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.