Heart Disease in Pregnancy

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Chapter 51

Heart Disease in Pregnancy

1. What cardiac physiologic changes occur during pregnancy?

    Hormonal changes cause an increase in both plasma volume (from water and sodium retention) and red blood cell volume (from erythrocytosis) during a normal pregnancy. A disproportionate increase in plasma volume explains the physiologic anemia of pregnancy. Maternal heart rate (HR) increases throughout the 40 weeks, mediated partially by increased sympathetic tone and heat production. Stroke volume subsequently continues to increase until the third trimester, when inferior vena cava (IVC) return may be compromised by the gravid uterus. Maternal cardiac output increases by 30% to 50% during a normal pregnancy. Systolic blood pressure drops during the first half of pregnancy and returns to normal levels by delivery. The physiologic changes related to cardiac output that occur during pregnancy are shown in Figure 51-1.

2. Are there independent vascular changes that occur during a normal pregnancy?

    The vascular wall weakens during pregnancy as a result of estrogen and prostaglandin, leading to increased risk for vascular dissection. As the placenta develops, it creates a low-resistance circulation. These factors, in addition to heat production, contribute to the reduced systemic vascular resistance (SVR) that is a normal part of pregnancy.

3. What are normal cardiac signs and symptoms of pregnancy?

4. What are pathologic cardiac signs and symptoms of pregnancy?

5. What are normal cardiac examination findings during pregnancy?

6. What are pathologic cardiac exam findings during pregnancy?

image Clubbing and cyanosis are not a part of normal pregnancy; desaturation for any reason is abnormal and warrants investigation.

image Elevated jugular venous pressure (JVP) is abnormal, reflecting elevated right atrial pressure. Although edema is common in this population, it is important to evaluate neck veins in any pregnant woman with peripheral edema.

image Pulmonary hypertension (right ventricular heave, loud P2, JVP elevation) findings should be investigated early. Women with preexisting pulmonary hypertension (pulmonary pressure greater than 75% of systemic pressure) should be counseled prior to pregnancy as to the risks.

image Systolic murmur 3/6 or louder and any diastolic murmur audible in pregnancy are considered abnormal and warrant evaluation.

image Audible S4 is unusual during pregnancy and may reflect underlying hypertension.

7. What are the cardiac changes that occur during labor and delivery?

    With each contraction, 300 to 500 mL of blood are autotransfused from the uterus into the maternal circulatory system. Cardiac output (CO) drops less with vaginal delivery than with cesarean, so vaginal delivery is recommended more commonly in patients with cardiac disease. Vacuum-assisted delivery is used to shorten stage II of labor for women who may not tolerate pushing. After delivery, intravascular volume increases from release of the IVC compression, HR slows, and blood pressure, CO, and HR generally normalize postpartum; however, CO remains elevated in lactating women while they continue to breast-feed.

8. Which women should undergo infective endocarditis (IE) prophylaxis at the time of delivery?

    IE prophylaxis is optional in vaginal delivery for patients with prior IE, prosthetic valves, and congenital heart disease (CHD) within the first 6 months of repair, or after 6 months if there is residual shunting, surgically constructed systemic-to-pulmonary shunts or conduits, or posttransplantation valvulopathy. It is not indicated in cesarean section, per 2007 American Heart Association (AHA) guidelines, although it is often given.

9. What maternal cardiac tests can be performed safely?

    All tests using radiation should be performed only after a thorough review and justification of the risks and benefits to the mother and fetus.

image Electrocardiograms and echocardiograms are safe, with no known risk to the fetus.

image Chest radiographs can be performed with proper pelvic shielding.

image MRI is considered safe (although there is little data during the first trimester).

image Low-level exercise tolerance testing to 70% of maternal maximal HR is safe with low risk of fetal distress or bradycardia.

image Transesophageal echocardiography (TEE) can be performed with appropriate sedation and monitoring.

image Cardiac catheterization, balloon valvuloplasty, angioplasty, and percutaneous intervention are invasive diagnostic and therapeutic tests that may be life saving to the mother with appropriate pelvic shielding for the fetus.

image Computerized tomography is relatively contraindicated due to radiation risk to the fetus.

image Nuclear imaging is contraindicated due to radiation risk to the fetus.

