Pregnancy-Associated Spontaneous Coronary Artery Dissection in a 32-Year-Old Woman With Postpartum Hemorrhage

Abstract

Background

Pregnancy-associated spontaneous coronary artery dissection (p-SCAD) is the leading cause of pregnancy-associated myocardial infarction.

Case Summary

A 32-year-old woman, G1P0, with gestational hypertension underwent cesarean delivery of twins, conceived with assisted reproductive technology. Because of uterine atony, she had postpartum hemorrhage requiring uterotonics and blood transfusion. She additionally tested positive for non-COVID coronavirus. On postoperative day 3, an electrocardiogram in the context of acute chest pain showed inferior and anterolateral ST-segment elevations. Coronary angiogram demonstrated type 2 SCAD of the left anterior descending artery and ostial second diagonal. Ejection fraction was mildly reduced (45%-50%) with apical hypokinesis. She was managed medically. Cross-sectional head to pelvis imaging was negative for fibromuscular dysplasia, aneurysm, and other dissections.

Discussion

To our knowledge, this is the first described case of p-SCAD after postpartum hemorrhage.

Take-Home Message

Etiologic assessment of SCAD should include hormonal, hemodynamic, and inflammatory stressors, whose roles remain incompletely understood but likely synergistic.

Visual Summary

History of Presentation

A 32-year-old woman (G1P0) presented for a scheduled cesarean delivery of dichorionic-diamniotic twins at 37 weeks of gestation due to fetal malpresentation in the setting of gestational hypertension. Her immediate postoperative course was complicated by uterine atony with 2.8 L of blood loss and a hemoglobin nadir of 6.3 g/dL, managed with uterotonics (misoprostol, methylergonovine, and oxytocin), vacuum-induced uterine tamponade, tranexamic acid, fibrinogen concentrate, and transfusion of 2 units of packed red blood cells. Despite significant blood loss, she remained hemodynamically stable without vasopressor support. On postoperative day 2 (POD2), she reported mild shortness of breath and a sore throat and tested positive for non-COVID coronavirus. On POD3, she awoke from sleep with acute chest pain radiating to her left arm, associated with shortness of breath and nausea. Vital signs demonstrated blood pressure 133/74 mm Hg (equivalent in the bilateral upper extremities), heart rate 79 beats/min, and oxygen saturation 100% on room air. Physical examination was notable only for pallor. The electrocardiogram demonstrated ST-segment elevation in the inferior and anterolateral leads (Figure 1). The initial high-sensitivity troponin I level was 37 ng/L (normal <40 ng/L) and peaked at 18,179 ng/L.

Take-Home Messages

• •Evaluation of SCAD warrants consideration beyond established risk factors to include hormonal, hemodynamic, and inflammatory stressors, whose roles remain incompletely understood but likely synergistic and significant.
• •Insight into the circumstances surrounding SCAD onset may, in part, help guide strategies aimed at preventing recurrence.

Figure 1.

12-Lead Electrocardiogram With Anterior-Inferior Injury

12-lead electrocardiogram showing anterior and inferior ST-segment elevation involving leads II, III, aVF, V₃-V₅.

Past Medical History

Her current and first pregnancy was achieved with intrauterine insemination and clomiphene citrate after the first treatment cycle. Results of routine prenatal laboratory testing and aneuploidy screening were normal, fetal growth tracked appropriately for gestational age, and she had no chronic hypertension. She was a former athlete who maintained a healthy lifestyle before delivery. At 36 weeks, she was found to have gestational hypertension and fetal malpresentation of twin A. Fetal malpresentation determined the mode of delivery, whereas gestational hypertension prompted early delivery, resulting in a scheduled cesarean delivery at 37 weeks. Additional medical history was notable for atopic dermatitis and childhood asthma, requiring nebulizer therapy between ages 5 and 6 years. Atopic dermatitis was quiescent through early adulthood but flared during pregnancy, prompting treatment with phototherapy and topical steroids. Lastly, she reported a previous trauma-associated concussion associated with transient headaches. There was otherwise no history of migraine or pulsatile tinnitus. There was no personal or family history of thrombophilia, autoimmune disease, or cardiovascular events.

Differential Diagnosis

The differential diagnosis included acute coronary syndrome, coronary vasospasm, pulmonary embolism, aortic dissection, and peripartum cardiomyopathy. Our patient had multiple peripartum cardiovascular risk factors, including postpartum hemorrhage (PPH), multiple gestation, and gestational hypertension. The postpartum period, especially the first week, is associated with a 4- to 5-fold increased risk of venous thromboembolism and a markedly increased risk of pregnancy-associated myocardial infarction, particularly spontaneous coronary artery dissection (SCAD).^1,2 Atherosclerotic plaque rupture was possible but less likely given her age and absence of traditional risk factors. Pregnancy-associated SCAD (p-SCAD) was high on our differential, given the timing, multiple risk modifiers, and typical demographics. Pulmonary embolism and aortic dissection were considered but lacked supportive clinical and hemodynamic features. Peripartum cardiomyopathy was less consistent with her abrupt and preferentially ischemic presentation. Coronary vasospasm was possible, particularly with recent methylergonovine exposure, though ultimately a diagnosis of exclusion.

