Postpartum STEMI in a Young Obese Female
Introduction:
ST-elevation myocardial infarction (STEMI) is a critical and often fatal condition, particularly
uncommon in younger individuals. This pathology entails transmural myocardial ischemia
caused by the obstruction of a coronary artery. In the postpartum period, young women
experience an increased prothrombotic risk, compounded by comorbidities such as obesity,
which further elevate the danger due to the hyper-estrogenic state.
Case Presentation:
A 31-year-old African American female with a history of morbid obesity (BMI 42) presented to
the hospital with central chest pressure beginning an hour prior to presentation. Of note, the
patient had recently delivered a live-born female newborn at 37 weeks 3 months prior to this
admission. She also endorsed emesis and dyspnea. Initial EKG showed concern for anterolateral
STEMI with elevations in the leads I / aVL / V1-V5 alongside ST depressions in leads III and
aVF. The cardiac catheterization lab was immediately activated. The patient underwent
successful percutaneous coronary intervention (PCI) with a drug-eluting stent (DES) of the
proximal left anterior descending (pLAD). During the PCI, the patient was noted to have a large
thrombotic occlusion. She was started on a 12-hour Eptifibatide drip. The post-catheterization
transthoracic echocardiogram (TTE) showed apical akinesis with high suspicion for an apical
clot. The patient was initiated on therapeutic enoxaparin and then subsequently underwent
contrast TTE which was inconclusive for clot resolution. She was discharged on Apixaban and
Ticagrelor along with Metoprolol Succinate for rate control and Losartan for hypertension.
Discussion:
This case underscores the unexpected risks faced by postpartum patients who are otherwise
healthy. The postpartum period is marked by an increased thrombotic risk, driven by elevated
production of coagulation factors and diminished fibrinolytic activity. Additionally, endothelial
damage incurred during childbirth predisposes patients to thrombus formation. The patient also
had pre-pregnancy obesity leading to both hyper-estrogenic and pro-inflammatory states. Young
women who are both pregnant and obese trigger elevated androgen aromatization in adipose
tissue leading to risk of high-clot burden. The patient also stated that she had a family history of
myocardial infarction in her mother signifying genetic interplay in the occurrence of STEMI.
