Acute MI symptoms can be mistaken for pregnancy symptoms, so vigilance is key. But how does one evaluate MI-related tissue damage in a pregnant woman? What therapies are safe for mother and fetus alike?

By Alexa Carroll, PA-C

The incidence of acute myocardial infarction (AMI) in pregnancy is as high as one in 10,000 patients.¹ Early diagnosis and treatment can avoid maternal and fetal complications; however, the diagnosis of AMI in a pregnant woman often is hindered because of a low suspicion level. Many of the symptoms associated with AMI mimic symptoms related to normal changes that occur during pregnancy.

How does one treat a pregnant woman with an AMI? Can she be treated like a "normal" patient with AMI? Health care providers and pregnant women must recognize the symptoms that might be associated with an AMI and not dismiss them as a normal part of pregnancy. And health care providers must be aware of management approaches that allow for the best possible outcome for mother and child alike.

The main management goals are maximizing myocardial oxygen delivery, minimizing myocardial oxygen requirements, preventing or quickly treating complications and achieving myocardial healing before delivery.²

AMI and Pregnancy: Case Report

A 39-year-old white woman at 34 weeks of gestation presented to an emergency department with a one-week history of intermittent heartburn and gastrointestinal distress that would come on gradually and last for about 30 minutes. The symptoms sometimes occurred after eating, and she had noticed some intolerance to fatty foods. Her symptoms seemed to improve after taking ranitidine and pantoprazole, and she assumed the heartburn and GI upset were a normal part of pregnancy.

She also reported having experienced in the past week two episodes of nonspecific chest discomfort radiating to her arms, which she dismissed as heartburn. However, she had been prompted to come to the ED after being awakened with persistent increasing retrosternal discomfort with some radiation to the neck, back and both arms. She described it as a "lousy" feeling in general. At presentation, the retrosternal discomfort had lessened. She admitted to some sweating and lightheadedness during the episode, but these symptoms had not occurred with previous episodes.

She denied shortness of breath, nausea, vomiting or change in her bowels. She also denied palpitations, diplopia, pain or tenderness in the lower extremities and pain or shortness of breath with activity.

History and Physical

Her past medical history included hypercholesterolemia above 300 mg/dL before her pregnancy, as well as kidney stones, human papillomavirus infection, varicella-zoster virus infection and depression. Her obstetric history included two previous full-term pregnancies. During her first pregnancy, she experienced pregnancy-induced hypertension, which resolved shortly after giving birth. C-section was performed because of cephalopelvic disproportion. Her second pregnancy was without difficulty, and a repeat C-section was performed.

This pregnancy had been without complications, with appropriate fetal growth throughout gestation and no evidence of hypertension or hyperglycemia.

Her family history is positive for premature coronary artery disease at age 55 in her mother. Her father has hypertension, and her brother has diabetes and is obese.

At admission, her medications included prenatal vitamins, ranitidine 150 mg twice a day and paroxetine 10 mg daily. She was not taking hypercholesterolemia medications. She denied alcohol use and was currently a nonsmoker but had smoked intermittently since her teenage years.

Physical examination revealed a pregnant woman in no acute distress who was cooperative, awake, alert and oriented. Her head was normal cephalic atraumatic, her neck was supple without carotid bruits or jugular vein distention and her trachea was midline.

Her heart was a regular rate and rhythm, with a grade II/VI ejection systolic murmur and a normal S1 and S2 without rubs or clicks. Her lungs were clear to auscultation bilaterally without ronchi, rales or wheezes. Her abdomen was soft, nontender and distended due to pregnancy, and bowel sounds were present. Extremities were without cyanosis or edema, and all peripheral pulses were palpable. There was no calf tenderness or signs of phlebitis. Central nervous system exam was unremarkable. Vital signs included a pulse of 78 beats per minute, blood pressure of 126/80 mmHg, respiration rate of 18 breaths per minute, tympanic temperature of 98.1 degrees and pulse oximetry of 98% on room air.

Differential Diagnosis

Differential diagnosis included gastroesophageal reflux disease, acute cholecystitis, pulmonary embolism and AMI. Because she was not experiencing symptoms during the evaluation, no medication or treatment was ordered. Routine blood work, cardiac enzymes and fetal monitoring were ordered. As precaution, an IV of 0.09% NaCl at 60 cc hour was started. The patient rested in the ED while awaiting test results; she was anxious to be discharged, blaming her symptoms on GI distress and heartburn.

