Late Postpartum Type 2 SCAD Presenting as STEMI in a Lactating Woman

SCAD is a rare etiology of ACS, commonly affecting young women in pregnancy or the immediate postpartum period. SCAD presenting several years after childbirth is uncommon, and its link to prolonged lactation is not well established. This case study describes a rare presentation of SCAD in a 41-year old lactating woman three years postpartum. The patient presented with acute STEMI despite having no conventional cardiovascular risk factors.

Coronary angiography confirmed a type-2 SCAD affecting the distal left anterior descending artery with marked coronary tortuosity. The patient was managed conservatively due to stable coronary flow and the increased risk of procedural complications with intervention. This case reinforces the importance of considering SCAD in young, breastfeeding mother even outside the early postpartum phase. The findings raise clinical awareness about prolonged lactation and its potential hormonal contribution to late-onset SCAD.

• A 41-year-old woman presented with an abrupt onset of substernal chest pain that developed suddenly while at home.
• She described earlier mild discomfort that briefly settled before bedtime but returned during sleep, waking her from rest and progressively worsening over several hours.
• The pain was non-radiating and initially not accompanied by other symptoms, though it persisted until relieved by aspirin administered by emergency medical services (EMS).
• Before the onset of pain, she noted experiencing significant emotional stress.

Introduction

Spontaneous coronary artery dissection (SCAD) refers to non-traumatic separation of the coronary artery wall layers—typically between the tunica intima and media or within the media—resulting in a false lumen. This false lumen has the potential to compress the true lumen, decreasing blood flow and causing myocardial ischemia or acute myocardial infarction. SCAD may occur due to atherosclerotic mechanisms, such as plaque rupture and intramural hematoma, or non-atherosclerotic causes, which are most commonly observed.

Non-atherosclerotic SCAD is strongly linked with conditions including fibromuscular dysplasia (FMD), peripartum status, hormonal changes, emotional or physical stress, connective tissue disorders, and idiopathic factors. SCAD represents up to 35% of acute coronary syndrome (ACS) cases in women younger than 50 and is the leading cause of pregnancy-associated myocardial infarction.

Although frequently associated with pregnancy and early postpartum vascular changes, SCAD also occurs independently of these periods and is often linked to underlying arteriopathies, emotional stress, and hormonal influences. Coronary artery tortuosity and FMD are increasingly recognised structural markers of vascular vulnerability in SCAD. However, the cardiovascular implications of prolonged lactation remain poorly described in the literature.

This case presents a rare non-atherosclerotic SCAD event in a woman with an extended breastfeeding history and marked coronary tortuosity, broadening current understanding of potential predisposing factors outside conventional peripartum timelines.

Medical History

• The medical history of the female patient was otherwise unremarkable, with no hypertension, diabetes, dyslipidaemia, smoking history, connective tissue disorders, or family history of premature coronary artery disease (CAD).
• She had a notable history of prolonged lactation, as she was still actively breastfeeding her 3-year-old child.

• On vital signs examination, the patient was hemodynamically stable, with a blood pressure of 122/76 mmHg, a heart rate of 68 beats per minute, a respiratory rate of 16 breaths per minute, a peripheral oxygen saturation of 99% on room air, and a temperature of 99°F.
• Physical examination revealed persistent facial melasma, which had been present since pregnancy.
• The initial electrocardiogram (ECG) demonstrated sinus rhythm without ST-T abnormalities, while cardiac biomarkers were considerably elevated.
• High-sensitivity troponin measured 143 pg/mL at admission, rising progressively to 796 pg/mL at 6 hours and peaking at 9513 pg/mL at 36 hours (reference range < 5–11.8 pg/mL), consistent with acute myocardial injury.
• Based on these findings, the woman was admitted with a diagnosis of non-ST-elevation myocardial infarction (NSTEMI), with an early differential including Takotsubo cardiomyopathy (broken heart syndrome) due to recent emotional stress.
• During the second hospital day, the patient experienced a recurrent episode of sudden, severe substernal chest pain, accompanied by nausea, vomiting, diaphoresis, and left arm radiation. Repeat ECG revealed ST-segment elevation in leads V3–V6 without reciprocal depression, prompting urgent coronary angiography.
• Coronary angiography showed marked tortuosity in all major coronary arteries, with the distal left anterior descending artery (LAD) demonstrating a sudden change in calibre, followed by a long tapered narrowing and subtotal occlusion, consistent with a type 2 SCAD.
• Echocardiography illustrated a preserved left ventricular ejection fraction of 55%, with a small area of apical hypokinesis. Mild dilation and hypokinesia of the right ventricle were also noted. A transthoracic echocardiogram excluded Takotsubo cardiomyopathy.
• Due to the distal involvement of the suspected lesion and the risk of exacerbating arterial injury, optical coherence tomography/intravascular ultrasound (OCT/IVUS) was deferred.
• No inpatient vascular imaging (computed tomography angiography/magnetic resonance angiography) was completed, as there was no immediate clinical indication; however, outpatient evaluation for FMD or related arteriopathies is planned.

