severe AS(aortic valve < 1 cm2 ) should limit their physical activity.Patients should have an electrocardiogram to look for ar-rhythmias and an echocardiogram to evaluate the aortic valve and ejection fraction. It is imperative to maintainan appropriate preload as these patients will not be ableto increase cardiac output, which is needed to maintainperfusion during the physiologic stresses of pregnancy.For the same reasons, hypotension and bradycardia shouldbe avoided. Useof a narcotic epidural is possible, but great care must be taken to avoid hypotension with placement of any epidural catheter. Patient symptoms should be moni-tored often to precisely decide on NYHA classi cation of the pregnant patient who has AS, and placental perfusion will need to be evaluated throughout the pregnancy.

Counseling patients who have a valvular lesion variesdepending on the type of lesion and degree of effect.Low-risk lesions such as issues with the tricuspid valve,pulmonary stenosis, mitral valve prolapse, and regurgi-tant lesions of the mitral or aortic valve are well toleratedin pregnancy and often do not require further evaluation.

Stenotic lesions of the mitral or aortic valve can causecomplications and must be more carefully managed dur-ing pregnancy. Combining maternal NYHA classi cationas well as maternal history with the valvular heart lesion(Table 4) can help in counseling the pregnant patient re-garding maternal and fetal risks.

Peripartum CardiomyopathyDiagnosis of peripartum cardiomyopathy classically is thedevelopment of cardiac failure (ejection fraction < 45%)

Table 5. Management of Valvular Lesions in PregnancyLesion Medical Management

PS Avoid: hypotension, bradycardia, myocardial depressants, excess blood lossMR Avoid: arrhythmia, bradycardia, increase in SVR, myocardial depressantsAR Avoid: arrhythmia, bradycardia, increase in SVR, myocardial depressantsMS Avoid: tachycardia, uid overload, decrease in SVR, hypotension, increase in PVR

Treatment: diuretics, b -blockers, maintain HR < 100 beats per minuteASa Avoid: hypotension, decrease in venous return, bradycardia

Treatment: b -blockers, aggressive uids to prevent hypotension

AR aortic regurgitation; AS aortic stenosis; HR heart rate; MR mitral regurgitation; MS mitral stenosis; SVR systemic vascular resistance;PS pulmonary stenosis; PVR peripheral vascular resistance.a No epidural.





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from the last month of pregnancy up to 5 months postpartum withno identi able cause for cardiac fail-ure. This condition can lead to ma-ternal mortality, and maternal deathis most common in the immediatepostpartum period. Management details regarding the patient whohas peripartum cardiomyopathy canbe found in Fig 3. Anticoagulant therapy is not prophylactically war-rantedunless the patienthas a knowncardiac thrombus or coronary artery disease.

Medication Use in PregnancyMedications can be used with carein the pregnant cardiac patient (Fig 4). Most cardiac medicationsused in pregnancy are the same asthose in the nonpregnant patient.For example, if a pregnant patient is experiencing supraventricular tachy-cardia requiring cardioversion oradenosine, both agents are safe inpregnancy and should be adminis-

tered if necessary. Speci c cardiacdrugs that should be avoided inpregnancy are angiotensin-convertingenzyme inhibitors and angiotensinreceptor blockers. Exposure to thesemedications in the rst trimester canlead to congenital malformations,including cardiac defects such asPDA, ASD, and VSD. In the latertrimesters, the fetus can experienceimpaired renal function causing de-creased amniotic uid (oligohy-

dramnios) and ultimately neonatalrenal failure. The low uid in uterocan lead to fetal pulmonaryhypoplasiaas well as contracted limbs and ab-normal bone formation. Furthermore, theneonateexposedto an angiotensin-converting enzyme inhibitor or angio-tensin receptor blocker in the second or third trimestercan experience retinopathy or hypotension.

Anticoagulation in PregnancyUnfractionated heparin (UFH) and low-molecular-weight heparin are considered safe in pregnancy and do not cross the placenta. UFH has a shorter half-life than

low-molecular-weight heparin (Table 6) and thereforeis often the preferred anticoagulant used when a preg-nancy nears term. Either drug may be reversed with prot-amine sulfate, with the obvious fact that reversal will befaster with UFH. In general, low-molecular-weight hep-arin is preferred to UFH because there is often lessfrequent dosing required, decreased risk for heparin-induced thrombocytopenia, and a lower rate of osteopo-rosis and skin reactions.

Figure 3. Management after diagnosis of peripartum cardiomyopathy. ACE [ angiotensin-converting enzyme; CAD[ coronary artery disease; CCB[ calcium channel blocker; IV [intravenous; LMWH[ low-molecular-weight heparin; LV [ left ventricular; SBP[ systolicblood pressure; UFH[ unfractionated heparin.





