ST elevation myocardial infarction in pregnancy
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ST Elevation Myocardial Infarction Microchapters |
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Differentiating ST elevation myocardial infarction from other Diseases |
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ST elevation myocardial infarction in pregnancy On the Web |
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Risk calculators and risk factors for ST elevation myocardial infarction in pregnancy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Physiological changes during pregnancy may increase the woman's risk of developing a myocardial infarction (MI). MI during the antepartum period is usually caused by an atherosclotic plaque rupture, whereas MI during the peripartum and postpartum period is usually caused by coronary artery dissection (commonly in the LAD). Diagnosis of MI among pregnant women is similar to that in the general population and requires clinical suspiccion, as well as ECG changes and troponin elevation. In contrast, elevated CK-MB concentration is unreliable, since CK-MB may normally increase during labor and post-delivery due to non-cardiac causes, namely placental and uterine leaks. During an MI, echocardiography is safe and may be performed to evaluate wall motion abnormalities, and fetal monitoring is recommended. Treatment is usually by percutaneous coronary intervention. If spontaneous coronary artery dissection occurs, a more thorough investigation for connective tissue diseases and vasculitis is warranted.
Acute MI in Pregnancy
- Incidence: 1 per 35,000 deliveries
- Maternal mortality rate: 5% to 18%, fetal mortality rate: 9%
- Common in third trimester until 1-2 months post-delivery
- Antepartum: Atherosclotic plaque rupture is the most common cause
- Perpartum or postpartum: Coronary artery dissection (LAD > RCA > LC > LM)
Risk Factors
- It is unknown if pregnancy itself is a risk factor in development of acute MI.
- The most important risk factors in the development of AMI in pregnancy are generally similar to those in the general population. Risk factors include:
- Age > 35 years
- Diabetes mellitus
- Hypertension
- Smoking
- Connective tissue diseases (e.g. Ehler Danlos syndrome)
- Vasculitis (e.g. Takayasu arteritis)
- Thrombophilia (e.g. antiphospholipid syndrome)
- Acute post-partum stress:
- Severe post-partum hemorrhage
- Post-partum infection
Pathophysiology
- During pregnancy, progesterone release results in structural changes in the vascular intima and media.
- Physiologically, cardiac output and blood volume increase during pregnancy, both of which may increase the risk of cardiovascular events.
Diagnosis
- Diagnosis similar to the general population by: Symptoms, ECG changes, and troponin.
- CK-MB concentrations may markedly increase during labor and post-delivery due to non-cardiac causes, namely placental and uterine leaks.
- Echocardiography is safe and may be performed to evaluate wall motion abnormalities.
- Fetal monitoring is recommended.
Treatment
- Percutaneous coronary intervention
- If spontaneous coronary artery dissection occurs, a more thorough investigation for connective tissue diseases and vasculitis is warranted.