Her complete blood count showed decreased hemoglobin at 11.1 g/dL and a hematocrit of 32.2%. All other cell indexes were within normal ranges. Chemistry profile showed slight hypokalemia at 3.5 mmol/L and hypocalcemia at 8.3 mg/dL. She had a slightly elevated glucose level at 114 mg/dL and slightly decreased carbon dioxide, total protein and albumin levels. All other electrolytes were within normal limits. None of the results was considered significant. Prothrombin time/partial thromboplastin time was within normal limits.

Results of arterial blood gas analysis showed a slight deviation from normal, but this was viewed as unremarkable. Urinalysis showed 14 white blood cells, 19 red blood cells and a small number of leukocytes, which were considered contamination.

Her episodes of GI distress and heartburn a week ago had prompted her obstetrician to perform an electrocardiogram (ECG), which showed normal sinus rhythm. A subsequent ECG in the ED showed normal sinus rhythm with nonspecific ST abnormalities, at a rate of 73 beats per minute. A chest X-ray performed while in the ED was normal.

Fetal heart tones were strong at 150 beats per minute. The patient was sent for a venous duplex ultrasound of the bilateral lower extremities, which showed no evidence of deep venous thrombosis. Ultrasound of the gallbladder revealed normal size and configuration, without evidence of cholelithiasis or biliary tract obstruction.

The first set of cardiac enzymes, taken at 16:24, showed an elevated troponin I level of 0.66 ng/mL, a slightly elevated creatine kinase (CK) level of 85 U/L and elevated CK-MB level at 6.1 ng/mL. Although initial cardiac enzymes did have some deviation from normal, it was not immediately concerning.

The second set of enzymes, taken at 20:30, showed a further elevated troponin I level of 2.02 ng/mL, an increasing CK of 138 U/L and an elevated CK-MB of 14 ng/mL. A repeat ECG again showed normal sinus rhythm with nonspecific ST and T abnormalities, at a rate of 82 beats per minute.

Acute Myocardial Infarction

While waiting for the final set of cardiac enzymes, the patient's family practitioner and obstetrician were notified. The increasing cardiac enzymes made it evident that the patient's symptoms, albeit brief and intermittent, were those of an AMI.

After speaking with her family practitioner and obstetrician, as well as a cardiologist, it was agreed that the patient should be admitted to the cardiac care unit for observation. The third set of cardiac enzymes at 01:10 showed elevated troponin I of 3.32 ng/mL, a CK of 157 U/L and an elevated CK-MB of 15.0 ng/mL.

The patient was placed on telemetry monitoring. While she was in the CCU, the lipid profile returned showing elevated total cholesterol (263 mg/dL) and triglycerides (277 mg/dL); low-density lipoprotein level was 166 mg/dL.

She was placed on IV heparin titrated every six hours. Since she was not experiencing AMI symptoms, the medical team decided to forego the use of nitroglycerin. While in the CCU, a third ECG again revealed normal sinus rhythm with nonspecific ST abnormalities, at rate of 78 beats per minute. Echocardiogram showed competent heart valves, mild concentric left ventricular hypertrophy and normal left ventricular systolic function.

Fetal ultrasound revealed a viable single uterine gestation with no abnormal fluid collections and an estimated gestational age 34 weeks, two days.

While in the CCU, the patient experienced no GI distress or chest discomfort, and telemetry monitoring showed no abnormalities. She was discharged from the CCU with a diagnosis of non-Q-wave AMI and hyperlipidemia.

Discharge and Delivery

She was discharged on metoprolol 25 mg twice a day, along with her previously prescribed ranitidine and paroxetine. She was given a transdermal nitroglycerin patch to use as needed if she began to experience chest pain. She was not prescribed dyslipidemia medication. Heparin was discontinued.

The patient was instructed to follow up with her cardiologist and obstetrician the week after discharge. After discharge, she experienced no further symptoms. She followed up with a high-risk maternity center and had a C-section scheduled. While it would be possible to deliver successfully at 34 weeks of gestation, considering the tremendous added stress on the heart it was decided to wait until as close to the due date as possible to have the C-section.

The patient had no further problems, and the baby was delivered via C-section approximately three weeks after her AMI. Precautions were taken to minimize blood loss in order to lessen stress on the heart. The patient had an uncomplicated delivery.

She had been recovering well at the high-risk maternity center until two days after delivery, when she experienced sharp stabbing chest pain and pressure with radiation to her arms. After ECG and lab tests suggested ischemia, she underwent successful open-heart double bypass surgery.

