Introduction

Acute myocardial infarction (AMI) is a rare entity in the parturient population occurring in 3 to 10 cases per 100,000 deliveries; however, it poses a great risk for the mother and her unborn baby with a high case fatality rate. This paper is intended to supplement existing acute coronary syndrome (ACS) protocols. Our intent is to allow the EP to initiate management and coordinate the several specialists involved. Whenever possible, the EP can be the key resource for applying best practice principles in what may be a complex clinical event.

Heart Disease: Heart disease is present in 0.5-1% of all pregnant women. Some statistics reported on AMI patients:

• The incidence of AMI is estimated at 6.2 per 100,000 deliveries.
• ACS presents as non-STEMI 40% of the time.
• Mortality of these patients ranges from 5.1% to 11%.
• This incidence is 3-4 times higher than the estimated age-associated risk for non-pregnant women.
• MIs tend to be big, affecting a large area of muscle, leading to heart failure and cardiogenic shock and therefore have a higher mortality rate.
• 38% of AMIs occurring during antepartum period, 21% intrapartum, and 41% in the 6-week postpartum period.
• Risk factors for AMI are commonly seen in pregnancy, such as diabetes mellitus, smoking, advanced maternal age (since 1981, the birth rate of women aged 40-44 years has doubled) , dyslipidemia, significant family history, and hypertension.
• Pregnancy induced risks: anemia, pre-eclampsia, eclampsia, and thrombophilia.
• AMI pathology: atherosclerosis with or without thrombosis 40%, thrombosis without atherosclerosis 8%, coronary artery dissection 27%, and normal coronaries 13%. Some have indicated that coronary dissection is the cause of 50%, then vasospasm, followed by thrombosis.

Pregnancy-related physiology:

Many key physiologic changes may contribute to the incidence and severity of AMI in pregnancy.

• Increase of stroke volume and heart rate producing increased myocardial oxygen demand.
• Decreased diastolic blood pressure and anemia contribute to decreased myocardial perfusion. Increasing myocardial damage vs. non-pregnant state.
• Labor: Increasing pain, uterine contractions, anxiety can all act to increase myocardial oxygen demand.
• Post delivery relief of, caval compression may produce increasing myocardium demands.

Diagnosis: Similar work up as in non-pregnancy.

Pregnancy variations:

• ECG being of lower sensitivity/ specificity in the pregnant patient. One study found ST-segment depression in 16/25 healthy patients undergoing cesarean delivery with regional anesthesia.

Troponin I levels are mildly elevated in preeclampsia, eclampsia, and gestational hypertension decreasing the utility of this exam in these patients. Of note, creatine kinase and creatine kinase MB fraction levels are mildly elevated (up to twofold) during and after delivery making serum troponin I level the most useful marker for myocardial injury during and after delivery in healthy women.

Management: Once ACS is identified in the pregnant patient, initiate usual ED protocols [STEMI alert if indicated] plus contact OB team for rapid fetal monitoring of a viable fetus and OB planning. However, the mother should be treated first, before delivery, due to the high mortality risk of delivery in untreated ACS.

Hypotension: If over 24 weeks gestation put patient in left lateral decubitus position to either treat or prevent hypotension from caval compression. Administer nitroglycerin and morphine sulfate as in non-pregnancy. As in non-pregnant patients, nitroglycerin is contraindicated if systolic blood pressure is below 90 mmHg or greater than or equal to 30 mmHg below baseline, severe bradycardia (< 50 beats per minute), tachycardia ( > 100 beats per minute) in the absence of symptomatic heart failure, or right ventricular infarction. If patient is hypotensive despite position change and discontinuation of nitroglycerin, give fluids and pressors as indicated.

Hypertensive emergency: If patient experiencing hypertensive crisis with ACS, consider preeclampsia. Initiate treatment as in non-pregnancy with nitro, morphine. Consider adding labetalol drip as needed. If possible, avoid lowering blood pressure below 140/90 mm Hg because of potential for uterine hypoperfusion.