10. What are the highest-risk maternal cardiac conditions during pregnancy?

    Moderate to severe mitral, aortic, and pulmonic stenosis are tolerated poorly during pregnancy. Patients should be counseled, with consideration of valvuloplasty or valve replacement before conception. These procedures can be performed during high-risk pregnancies if the patient decompensates. Pulmonary hypertension (pHTN) is also a high-risk condition, with historic maternal mortality rates of 30% to 56%. Although mortality remains unacceptably high, improvements in both the treatment of pHTN as well as the management of high-risk pregnancy have led to significant mortality reductions. Women with pHTN should be counseled regarding these risks. See Question 14 for discussion of CHD.

11. Are regurgitant lesions equally risky?

    Both mild to moderate aortic insufficiency and mitral regurgitation are tolerated well during pregnancy. The reduction in SVR can lessen the degree of regurgitation. Only patients with severe symptomatic regurgitation (New York Heart Association [NYHA] classes III or IV) should be considered for valve replacement before pregnancy. The only indication for valve replacement for regurgitant lesions during pregnancy is infective endocarditis.

12. What are maternal complications seen in pregnant women with cardiac disease? What are some predictors of fetal complications?

    Pulmonary edema, stroke, arrhythmia, and cardiac death are complications noted in a study of 599 such pregnancies. Fetal complications were seen more often in pregnancies with maternal cyanosis, left heart obstruction, anticoagulation, concomitant smoking, multiple gestations, and heart failure symptoms greater than NYHA class II.

13. How are pregnant women anticoagulated during pregnancy?

    Because warfarin is contraindicated during the first trimester and at term, 2012 American College for Chest Physicians (ACCP) guidelines recommend one of the following grade 1A strategies:

Long-term anticoagulants should be resumed postpartum with all regimens, as early as the same evening. Low-dose aspirin can be optionally added for high-risk patients with mechanical heart valves. Mothers taking warfarin may nurse after delivery.

14. How are the common congenital lesions tolerated during pregnancy?

    In developed countries, congential heart disease (CHD) has superseded rheumatic heart disease as the most common preexisting heart disease in pregnancy. Repaired atrial septal defects (ASDs) and ventricular septal defects (VSDs) confer no increased cardiac risk. Unrepaired left-to-right intracardiac shunts (ASD and VSD) are well tolerated because of the reduction in SVR, which decreases left-to-right shunting during pregnancy. Patients are at an increased risk for paradoxical embolization if they develop deep vein thrombosis.

    Right-to-left (cyanotic) shunting is poorly tolerated in pregnancy. Women with tetralogy of Fallot should undergo repair before contemplating pregnancy. Right-to-left shunting worsens during pregnancy because of reduction of SVR. Women with Eisenmenger syndrome risk a 30% to 50% maternal mortality with pregnancy. Women with such high risk are counseled to avoid pregnancy or undergo therapeutic termination.

15. Which cardiac arrhythmias can complicate pregnancy?

    Patients may develop atrial and ventricular ectopy because of myocardial stretch. Reentrant pathways may emerge leading to atrial arrhythmias. These can be treated acutely with vagal maneuvers or adenosine if the mother is unstable. Recurrent supraventricular arrhythmias can be prevented with digitalis or beta-adrenergic blocking agents (β-blockers). Symptomatic ventricular arrhythmias are treated medically or with implantable cardioverter-defibrillators. If a pregnant woman suffers a cardiac arrest, the viable baby should be delivered after 15 minutes if there is no return of spontaneous maternal circulation.

16. How do you treat a pregnant woman with an acute myocardial infarction?

    Pregnant women with ST segment elevation myocardial infarction (STEMI) should be taken to the catheterization laboratory for primary balloon angioplasty. Heparin can be used safely; however, there is little data on the use of stents, as clopidogrel has not been extensively studied in pregnancy. β-Blockers and low-dose aspirin can be used in pregnancy, but angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and statins should be avoided. Risk factors should be treated.

