A Pregnant Woman Is Presenting With Chest Pain. How Should I Approach Treatment?
The key to treatment is to ascertain the etiology of chest pain in this woman. The differential diagnosis of chest pain in the pregnant woman includes gastrointestinal, musculoskeletal, cardiovascular, and pulmonary etiologies. Accurate and timely treatment depends on a thorough history and physical examination with appropriate diagnostic testing. Special attention should be paid to findings on the physical examination. For example, any murmur suggesting the presence of valvular disease or hypertrophic cardiomyopathy should prompt further evaluation with an echocardiogram. We will begin by reviewing some causes of chest pain in this special population.
Gastroesophageal Reflux Disease
Heartburn is common, occurring in two-thirds of pregnancies. During pregnancy, the lower esophageal sphincter tone is decreased due to increased pressure from the expanding uterus, as well as increased levels of progesterone and estrogen.1 A reliable history and symptoms of heartburn can avoid unnecessary additional testing and allow the clinician to proceed with appropriate treatment of gastroesophageal reflux disease. However, chest pain associated with dyspnea, presyncope, nausea, diaphoresis, exertion, or unresponsive to antireflux treatment is worrisome and indicates the need for further evaluation.
Musculoskeletal
Costochondritis and fibromyalgia are examples of noncardiac causes of pain. Costochondritis is characterized by reproducible chest wall tenderness. It is exacerbated by movement and deep inspiration. The diagnosis is made on clinical grounds. Use of nonsteroidal anti-inflammatory drugs or high-dose aspirin are not recommended during the third trimester, due to risk of premature closure of the ductus arteriosus.
Myocardial Infarction
Myocardial infarction (MI) during pregnancy is rare with an incidence of 6 per 100,000.2 The risk of MI increases 3- to 4-fold during pregnancy compared to nonpregnant women. Seventy-three percent of cases of acute MI occurred during pregnancy, while 27% occurred during the postpartum period.2 Other possible causes of acute MI include coronary artery dissection, thrombosis, and coronary vasospasm. Spontaneous coronary artery dissection is more common during the early postpartum period. It has been postulated that increased levels of progesterone lead to weakening of the intima and media layers and play a role in the pathophysiology of dissection.3 The electrocardiogram (ECG) and cardiac biomarkers aid in the diagnosis of MI. Echocardiography identifies wall motion abnormalities, which help guide further management.
The treatment of MI in the pregnant patient is similar to that of the nonpregnant woman with specific additional considerations. Due to its large molecular size, heparin is safe for use during MI in pregnancy, as it does not cross the placenta. If coronary angiography is available, thrombolytic therapy is not recommended as first-line therapy. While it may be lifesaving, especially when PCI is unavailable, complications include maternal hemorrhage, preterm delivery, and abruptio placentae. In addition, pregnancy is a relative contraindication for the use of fibrinolytic therapy and may extend the dissection flap in a coronary dissection.2 PCI is preferable for ST-elevation MI (STEMI) as coronary angiography can also diagnose coronary dissection. Medical treatment with the use of beta-blockers, low-dose aspirin, and nitrates is appropriate for an MI.4 The use of statins, angiotensin converting enzyme (ACE) inhibitors, and angiotensin receptor blockers, however, are contraindicated during pregnancy (Table 1). A conservative strategy consisting of medical therapy is recommended for stable non-ST-elevation MI (NSTEMI), rather than an early invasive strategy. Fetal monitoring is indicated during the acute illness.5
Successful coronary revascularization has been reported during pregnancy. During coronary angiography, abdominal shielding, using a radial approach, and shorter fluoroscopy times reduce radiation exposure to the fetus. Bare-metal stents are preferred, as the safety of drug-eluting stents is unknown. In addition, dual antiplatelet therapy increases the risk of bleeding during the peripartum period. Currently, data regarding coronary artery bypass grafting remain limited.
FDA Pregnancy Risk Classification
A—Controlled studies in pregnant women fail to demonstrate a risk to the fetus in the first trimester with no evidence of risk in later trimesters
B—No evidence of risk in humans
C—Animal studies have demonstrated adverse effects on the fetus, but no controlled studies in pregnant women; or no animal or well-controlled studies are available
D—Studies have demonstrated a risk to the fetus. However the benefits may outweigh the potential risks
X—Contraindicated in pregnancy or women who may become pregnant
Pulmonary Embolism
Pulmonary embolism (PE) must be considered in the pregnant patient with chest pain and dyspnea. Pregnancy is a prothrombotic state with all features of Virchow’s triad (venous stasis, endothelial injury, and hypercoagulability). It is associated with increased levels of coagulation factors I, II, VII, VIII, IX, X, and a decrease in protein S. In women with a high clinical suspicion for a PE (ie, chest pain and lower extremity edema or tenderness), it is reasonable to begin with Doppler ultrasound of the lower extremity. If positive, anticoagulation can be initiated. If both chest x-ray and Doppler studies are negative, ventilation/perfusion scan (V/Q) is appropriate. If the V/Q scan is indeterminate or the CXR is abnormal, a computed tomography (CT) angiogram (with abdominal shielding) should be performed to exclude a PE. Patients should be treated with low-molecular weight or unfractionated heparin once a PE is diagnosed. Warfarin should not be used during the first trimester due to its teratogenicity. Anticoagulation for a period of 3 months is recommended as pregnancy is considered a reversible risk factor. However, an extended period or indefinite therapy may be recommended depending on other thromboembolic risk factors.4
Pulmonary Hypertension
Severe pulmonary hypertension (PHTN) may also cause chest pain and usually occurs in association with dyspnea. The normal physiologic changes of pregnancy are not well tolerated in this patient population and symptoms often worsen during the second and third trimesters. Severe PHTN is associated with a 30% to 50% maternal mortality and increased fetal risk. As a result, it is considered a contraindication to pregnancy. There is no consensus for the treatment of pulmonary hypertension in pregnancy. The specific management options exceed the scope of this clinical summary and require the collaborative input of a pulmonologist, cardiologist, and obstetrician.
