Acute Myocardial Infaction in pregnancy (MI) Acute Coronary Syndrome (ACS)

1. What every clinician should know

The incidence of cardiac disease among pregnant women is around 0.5-1%. Cardiac disease is the main cause of mortality among parturint in developed countries, and it remains the worst cause of all indirect maternal deaths.

Acute myocardial infarction (AMI) in women of reproductive age (16 – 45 years of age) is a rare event. During pregnancy, the risk of AMI is increased three to four fold, compared to non-pregnant women. Incidence of AMI has been reported to be between 1:16,129 to 1:35,700 deliveries. This incidence is likely to increase due to a continuing trend of childbirth in older women, the use of reproductive technologies that allow older and postmenopausal women to conceive, the increased use of oral contraceptives in women over 35 years of age, and substance abuse during pregnancy (especially cocaine).

AMI during pregnancy or immediate post partum period is associated with a higher maternal and fetal mortality. Maternal deaths from acute coronary syndrome (ACS) and ischemic heart disease (IHD) rose four fold from 2000 – 2002 to 2003 – 2005 in the UK.

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Maternal mortality rate from AMI is around 7% (range 5% – 37%). Mortality with AMI during the peripartum period is higher (18%) compared to both the antepartum and postpartum periods (9%). Mortality may be as high as 50% during cesarean sections. Outcome is better during early pregnancy. Improvement in survival might be related to improved strategies for identifying and treating ACS, including rapid thrombolysis and percutaneous interventions (PCI).

Risk factors for AMI during pregnancy include: history of hypertension, obesity, diabetes mellitus, and hyperlipidemia, family history of MI, thrombophilia, smoking, age greater than 35 years (30% for those older than 35 years, compared with 10%), and multiparity (78% compared with 61%), including non-Hispanic white (40% compared with 35%) and black race (15% compared to 7%). As an example, the risk for AMI during pregnancy is 30 fold higher in women over 40 compared with those less than 20 years of age. Obstetric risk factors for AMI include preeclampsia, postpartum infection, postpartum hemorrhage, and the requirement of a blood transfusion.

Acute coronary syndrome (ACS) is a term used in patients when there is clinical suspicion of myocardial ischemia. There are three types of ACS: unstable angina (UA), ST elevation myocardial infarction (STEMI), formerly known as Q wave MI, and non-ST elevation myocardial infarction (NSTEMI), formerly known as non-Q wave MI. Biomarker changes are present in both STEMI and NSTEMI events.

2. Diagnosis and differential diagnosis

The diagnosis of AMI is the same among parturient as in non-pregnant patients, and is made based on history, physical findings, ECG changes, and cardiac markers. Normal changes during pregnancy as well as fetal safety influence some of the diagnostic criteria and approaches.

Among non pregnant patients, the most significant symptoms include chest pain, dyspnea, diaphoresis, poor exercise tolerance, and syncope. It is important to note that all of these symptoms may occur in normal pregnant patients without MI, which sometimes can delay the diagnosis of AMI.

ECG and enzyme values remain the gold standard in diagnosis. ECG changes may not be as reliable and may mimic ischemia even in normal parturients. It is important to remember that even during a normal pregnancy, the ECG may show sinus tachycardia, a leftward shift, ST-segment depression, flattened or inverted T waves, and a Q wave in lead III. Because these changes can be seen during a normal pregnancy, serial ECG changes are more meaningful than isolated ECG changes.

The diagnosis of MI is based on the rise and gradual fall of tropinin and a more rapid rise of creatine kinase-MB (CK-MB), with at least one of the following: ischemic symptoms, development of pathologic Q waves of ≥0.04 sec on ECG, ECG changes indicative of ischemia (ST segment elevation or depression or a new bundle branch block), imaging evidence of new loss of viable myocardium, or a new regional wall motion abnormality.

It is important to note that during the peripartum period:

  • Measurement of the plasma troponin-1 level is useful in patients with suspected peripartum myocardial infarction because these levels remain within the normal range unless myocardial injury has occurred.

  • The serum CK-MB fraction may increase two fold 30 minutes after delivery in the absence of myocardial ischemia.

Holter monitoring and echocardiography (ECHO) are noninvasive, useful, and safe evaluations during pregnancy. While Holter monitoring may not be completely reliable, ECHO can evaluate for the presence of any wall-motion abnormalities.

The differential diagnosis of chest pain during pregnancy should include:

  • preeclampsia

  • hemorrhage

  • sickle cell crisis

  • acute pulmonary embolus

  • aortic dissection

  • heartburn (most common cause of chest pain during pregnancy)

Chest pain should never be ignored, and if the chest pain is significant, cardiac consult should be requested.

3. Management


Maternal AMI must be treated prior to delivery. The maternal risk associated with delivery without treating ACS is very high. Mode of delivery should optimize the maternal clinical status and obstetric consideration for the fetus. Cardiac consult is of utmost importance, and close multispecialty management is mandatory.

Treatment should be directed towards relief of ischemic pain, hemodynamic stability, initiation of reperfusion therapy with primary percutaneous coronary intervention (PCI) or fibrinolysis, and antithrombotic therapy and beta blocker therapy to prevent life threatening ventricular arrhythmias and recurrent ischemia. The pharmacologic agents (e.g., nitrates, beta-adrenergic receptor antagonists, and calcium channel antagonists) used to treat myocardial ischemia in non-pregnant patients are also used during pregnancy.