Investigations

An emergency coronary angiogram 1 hour after symptom onset showed type 2 SCAD of the distal left anterior descending artery and ostial second diagonal branch (Figure 2, Video 1). Left ventriculography showed an ejection fraction (EF) of 45% to 50% with apical hypokinesis. She was noted to have an elevated left ventricular end-diastolic pressure of 18 mm Hg. Transthoracic echocardiography confirmed reduced EF with segmental wall motion abnormality. Head to pelvis computed tomography angiography during hospitalization showed no evidence of fibromuscular dysplasia, aneurysm, or other dissection.

Figure 2.

Emergency Coronary Angiogram (Left Anterior Oblique Projection)

Coronary catheterization demonstrates type 2 spontaneous coronary artery dissection of the distal left anterior descending artery and ostial second diagonal branch.

Management

Given the patient's clinical and hemodynamic stability, absence of malignant arrhythmias, and lack of high-risk anatomical features, she was treated medically with aspirin, antianginals, and metoprolol. She was admitted to the cardiac care unit for monitoring under the guidance of a multidisciplinary cardio-obstetrics team. She received one dose of furosemide and was started on low-dose enalapril in addition to daily aspirin and metoprolol. There was no evidence of recurrent ischemia during the remainder of the hospitalization. She was transferred back to the obstetrics service on POD5 and discharged on POD7 with close follow-up.

Outcome and Follow-Up

Interval echocardiography at 2 months showed recovered EF. Cardiac magnetic resonance demonstrated normal biventricular size and function, with mild-to-moderate apical hypokinesis and a near-transmural infarction of the distal septum and medial apex comprising a small total scar burden of 4%. The patient remains on low-dose metoprolol and baby aspirin, with well-controlled blood pressures. She was referred for cardiac rehabilitation but chose to defer enrollment and had resumed moderate-intensity exercise at short-term follow-up. She has no immediate plans for future pregnancy. She is currently using barrier contraception but was counseled on the superior efficacy and reliability of long-acting reversible contraception. She completed 6 months of lactation uneventfully.

Discussion

This case highlights multiple established risk factors for p-SCAD, including multiple gestation, gestational hypertension, and fertility treatment.^3,4 Our patient's age, early postpartum presentation, multivessel involvement including the left anterior descending artery, and reduced EF are characteristic features of p-SCAD.⁵ The hormonal milieu of twin gestation, compounded by exogenous hormone exposure from fertility treatment, may have increased vascular vulnerability and predisposed our patient to p-SCAD. Specifically, multiple gestation pregnancies are associated with up to 50% higher circulating levels of estradiol and progesterone compared with singleton pregnancies.⁶ These hormones promote connective tissue remodeling within coronary arteries that can weaken the vessel wall, especially under conditions of increased hemodynamic stress.⁴

PPH is a recognized risk factor for pregnancy-associated myocardial infarction, but the association between p-SCAD and PPH is not well characterized.⁷ Although prior literature has documented cases of p-SCAD with subsequent delivery complicated by PPH, this case appears to be the first in which PPH preceded the onset of p-SCAD.⁶ It is conceivable that the rapid autotransfusion of uterine blood after delivery, followed by substantial PPH (with loss of approximately one-half of her blood volume) and subsequent resuscitation, collectively imposed hemodynamic strain that served as an inciting factor in our patient. Moreover, methylergonovine, a potent vasoconstrictor with known proischemic and vasospastic effects, may have further contributed to arterial vulnerability.

Current expert consensus advises caution with future pregnancy after SCAD, given the lack of established risk factors or preventive strategies for recurrence and the heightened severity typically seen in pregnancy-associated cases. Although limited to small observational studies, available data suggest a 3% to 11% recurrence rate within 12 months of pregnancy in patients who become pregnant after SCAD.^8,9 Recurrence rates across all SCAD cohorts range from 2.1% to 29%, with the more contemporary studies reporting rates between 2.1% and 14.8%.^3,10,11 These risks were reviewed with the patient in detail during postpartum follow-up. She was counseled that future pregnancy carries a meaningful risk of recurrent SCAD, including life-threatening maternal morbidity, and that risk stratification strategies remain limited. We reviewed the role of a gestational carrier as well as adoption as alternative pathways for expanding her family. Should our patient elect to pursue another pregnancy, we would advise deferring conception for at least 1 year after the index event, avoiding multifetal gestation and high-dose exogenous hormonal stimulation, and obtaining preconception echocardiographic assessment and stress testing.⁸ Given the more distal location of the dissection, the role of coronary computed tomography angiography prepartum may be limited.¹² A multidisciplinary Pregnancy Heart Team would provide close surveillance, with echocardiography in each trimester, continuation of β-blocker therapy, close blood-pressure control, and telemetry monitoring throughout labor and the postpartum hospitalization. With a history of SCAD, future use of methylergometrine would be contraindicated.¹³

Conclusions

To our knowledge, this is the first report of p-SCAD occurring after a pregnancy complicated by PPH. What further distinguishes this case is the clustering of several p-SCAD risk modifiers—fertility therapy, multiple gestation, PPH, and viral illness—raising questions about the synergistic effects of conception-, pregnancy-, and delivery-related stressors on coronary arterial integrity. Future research is needed to clarify the mechanisms by which hormonal, hemodynamic, and inflammatory factors interact to precipitate SCAD in the peripartum setting. There is also a need for consensus on risk stratification and counseling for patients with a history of p-SCAD who are considering future pregnancy.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Emergency Coronary Angiogram (Left Anterior Oblique Projection)

Type 2 spontaneous coronary artery dissection of the distal left anterior descending artery and ostial second diagonal branch.