17. How do women with hypertrophic cardiomyopathy (HCM) tolerate pregnancy?

    Management is similar to the nongravid state. Women with HCM will experience left ventricular end-diastolic pressure (LVEDP) elevations because of increased blood volume of pregnancy. If the LV is able to dilate, outflow obstruction may be reduced. At the time of delivery, anesthesia is critical to reduce sympathetic stimulation from pain; most anesthetic agents reduce myocardial contractility. Preload and afterload changes during delivery must be minimized to avoid increased outflow obstruction. Short-acting vasoconstrictors, diuretics, or volume adjustments may be necessary.

18. What are the recommendations for patients with Marfan syndrome?

    Women with Marfan syndrome are at risk for aortic dissection because of the additional vascular changes of pregnancy. Genetic counseling should be performed before conception because of autosomal dominant transmission. Those with an aortic root diameter of more than 40 mm are at highest risk and are advised to avoid pregnancy. Management includes β-blockers, serial echocardiograms, and bed rest to avoid further root dilation. Type A dissection (involving the ascending aorta) should be managed surgically, with delivery of the viable fetus before repair. Type B dissection (descending aortic involvement) can be managed medically with labetalol or nitroprusside.

19. Which commonly used cardiac medications should be avoided during pregnancy?

    Common cardiac medications that should be avoided during part or all of pregnancy are listed in Box 51-1.

Box 51-1   SAFETY OF CARDIAC MEDICATIONS IN PREGNANCY

ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker; LMWH, low-molecular-weight heparin; UFH, unfractionated heparin.

20. What is peripartum cardiomyopathy (PPCM)?

    This is a syndrome of congestive heart failure diagnosed from the last month of pregnancy up to 5 months postpartum, with demonstration of reduced systolic function by echocardiogram, without identifiable or reversible cause. This is distinct from preexisting cardiac disease, which usually presents before the final month due to physiologic changes of pregnancy. Women with PPCM are treated with standard heart failure medications (hydralazine/nitrates while pregnant; ACE inhibitors after delivery). Prognosis is determined by degree of systolic function recovery. Maternal risk is higher during subsequent pregnancies if LV ejection fraction (EF) dysfunction (EF < 40%) persists. B-type natriuretic peptide (BNP) levels do not rise in a normal pregnancy; increased levels suggest cardiomyopathy, preeclampsia, eclampsia, and/or diabetes.

Bibliography, Suggested Readings, and Websites

1. Bates, S.M., Greer, I.A., Middeldorp, S., et al. VTE, thrombophilia, antithrombotic therapy, and pregnancy: antithrombotic therapy and prevention of thrombosis, ed 9: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141:e691S–e736S.

2. Bédard, E., Dimopoulos, K., Gatzoulis, M.A. Has there been any progress made on pregnancy outcomes among women with pulmonary arterial hypertension? Eur Heart J. 2009;30:256–265.

3. Bonow, R.O., Carabello, B.A., Kanu, C., et al. ACC/AHA Guidelines for management of patients with valvular heart disease. Circulation. 2006;114:493–496.

4. Drenthen, W., Pieper, P., Roos-Hesselink, J., et al. Outcome of pregnancy in women with congenital heart disease: a literature review. J Am Coll Cardiol. 2007;49:2303–2311.

5. Elkayam, U., Bitar, F. Valvular heart disease in pregnancy, parts I (native) and II (prosthetic). J Am Coll Cardiol. 2005;46:223–230. 403–410

6. James, A.H., Brancazio, L.R., Price, T. Aspirin and reproductive outcomes. Obstet Gynecol Surv. 2008;63:49–57.

7. Kusters, D.M., Lahsinoui, H.H., van de Post, J.A. Statin use during pregnancy: a systematic review and meta-analysis. Expert Rev Cardiovasc Ther. 2012;10:363–378.

8. Reimold, S.C., Rutherford, J.D. Clinical practice: valvular heart disease in pregnancy. N Eng J Med. 2003;349:52–59.

9. Weiss, B.M., Zemp, L., Seifert, B., et al. Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. J Am Coll Cardiol. 1998;31:1650–1657.

10. Wilson, W., Taubert, K., Gewitz, M., et al. Prevention of infective endocarditis: Guidelines from the AHA. Circulation. 2007;116:1736–1754.

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