Discussion

The highest incidence of AMI appears to be in multigravidas older than 33, in the third trimester.^3,4 The maternal mortality rate is nearly 45%, and death occurs either at the time of the MI or within two weeks.⁵ One population-based study performed in California over the course of 10 years showed an increase in the number of AMIs in pregnant women over that time. During the first year, the incidence was one in 73,400 patients; incidence increased to one in 24,600 patients in the final year of the study.¹

The risk factors for an AMI in pregnancy are the same as those in nonpregnant patients. Risk factors include family history, familial and patient hypercholesterolemia, diabetes, smoking, stress and previous use of oral contraceptives.⁴

Diagnosis can be suggested by history, but it is not always clear-cut. Symptoms associated with the normal changes of pregnancy include dyspnea, orthopnea, edema, exercise intolerance and epigastric pain. These symptoms also are associated with MI, presenting a diagnostic challenge during pregnancy.² Changes in the coagulation and fibrinolytic cascade and increased fibrinogen and prothrombin that make pregnancy a hypercoagulable state, leading to an increased risk of thrombosis.^2,3 Furthermore, increases in blood volume, stroke volume and heart rate can increase myocardial oxygen demand, which could contribute to an AMI and also cause further complications after an AMI.⁵

Pregnancy limits the diagnostic procedures, medications and therapies that can be used to treat symptoms. Echocardiography allows noninvasive evaluation of the anatomy and function of multiple areas of the heart, thus allowing the extent of myocardial damage to be assessed.^2,3 Cardiac catheterization and angiography allow for direct visualization of coronary arteries and can help determine the extent of disease. However, significant radiation is involved, so these procedures ideally are performed after delivery.²

Medical Management of AMI

Beta-blockers often are started soon after MI due to their antihypertensive and antiarrhythmic properties, as well as their ability to decrease heart rate. While they generally are a good choice in treating AMI in pregnancy, they often require monitoring due to potential fetal complications.^3,6 Among the reported beta-blocker-related complications are fetal growth retardation, fetal bradycardia, fetal hypoglycemia and decreased neonatal respiratory rate.⁴

Angiotensin-converting enzyme inhibitors are contraindicated during pregnancy due to increased incidence of fetal renal abnormalities and death.7 Nifedipine has been used in the treatment of hypertension, preeclampsia and myocardial ischemia during pregnancy, but limited information is available on the effectiveness and safety of other calcium-channel blockers.⁴

Anticoagulation can help prevent thrombus formation and can break up a thrombus that might have caused infarction. Warfarin is a pregnancy category D drug that crosses the placental barrier and is contraindicated in pregnancy.⁸ Heparin is in category C and is the anticoagulant of choice in pregnancy; because of its large molecular size, it does not cross the placental barrier, and it is not teratogenic.³ It is recommended that heparin therapy be discontinued 24 hours before elective induction of labor.⁴ The use of aspirin, a category D drug, as an antiplatelet agent is controversial. There is evidence of increased risk of hemorrhage and congenital abnormalities when aspirin is used in the third trimester.4 Nevertheless, aspirin has been used successfully in hypertensive pregnant women.⁸ Clopidogrel, in pregnancy category B, has been used throughout pregnancy, and while it may be more effective than aspirin, evidence is not yet conclusive.⁹

Pain relievers are an essential part of AMI treatment because they can help reduce the increased cardiac workload produced by pain.² Non-opiate analgesics may be used during pregnancy. In the third trimester, morphine sulfate, a pregnancy category B drug, can be used to prevent or relieve chest pain.^2,3 Note that if morphine is used shortly before delivery, it will cross the placental barrier and can cause neonatal respiratory depression.⁴

In most MI cases, thrombolytic therapy is considered a first-line therapy. However, it is contraindicated during pregnancy, although some authors suggest that it is a relative contraindication. Streptokinase and tissue plasminogen activator have been used successfully in pregnant patients without complications, but there is evidence of increased maternal mortality, pregnancy loss and hemorrhage.⁸

Nitroglycerin, a vasodilator that allows for increased blood and oxygen to tissue, can be used to prevent or relieve chest pain.^2,8 Even though nitroglycerin is in pregnancy category C, there are no known adverse effects during pregnancy.⁴

Pregnant women who experience an AMI are at increased risk for arrhythmias, which can impede cardiac output, blood pressure and myocardial and placental perfusion.² Certain anti-arrhythmia agents can be used during pregnancy and are very effective. Digoxin is effective in controlling supraventricular arrhythmias during pregnancy. Lidocaine, a pregnancy category B drug, is the drug of choice for treatment of ventricular arrhythmias.⁸