Treatment of myocardial ischemia while maintaining cardiac output improves cardiac function, which should increase the uteroplacental perfusion. Follow the MONA protocol (morphine, oxygen, nitroglycerine, and aspirin) while awaiting an expert opinion. Conversely, an overly aggressive therapy may adversely affect the fetus. For example, intravenous nitroglycerin or morphine can result in a sudden reduction in preload, which may reduce maternal cardiac output and uteroplacental prefusion.

Other associated diseases which may adversely reduce myocardial oxygen supply (e.g. anemia, hypotension, and hypoxia), increase myocardial oxygen demand (e.g., hypertension, infection, and thyrotoxicosis) or effect both (substance abuse) should be treated promptly. It is prudent to monitor the fetal heart rate (FHR) in these patients.

Urgent PCI is the treatment of choice. Bare metal stents are usually preferred over drug-coated (drug eluting – DES) stents. DES stents require prolonged prophylactic clopidrogel to avoid thrombosis during delivery and have to be discontinued to avoid major bleeding during delivery.

The fetal radiation dose from PCI is low. Appropriate lead shielding is mandatory for fetal protection, so the maternal back and the abdomen should be protected appropriately and the field size coned down to the area of interest. Cardiac catheterization and interventional procedures are associated with a fetal radiation exposure of up to 0.1 gray (Gy) units (1 Gy = 100 rad), depending on the extent of the procedure.

In general, as long as the organogenesis is complete, this level of exposure should not alter maternal management if catheterization is indicated. There is an increased risk to the fetus of dying of cancer within 15 years, which for a 60 minute screening in the antero-posterior (AP) projection, is estimated at 1:80,000. As for all procedures that require a pregnant woman to lie prone, a wedge should be placed under the right hip to prevent uterine compression of the inferior vena cava.

tPA (tissue Plasminogen Activator) can also be considered in patients who are candidates for thrombolytic treatment, but care has to be taken because it may increase the risk of placental abruption, intrauterine hemorrhage, and fetal demise, as well as increased blood loss if any operative procedures have to be performed immediately following.


Continuous ECG and SpO2 during labor or cesarean section and invasive monitoring, such as intra-arterial catheter and pulmonary artery catheter, should be considered in patients with either MI or ventricular or valvular dysfunction.

Prevent hypocapnia and catecholamines, as they produce coronary artery vasoconstriction. Avoid pain and hyperventilation. Prevent sudden hypotension, which may reduce coronary perfusion. Prevent hypertension and tachycardia, as they increase myocardial oxygen demand. Remember some drugs can cause coronary steal.


The patient should be monitored closely for any symptoms or ECG changes of MI, preferably in an ICU for the first 24 hours. If cardiopulmonary bypass surgery is necessary, the risk of maternal mortality from this surgery is 13% and the risk of fetal loss is 30%.

In patients with ACS secondary to cocaine abuse, it is important to administer benzodiazepines early during treatment and to avoid using beta blockers due to the possible exacerbation of coronary vasoconstriction.

Avoid methylergonovine during the third stage of labor because it can precipitate coronary artery spasm.

4. Complications

A. Congestive heart failure, coronary dissection, maternal collapse, and fetal demise are complications of AMI.

B. Coronary dissection and irradiation to the fetus are complications from PCI. Placental abruption can occur from t-PA treatment.

5. Prognosis and outcome

A. Severity of the underlying condition precipitating the MI and the myocaridal function correlate with outcome for these patients.

B. Timing of the event in relation to pregnancy and delivery also plays an important role in fetal and maternal outcomes. AMI during labor and the third trimester are associated with higher mortality.

C. MI with refractory congestive heart failure during pregnancy has worse outcomes for the mother and fetus, and early cesarean delivery should be undertaken.

D. Vaginal delivery is preferred over cesarean section in patients where AMI occurred prior to the peripartum period. Vaginal delivery should be undertaken with a dense epidural block to prevent an increase in cathecholamines and pain during delivery. Sympathectomy associated with epidural block reduces preload as well as afterload, thereby reducing oxygen demand. Cesarean delivery should be considered mainly for obstetric indications. Epidural is the anesthetic of choice, which can also be used for postoperative pain management.

6. What is the evidence for specific management and treatment recommendations

Roth, A, Elkayam, U. “Acute myocardial infarction associated with pregnancy”. J Am Coll Cardiol.. vol. 52. 2008. pp. 171-80. (Review article on MI in pregnancy with treatment alternatives.)

James, AH, Jamison, MG, BIswas, MS, Brancazio, LR, Swamy, GK. “Acute myocardial infarction in pregnancy: a United States population-based study”. Circulation. vol. 113. 2006. pp. 1564-71.

El-Deeb, M, El-Menyar, A, Gehani, A, Sulaiman, K. “Acute coronary syndrome in pregnant women”. Expert Rev Cardiovasc Ther.. vol. 9. 2011. pp. 505-15. (Review article of ACS in pregnancy, includes review of case reports in literature.)

O’Gara, PT, Kushner, FG, Ascheim, DD, Casey, DE, Chung, MK. “2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines”. J Am Coll Cardiol. vol. 61. 2013. pp. e78-140.

Jneid, H, Anderson, JL, Wright, RS, Adams, CD, Bridges, CR, Roos-Hesselink, J, Duvekot, JJ, Thorne, SA. “2012 ACCF/AHA focused update of the guideline for the management of patients with unstable angina/non–ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines”. J Am Coll Cardiol. vol. 60. 2012. pp. 645-81.