Aortic Dissection
During pregnancy, several hemodynamic and hormonal changes contribute to histological changes in the aorta, which may increase the risk of aortic dissection. Dissection occurs most commonly in the third trimester or early postpartum, hence should be considered in the appropriate clinical setting. Risk factors for aortic dissection include hypertension, connective tissue disease (including Marfan’s syndrome), pregnancy, trauma, congenital aortic anomalies (bicuspid aortic valve or coarctation), and aortitis. A transesophageal echocardiogram or CT scan, with abdominal shielding, is appropriate for diagnosing aortic dissection. This is important since treatment with heparin is indicated with acute MI, but could be catastrophic in the woman with aortic dissection. Aortic dissection is a medical emergency and requires immediate treatment and consultation with a cardiologist and cardiothoracic surgeon.
Diagnostic Tools in the Assessment of Pregnant Patients With Chest Pain9
In most pregnant women, the 12-lead electrocardiogram (ECG) is normal. However, there can be variability of the ST segment and T wave during pregnancy and during induction of anesthesia.6,7 ECGs may mimic left ventricular hypertrophy or left axis deviation. Hence, the ECG has to be interpreted with clinical symptoms in mind.
The transthoracic echocardiogram (TTE) is essential in the evaluation of a pregnant patient with chest pain. TTE poses no radiation exposure to the mother or fetus. It provides valuable noninvasive information regarding hemodynamics and cardiac structure and function. Valvular stenosis or regurgitation, congenital heart defects (atrial or ventricular septal defects), and aortic root disease can be diagnosed using echocardiography.
Exercise testing is appropriate for evaluation of ischemia in pregnant women. Stress echocardiography using cycle ergometry or treadmill walking is the test of choice. A submaximal stress test to reach 70% of age-predicted maximal heart rate with fetal monitoring is recommended. Maximal exercise should be avoided as fetal bradycardia has been reported.8
Radiation exposure is a concern in pregnant women who require additional diagnostic testing. Effort should be made to minimize exposure of the fetus using abdominal shielding. When dyspnea, edema, and orthopnea are present, a chest radiograph is indicated if congestive heart failure is suspected. CT may be necessary with a high clinical suspicion of pulmonary embolism, an elevated D-dimer, but normal lower extremity duplex. Radionuclide stress testing should be avoided, especially during organogenesis, due to radiation risks to the developing fetus.
Summary
The differential diagnosis of chest pain in the pregnant woman is broad, and the key to accurate diagnosis and treatment begins with a focused history and physical examination. This guides appropriate testing, minimizes unnecessary radiation, and avoids missing life-threatening clinical syndromes. The pregnant patient can have a range of benign to serious clinical conditions, and appropriate diagnostic tests are part of the evaluation.
References
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2. James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myocardial infarction in pregnancy: a United States population-based study. Circulation. 2006;113(12):1564-1571.
3. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll Cardiol. 2008;52:171–180.
4. Bates SM, Greer IA, Pabinger I, Sofaer S, Hirsh J; American College of Chest Physicians. Venous thromboembolism, thrombophilia, antithrombotic therapy, and pregnancy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133(6 Suppl): 844S-886S.
5. 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. Eur Heart J. 2011;32:3147-3197.
6. Wenger, NK, Hurst JW, Strozier VN. Electrocardiographic changes in pregnancy. Am J of Cardiology. 1964;13(6):774-778.
7. Schwartz DB, Schamroth L. The effect of pregnancy on the frontal plane axis. J Electrocardiol. 1979;12(3):279-281.
8. Carpenter MW, Sady SP, Hoegsberg B, et al. Fetal heart rate response to maternal exertion. JAMA. 1988;259:3006-3009.
9. Elkayam U, Gleicher N. Cardiac evaluation during pregnancy. In: Elkayam U, Gleicher N, eds. Cardiac Problems in Pregnancy. 3rd ed. New York, NY: Wiley-Liss; 1998:23–32.