Other Interventions

Angioplasty with stenting has been performed successfully in pregnancy. However, the risk of radiation to the fetus must be considered. A radial approach to stenting has been shown equally as successful as the femoral approach.⁸ Some have considered immediate coronary angioplasty or percutaneous transluminal coronary angioplasty with or without stenting as the gold standard for treating AMI in pregnancy.² Coronary artery bypass grafting has been performed on pregnant patients with success and has a similar mortality rate in both pregnant and nonpregnant patients.⁸ It is suggested that if a patient is further along than 28 weeks, a C-section should be performed prior to bypass.⁸

Cardiopulmonary resuscitation during pregnancy follows the same guidelines as in nonpregnant patients. It is recommended that a pillow or similar object be placed under patient's flank and pelvis to attempt to avoid uterine compression. Pregnancy challenges CPR's effectiveness. The thorax is less compressible, and there may not be enough force for sufficient cardiac output. The elevated diaphragm that occurs during pregnancy hinders artificial respirations.^2,3 Some authors suggest that up until 24 weeks (the onset of fetal viability), CPR is aimed entirely at saving the mother. The goal after 24 weeks is to save both the mother and the fetus.³ Cardioversion also has been used during pregnancy with no fetal injury.⁸

AMI and Delivery

When a woman has had an AMI prior to delivery, it is in the best interest of both the mother and the fetus to prolong delivery until the MI has had time to heal. It is recommended that if the woman is not at term, delivery should be delayed two to three weeks if possible.⁴

Significant changes in cardiac output and volume occur during labor and delivery. Each contraction pushes an estimated 300 to 500 mL of blood into the central circulation, causing increased stroke volume and cardiac output during delivery.⁵ This, combined with the added cardiovascular stress caused by the pain and anxiety associated with delivery and the damaged myocardial tissue, further complicates the treatment of an AMI when planning for delivery.⁵ Therefore, labor and delivery should be planned carefully to ensure proper monitoring of mother and child.

C-section and vaginal delivery have respective risks and benefits. Some experts suggest that uncomplicated vaginal delivery under epidural anesthesia is the preferred delivery method,⁸ especially if measures are taken to reduce cardiac workload and oxygen demand.⁴ Vaginal delivery obviates major surgery and its possible complications.

C-section allows for time management and can expedite delivery, avoiding a long stressful labor and reducing maternal physical stress. However, cardiac output can increase 50% during a C-section because of hemodynamic changes associated with blood loss.⁵

After delivery, a woman who has had an AMI during pregnancy is at markedly increased risk for a repeat AMI.² This mainly relates to the vast hemodynamic changes that occur during and after delivery, such as large fluid shifts into the intravascular space, a slow return of cardiac output, return of blood volume and normal vascular resistance.²

Whether women who have had an AMI during pregnancy should have subsequent children has been a subject for debate. The decision to have more children is entirely individualized, based on such factors as myocardial damage, residual left ventricular function, underlying coronary anatomy and any ongoing ischemia of myocardial tissue.⁴

References

1. Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarction in pregnancy and the puerperium: a population-based study. Obstet Gynecol. 2005;105(3):480-484.

2. Kirkland CJ. Myocardial infarction during pregnancy. J Perinat Neonatal Nurs. 1991;5(2):38-49.

3. Badui E, Enciso R. Acute myocardial infarction during pregnancy and puerperium: a review. Angiology. 1996;47(8):739-756.

4. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll Cardiol. 2008;52(3):171-180.

5. Tucker D, Liu D, Ramoutar P. Myocardial infarction at term: a case report to consider management options. J Obstet Gynaecol. 1996;16(6):522-524.

6. Iung B. Rheumatic heart disease. In: Oakley C, Warnes CA, eds. Heart Disease in Pregnancy. 2nd ed. Malden, MA: Blackwell Publishing; 2007:79-95.

7. Martin SR, Foley MR. Cardiac disease in pregnancy. In: Queenan JT, Spong CY, Lockwood CJ, eds. Management of High-Risk Pregnancy. 5th ed. Malden, MA: Blackwell Publishing; 2007:143-162.

8. Lange SS, Jenner M. Myocardial infarction in the obstetric patient. Crit Care Nurs Clin North Am. 2004;16(2):211-219.

9. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324(7329):71-86.

Alexa Carroll is a PA in Dallas, Pa. She indicates no relationships to disclose related to the contents of this article.