ST-segment elevation myocardial infarction (STEMI) caused by spontaneous coronary artery dissection (SCAD) in a
Jaspreet Padam1, Michael Cenkowski1, Shravankumar Nosib2,3
1Medicine, Royal University Hospital, Saskatoon, Saskatchewan, Canada.
Insights
A postpartum woman with a history of pre-eclampsia and von Willebrand disease (VWD) experienced an ST-segment elevation myocardial infarction due to coronary artery dissection. Conservative management and dual antiplatelet therapy led to an uncomplicated recovery without bleeding complications.
Area of Science:
- Cardiology
- Obstetrics
Background:
- Acute coronary syndromes in postpartum women are rare but serious.
- Pre-eclampsia and von Willebrand disease (VWD) are significant risk factors that can complicate management.
Observation:
- A postpartum woman presented with chest pain, ECG changes, and elevated cardiac biomarkers consistent with myocardial infarction.
- Point-of-care ultrasound revealed apical hypokinesis; coronary angiography showed a distal left anterior descending artery dissection with TIMI 3 flow.
Findings:
- The patient was diagnosed with ST-segment elevation myocardial infarction secondary to coronary artery dissection, not plaque rupture.
- Conservative management, including a modified 3-month dual antiplatelet therapy course due to VWD, resulted in an uncomplicated hospital course.
Implications:
- This case highlights the importance of considering coronary artery dissection in postpartum women presenting with acute coronary syndromes, especially with relevant comorbidities.
- Conservative management can be effective in selected cases of spontaneous coronary artery dissection, even in patients with bleeding risks like VWD.
Abstract:
A postpartum woman in her early 40s, with a history of pre-eclampsia and von Willebrand disease (VWD), presented to the emergency room with chest pain suggestive of an acute coronary syndrome. Initial workup revealed an evolving anterior wall ST-segment elevation myocardial infarction on ECG and elevated cardiac biomarkers, confirming myocardial damage. Point-of-care ultrasound showed apical hypokinesis and coronary angiography revealed a distal dissection of the left anterior descending coronary artery. There was TIMI 3 flow and no evidence of plaque rupture. No percutaneous coronary intervention was performed and the patient was managed conservatively.Fibromuscular dysplasia was ruled out on screening CT angiography. Dual antiplatelet therapy was initiated for an amended course of 3 months given the history of VWD. Our patient had an uncomplicated course in the hospital with a downward trend in their cardiac biomarkers, resolving anterior ST elevation on serial ECGs, and no bleeding complications.
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