• The patient was initially managed for NSTEMI with standard medical therapy, including aspirin, clopidogrel, heparin, metoprolol, and atorvastatin.
• Following coronary angiography, which confirmed a distal LAD dissection consistent with type 2 SCAD, the management strategy was modified. Anticoagulation, additional antiplatelet therapy, and statin therapy were discontinued to minimize the risk of worsening the dissection.
• The patient was transitioned to a conservative treatment approach, receiving low-dose metoprolol succinate 12.5 mg daily and aspirin monotherapy.
• The woman remained hemodynamically stable, with complete resolution of chest pain and no recurrent ischemic symptoms. She was discharged on hospital day 5 on a conservative regimen of beta-blocker and aspirin, consistent with contemporary SCAD management recommendations.

Discussion

This case illustrates an uncommon presentation of SCAD occurring three years postpartum in a woman who was still breastfeeding, extending the recognized window of vulnerability well beyond the early peripartum period. SCAD typically affects younger women without traditional atherosclerotic risk factors, and this case reinforces the need for clinicians and women’s health specialists to consider SCAD in young women presenting with chest pain or myocardial infarction, even years after pregnancy.

A striking feature in this patient was the pronounced coronary tortuosity, a trait frequently associated with SCAD and often indicative of an underlying arteriopathy. Although she lacked phenotypic signs of connective tissue disease, such anatomical findings justify further evaluation for conditions such as FMD or heritable vascular disorders. Identifying such contributors is fundamental, given their association with recurrence and systemic vascular involvement.

From a mechanistic standpoint, this case supports growing interest in hormonal influences on vascular integrity. While SCAD is classically linked to pregnancy-related hormonal fluctuations, prolonged lactation may also modify collagen structure and arterial wall resilience. Although this association remains speculative, it warrants further exploration due to potential implications for risk stratification in postpartum women.

Conservative management was appropriate given the distal vessel involvement and clinical stability, aligning with evidence that most SCAD lesions heal spontaneously. Long-term follow-up remains critical, as recurrence can occur in new coronary segments and may be associated with ongoing emotional or hemodynamic stress. Overall, this case broadens the clinical context in which SCAD should be considered and highlights the importance of individualized management and continued vascular assessment in affected patients.

Learning

• SCAD should be considered in young women presenting with ACS, even years beyond childbirth, particularly when traditional atherosclerotic risk factors are absent.
• Coronary tortuosity, distal vessel involvement, and hormonal influences from prolonged lactation may collectively raise arterial vulnerability and expand the recognized spectrum of SCAD presentations.
• Unexpected right-ventricular dysfunction, as seen in this case, may represent an underappreciated component of SCAD and warrants closer evaluation in similar patients.
• Conservative therapy remains the preferred strategy in stable type 2 SCAD, given its high rate of spontaneous healing and the risks associated with revascularization.
• Long-term management should include surveillance for recurrent events, assessment for underlying arteriopathies such as FMD, and patient counseling regarding stress reduction and future cardiovascular risk.