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Warfarin, however, crosses the placenta and is usually not used in pregnancy. Use in the rst trimester warrantsconcern for fetal malformations such as nasal and limb

hypoplasia, optic atrophy, and impaired mental status.The risk of this syndrome, referred to as warfarin

embryopathy, is estimated by Hirschand Fuster to be 4% to 10%. More-over, use of warfarin during em-bryogenesis in the rst trimester isrelated to higher miscarriage rates.During the latter part of pregnancy,use of warfarin can have a deleteri-ous effect on the fetus, sometimesresulting in intracranial hemor-rhage. It is also important to notethe long half-life of warfarin, espe-cially when compared with theother anticoagulant choices (Table6). In a study byChan etal, warfarin was found to be more effective thanUFH in preventing venous throm-boembolism in patients who haveolder-generation mechanical heart valves. With the risks of warfarin,and the availability of other anti-coagulant agents that are highly effective in preventing venousthromboembolism, warfarin isnot routinely used in the pregnant patient.

Systemic BacterialEndocarditis ProphylaxisPregnant patients who have cardiaclesions do not require antibioticprophylaxis. Currently, the Ameri-can College of Obstetricians andGynecologists, as well as the Amer-ican Heart Association, recommendsystemic bacterial endocarditis pre-

vention with a vaginal or cesarean delivery only if infec-tion is present in speci c cardiac lesions (Table 7). Theantibiotics recommended are as follows: ampicillin, cefa-

zolin, ceftriaxone, clindamycin, or amoxicillin. Becausecefazolin, ceftriaxone, and clindamycin do not cover en-terococcus, vancomycin should be added to those regi-mens. Antibiotics should be administered 30 to 60minutes before delivery.

ConclusionsCardiac lesions in pregnancy are often well tolerated, but those that are not warrant a cardiac evaluation as well ascareful management in the antepartum and peripartumperiods. Many patients, speci cally those who have peri-partum cardiomyopathy, are at a higher risk of death in

Figure 4. Fetal effects of cardiac medications in pregnancy. Drug classes are given inparentheses. The classes are: (A), human studies show no risk to fetus; (B), animal studiesshow risk or no risk to fetus, but human studies show no risk to fetus; (C), animal studieshave shown adverse risk to fetus, but human studies are lacking; (D), human studies showevidence of fetal risk. Class C and D may have medical benets for the mother that couldoutweigh risk to fetus. IUGR[ intrauterine growth retardation.

Table 6. AnticoagulationMedications

Anticoagulant Half-Life

Unfractionated heparin 6090 minLow-molecular-weight heparin 4.5 h (single dose)

7 h (multiple doses)Warfarin 1.52.5 d





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the immediate postpartum period. One cannot forget that the postpartum period is an important time to watchthe cardiac patient closely because third-spacing andincreased cardiac output can put added stress on an al-ready inadequately functioning heart. It is important toproperly identify the exact cardiac lesions a pregnant woman presents with and closely monitor her symptoms(with assistance of NYHA classi cation) so that she canbe properly counseled, managed, and treated throughout her pregnancy.

Suggested Reading American College of Obstetricians and Gynecologists. Practice

bulletin no. 120: use of prophylactic antibiotics in labor anddelivery. Obstet Gynecol . 2011;117:1472 1483

American College of Cardiology/American Heart Association Task Force on Practice Guidelines; Society of Cardiovascular Anes-

thesiologists; Society for Cardiovascular Angiography and Inter- ventions; Society of Thoracic Surgeons; Bonow RO, CarabelloBA, Kanu C, et al. ACC/AHA 2006 guidelines for themanagement of patients with valvular heart disease: a report of the American College of Cardiology/American Heart AssociationTask Force on Practice Guidelines (writing committee to revise the1998 Guidelines for the Management of Patients With ValvularHeart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society forCardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. Circulation . 2006;114(5):e84 e231

Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focusedupdate incorporated into the ACC/AHA 2006 Guidelines forthe Management of Patients With Valvular Heart Disease:a report of the American College of Cardiology/AmericanHeart Association Task Force on Practice Guidelines (WritingCommittee to revise the 1998 guidelines for the management of patients with valvular heart disease) endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of ThoracicSurgeons. J Am Coll Cardiol . 2008;52(13):e1 e142

Chan WS, Anand S, Ginsberg JS. Anticoagulation of pregnant women with mechanical heart valves: a systematic review of theliterature. Arch Intern Med . 2000;160(2):191 196

Chang J, Elam-Evans LD, Berg CJ, et al. Pregnancy-relatedmortality surveillance United States, 1991-1999. MMWR Surveill Summ . 2003;52(2):1 8

Donnelly JE, Brown JM, Radford DJ. Pregnancy outcome andEbstein s anomaly. Br Heart J . 1991;66(5):368 371

Francois K. Postpartum hemorrhage. In: Foley MR, Strong TH,Garite TJ, eds. Obstetric Intensive Care Manual . 3rd ed.New York, NY: The McGraw-Hill Companies Inc; 2010:27 37

Hirsch J, Fuster V. Guide to anticoagulant therapy. Part 2: oralanticoagulants. American Heart Association. Circulation . 1994;89(3):1469 1488

Lupton M, Oteng-Ntim E, Ayida G, Steer PJ. Cardiac disease inpregnancy. Curr Opin Obstet Gynecol . 2002;14(2):137 143