Medical Management: Medications generally used for ACS patients have a positive risk benefit profile in pregnancy. Some pregnancy related issues:

• Morphine: Communicate doses and times to delivery team so the effect on the fetus can be anticipated if delivered while medications are in the system.
• Nitrates: avoid maternal hypotension resulting in placental hypoperfusion. Tocolytic effect may slow labor.
• ASA: no significant issues.
• Heparin (unfractionated and low molecular weight), and clopidogrel: bleeding risks related to delivery, spinal anesthesia.
• beta-blockers: potential transient neonatal bradycardia, hypoglycemia, hypotension. Communicate dosing information to delivery team.
• Amiodarone: May lead to transient neonatal hypothyroidism, usually not associated with goiter. It is unrelated to either the dose or duration of amiodarone treatment. Exposure to amiodarone may also be associated with neurodevelopmental abnormalities, even in the absence of thyroid disease, but completely normal development has also been reported. Notify delivery team, even after relatively short treatment duration, so that evaluation for and treatment of neonatal hypothyroidism can begin in a timely manner.
• Oxytocin: If OB initiates oxytocin,be aware that it may induce chest pain, transient profound tachycardia, hypotension, and concomitant signs of myocardial ischemia with marked ECG changes. The effects are related to oxytocin; however, the patient needs to be watched carefully for possible AMI.

Post-acute phase testing: Patient should be evaluated further with minimally/non-invasive testing, such as echo and stress testing.

PCI: As in non-pregnancy, heparin and clopidogrel are given prior to procedure. Bare metal stents are preferred to drug eluting stents because the risk of stent thrombosis is lower when clopidogrel has to be stopped for delivery. Aspirin should be continued. Fetal radiation dose from PCI is low. One study showed if maternal back and abdomen are protected and the area is coned down, increased risk to the fetus of dying of cancer within 15 years from 60 minutes is ~1:80000. Another states that coronary angiography exposes patients to 2.5-5.0 mSv and PCI exposes patients to 5.0-15.0 mSv, which are both below the threshold for teratogenicity at any gestational age. Care should be taken during the procedure due to fragility of vascular structures and risk of coronary dissection.

Thrombolysis: If PCI is not available, then treatment should continue as in the non-pregnant patient. There is little data on thrombolysis for MI in pregnancy. These medications are unlikely to cross to the placenta but have been associated with first-trimester pregnancy loss, preterm labor, maternal hemorrhage, abruption placenta, and fetal death. In comparison, complication rate for thrombolysis in pulmonary embolism is only 1%. Generally these patients should be considered for lytic therapy, if timely PCI is not available.

CABG: A small amount of information is available for CABG in pregnancy. However, one study states that maternal mortality from cardiopulmonary bypass surgery is up to 13% and the risk of fetal loss is near 30%.

Post-Cardiac Arrest Hypothermia: For the non pregnant post arrest patient, this therapy has become one accepted standard intervention. The data on use in pregnancy is limited but some hospital protocols may list pregnancy as a contraindication. Many clinicians follow the dictum that saving the mother takes precedence over potential risks to the fetus. Therefore, they will initiate therapeutic hypothermia in these patients. Consider proactively discussing this issue with your perinatology, OB, cardiology consultants to optimize hospital protocols to address this situation.

A pertinent letter was in 2011 New England Journal of Medicine:: In a review of therapeutic hypothermia in comatose survivors of cardiac arrest, Holzer includes pregnancy as a contraindication to hypothermia. Successful induced hypothermia after cardiac arrest in a pregnant woman at 13 weeks of gestation, with subsequent term delivery and normal development of her newborn, has been reported. Also, intraoperative hypothermia administered during cardiac surgery in pregnant women with successful delivery of the fetuses has been described. Varying degrees of hypothermia were used during these operations, with similar positive outcomes. There are theoretical risks to the fetus. In one study, fetal death occurred in up to 24% of mothers undergoing cardiopulmonary bypass with the concurrent use of hypothermia; however, whether this rate of death was attributed to hypothermia or the stress of cardiac surgery with hypothermia remains unknown.Induced hypothermia improves neurologic morbidity and mortality. Conversely, no evidence exists to support harm associated with hypothermia during pregnancy, and evidence does exist to suggest the safety of this practice. Thus, we believe that the potential benefit of induced hypothermia outweighs the theoretical but unproven risks to the fetus, mother, or both.

[References and this article with citations are available online at www.acepnews.com].

Dr. Roemer is an Associate Professor in the Department of Emergency Medicine, OU School of Community Medicine, Schusterman Center, in Tulsa, Okla.; Dr. Brown is a Resident Physician in the Department of Emergency Medicine, OU School of Community Medicine, in Tulsa, Okla.; Dr. Katz is a Clinical Professor, Department of Obstetrics and Gynecology, Oregon Health Sciences University, and Medical Director, Women’s Services, Sacred Heart Medical Center, Center for Genetics and Maternal-Fetal Medicine, in Eugene, Ore.; Dr. Rousan is a Cardiology Fellow, at the University of Oklahoma, OU Health Sciences Center, in Oklahoma City, Okla.