Background

Worldwide, cardiac disease is a leading cause of death in many resource-rich countries.³ In the United Kingdom, the most common cause of maternal death is cardiac disease, of which acquired conditions account for the majority.⁵ In the recent UK Confidential Enquiry into Maternal Deaths, Saving Lives, Improving Mothers’ Care,⁵ there were 49 deaths from cardiac disease, with ischemic heart disease (IHD) accounting for 20 percent. These deaths were due to either an acute myocardial infarction (MI) or preexisting IHD, where death was presumed to be due to an arrhythmia or heart failure.

IHD is rare in women of childbearing age.⁶ In the UK Obstetric Surveillance System (UKOSS) study of MI in pregnancy (2005–10), the incidence of MI complicating pregnancy or the first week postpartum was 0.7 per 100,000 maternities.² The rate of maternal and fetal demise is high following MI in pregnancy: maternal mortality rates between 5 and 11 percent have been reported, with most deaths occurring peri-infarct or in the peripartum period.^7–9 Fetal mortality is around 9–13 percent,⁹ with most deaths occurring in association with maternal death. The outcome of pregnancy in women who have suffered an MI before pregnancy may be better. In 2007, the European Registry on Pregnancy and Heart Disease was initiated by the European Society of Cardiology (ESC) to collect data on women with structural heart disease or IHD.¹⁰ Between 2007 and 2011, pregnancy occurred in 20 women who had suffered an MI previously, with only one woman suffering a new acute coronary syndrome (ACS). Overall, a total of six women had ACS during pregnancy, and all of them survived.

Risk Factors

The risk factors for ACS in pregnancy are the same as those for the general population:²

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  Diabetes mellitus

  
  
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  Hypertension

  
  
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  Obesity

  
  
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  Smoking

  
  
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  Family history

  
  
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  Hypercholesterolemia

Advanced maternal age is a significant risk factor for MI. In the UKOSS study of MI in pregnancy, the mean age of women suffering an MI was 37 years compared with 29 years in the control group.² The risk of MI is 30 times greater in women over age 40 compared with those under 20 years of age.^{3, 7} This is a concerning observation in view of the increasing tendency of women in developed countries to delay having children.

Pregnancy itself increases the risk of ACS three- to fourfold.³ Increased circulating blood volume and increased cardiac output in pregnancy result in an increase in myocardial oxygen demand. At the same time, the physiologic anemia and reduction in diastolic blood pressure reduce myocardial oxygen supply.¹¹ Blood vessel walls are more vulnerable to damage during pregnancy: shearing forces are increased, and blood vessel walls are weakened by elevated levels of estrogen and progesterone.⁴ When these factors are combined with the prothrombotic state of pregnancy, clot formation and subsequent ischemia are more likely. Other pregnancy-specific risk factors identified by UKOSS include twin pregnancy and preeclampsia.²

Pathophysiology

ACS is usually the result of atherosclerotic plaque rupture or instability. When complicated by overlying thrombus formation, complete occlusion to blood flow may result, producing an MI. However, in pregnancy, this mechanism accounts for only 40–50 percent of cases of MI.^{2, 9, 12} The other mechanisms contributing to MI are coronary dissection (16–27 percent), which is a rare event in the nonpregnant population at 1 percent or less, and coronary thrombus occurring in normal coronary arteries (6–21 percent), which is thought to occur from paradoxical embolism through a patent foramen ovale. Normal coronary arteries at angiography have been found in up to 29 percent of patients.^{2, 9, 12}

Diagnosis

IHD may present as stable angina or as an acute coronary syndrome (ACS). ACS consists of three different clinical entities: unstable angina, non-ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI). Patients with unstable angina may present with chest pain at rest or on minimal exertion but have no rise in cardiac enzymes or 12-lead ECG changes. NSTEMI patients have chest pain associated with raised cardiac enzymes, and the ECG may show ST-segment depression or T-wave changes. Patients with STEMI typically have severe chest pain associated with elevated ST segments or new left bundle-branch block and raised cardiac enzymes.

In pregnant women, the diagnosis of ACS is the same as in nonpregnant patients, consisting of a triad of history and examination, 12-lead ECG, and troponin levels. STEMI is a clinical diagnosis and does not rely on waiting for cardiac enzyme results because this would delay prompt treatment. ACS may present atypically in pregnant women, making the diagnosis more challenging. Classic central crushing chest pain may be absent, and atypical symptoms such as abdominal or epigastric pain, vomiting, and dizziness may be attributed to pregnancy per se rather than ACS.¹ Previous recommendations from the Confidential Enquiries into Maternal Deaths in the UK recommend that any women who is suffering chest or epigastric pain severe enough to warrant opioid analgesia should have appropriate investigations to rule out cardiac disease.¹ The 12-lead ECG in pregnant women may also be more difficult to interpret because nonspecific ST-segment and T-wave changes may occur due to pregnancy.

The differential diagnoses for ACS in pregnancy are acute pulmonary embolism, preeclampsia, and aortic dissection. Echocardiography may be a useful tool to identify wall motion abnormalities suggestive of ischemia, and exercise treadmill testing can be performed in pregnancy, although this test has a high false-positive rate.¹³ There have been no reported adverse effects from dobutamine stress echocardiography, and more recently cardiac MRI has been used in the second and third trimesters of pregnancy.¹³ Coronary angiography can be both diagnostic and therapeutic (see below).