Martin SR, Hill AJ, Foley MR. Cardiac disease in pregnancy. In:Queenan JT, Spong CY, Lockwood CJ. eds. Queenan s Management of High-Risk Pregnancy . 6th ed. Oxford: Wiley-Blackwell; 2012:260 291

Simpson LL. Maternal cardiac disease: update for the clinician.Obstet Gynecol . 2012;119(2 pt 1):345 359

Vandvik PO, Lincoff AM, Gore JM, et al; American College of Chest Physicians. Primary and secondary prevention of cardiovascular disease: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest PhysiciansEvidence-Based Clinical Practice Guidelines [published correc-tion appears in Chest . 2012;141(4):1129]. Chest . 2012;141(suppl 2):e637S e668S

Table 7. Cardiac Lesions RequiringSystemic Bacterial EndocarditisProphylaxis When Infection IsPresent Prosthetic cardiac valve or prosthetic material for valve

repair History of infective endocarditis Unrepaired cyanotic CHD (palliative shunts, conduits) Completely repaired CHD with prosthetic materials if

done < 6 mo ago Repaired CHD with residual defects

CHD

congenital heart disease.

American Board of Pediatrics Neonatal-PerinatalMedicine Content Specications Know the effects on the fetus and/or

newborn infant of maternal cardiacdisease and its management.

Know the effects on the fetus and/ornewborn infant of maternalthromboembolic, or potentialthromboembolic (eg articial valve), disorders and theirmanagement, including the use of anticoagulant agents.





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Starting with 2012 NeoReviews , AMA PRA Category 1 Credit TM can be claimed only if 60% or more of the questionsare answered correctly. If you score less than 60% on the assessment, you will be given additional opportunities toanswer questions until an overall 60% or greater score is achieved.

1. A 25-year-old woman is in her second trimester of pregnancy. She has been referred to the high risk obstetric

clinic for cardiac disease. Prior to more extensively reviewing her history, doing a physical exam, and additionalevaluation, you think about some of the most common congenital heart diseases seen in the pregnant patientand consider their relative consequences during pregnancy. Which of the following is correct about possiblecongenital heart disease in this pregnant woman?A. Atrial septal defect is one of the least common lesions encountered in the pregnant patient.B. If coarctation of the aorta is present, Valsalva maneuver during the second stage of labor should be encouraged.C. Most patients with Tetralogy of Fallot who become pregnant have had no previous operation on their

cardiac lesion.D. Patent ductus arteriosus is encountered often and is tolerated poorly in pregnancy.E. The leading causes of maternal mortality during pregnancy consist of cardiomyopathy, pulmonary

hypertension, aortic dissection and myocardial infarction.

2. You consider some of the physiologic changes that occur during pregnancy that may affect cardiovascularstatus and their clinical implications for the mother and the fetus. Which of the following is correct?A. Blood volume increases.B. Cardiac output decreases.C. Heart rate decreases.D. Stroke volume decreases.E. Systemic vascular resistance increases.

3. You notice that this mother is tall, and you consider the possibility of Marfan syndrome. Which of thefollowing is correct about a pregnant woman with Marfan syndrome?A. It would be very unusual for her to have a baby who also has Marfan syndrome.B. Marfan syndrome is autosomal recessive and seldom is accompanied by cardiac complications.C. Pre-pregnancy aortic repair is not indicated if the dilation of the aorta is more than 4.5 cm because the risk

of rupture is low, especially if the mother is asked to do strong Valsalva maneuvers during the second stage

of labor.D. Pre-pregnancy aortic repair is required even if the aorta does not show dilation.E. The main concern is that dilation of the aortic root could lead to dissection and aortic rupture.

4. After the physical exam, you are concerned that the woman has a valvular abnormality of her heart. Which of the following is correct?A. Mitral stenosis is the least common valvular lesion found in pregnancy.B. Most of the valvular lesions seen in pregnancy are acquired from rheumatic fever.C. Physical exertion need not be limited in pregnant women with aortic stenosis when their valves are stenotic

to more than 1/4 th of normal.D. Regurgitant lesions in the mitral and aortic valves are much more worrisome than stenotic lesions of these

valves.E. There is no need for anticoagulation in a woman who has mitral stenosis and atrial brillation.





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5. In terms of cardiac medications used in pregnancy, which of the following is correct?A. Adenosine should not be administered to a pregnant patient who is experiencing supraventricular

tachycardia.B. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers should be avoided in the rst

trimester because they can lead to congenital malformations and in the later trimesters the fetus canexperience impaired renal function that can result in oligohydramnios.

C. Antibiotic prophylaxis should not be used in pregnant women with cardiac lesions even if they haveinfective endocarditis.

D. Unfractionated heparin and low molecular weight heparin are safe for the fetus because they readily crossthe placenta.

E. Warfarin is a safe drug to use for anticoagulation during all stages of pregnancy.





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DOI: 10.1542/neo.13-11-e6512012;13;e651 Neoreviews

Alexandria J. Hill and Luis D. PachecoCardiovascular Disease in Pregnancy

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Enfermedad Cardiovascular Materna