Postpartum spontaneous coronary artery dissection – a case report

Abstract

Spontaneous coronary artery dissection (SCAD) is an increasingly recognized non-atherosclerotic cause of acute coronary syndrome (ACS), particularly affecting young women in the peripartum or postpartum period. We report the case of a 39-year-old woman, 3 months postpartum and breastfeeding, who presented with acute central chest pain radiating to the left arm and associated dyspnea. She had no cardiovascular risk factors. Her electrocardiogram showed dynamic T-wave inversions in the anterolateral leads, and high-sensitivity troponin-T was elevated at 454 ng/L. Transthoracic echocardiography demonstrated a left ventricular ejection fraction of 45% with apical hypokinesis. Coronary angiography demonstrated a 99% stenosis in the mid-left anterior descending artery, consistent with type 2 SCAD. The patient was hemodynamically stable and managed conservatively with beta-blocker, ACE inhibitor, and dual antiplatelet therapy. Breastfeeding was discontinued following shared decision-making due to concerns over medication safety. Screening for fibromuscular dysplasia with CT angiography of the carotid and renal arteries was unremarkable. At 6 months, CT coronary angiography showed complete resolution of the dissection and normal coronary anatomy, allowing cessation of antiplatelet therapy in line with the patient’s preference to resume breastfeeding. Interval echocardiography also demonstrated recovery of left ventricular ejection fraction to 62%. This case highlights the importance of considering SCAD in young postpartum women presenting with ACS. Prompt diagnosis and tailored conservative management can result in excellent outcomes. Longitudinal imaging, medication review, and reproductive counselling are essential in the follow-up of such patients with the need for patient-centered care in the context of breastfeeding and future pregnancies.

Case report

A 39-year-old female presented to the emergency department with acute-onset central chest tightness radiating to the left arm, accompanied by shortness of breath. She had no known cardiovascular risk factors and no family history of ischaemic heart disease. She was 3 months post-partum and actively breastfeeding. On admission, her heart rate was 57 beats per minute, her blood pressure was 99/70 mmHg, and she was saturating well on room air. Cardiac and pulmonary examination was normal.

Serial electrocardiograms (ECGs) revealed dynamic T-wave inversions in the anterolateral leads. Peak high-sensitivity troponin-T was elevated at 454 ng/L (upper limit of normal <16 ng/L). Basic biochemical investigations, full blood count and chest X-ray were unremarkable.

Cardiology was consulted due to raised troponins. A transthoracic echocardiography (TTE) demonstrated a left ventricle ejection fraction (LVEF) of 45%, apical hypokinesis with no significant valvulopathies. There was no right heart strain noted. Due to concerns for acute coronary syndrome, the patient underwent coronary angiography, which identified a 99% stenosis of the mid-left anterior descending artery with TIMI 2 flow (Figure 1), with angiographic features consistent with type 2 spontaneous coronary artery dissection (SCAD). The remaining coronary arteries were normal.

Figure 1.

(a–c): Coronary angiography in a 39-year-old post-partum female presenting with chest pain, elevated troponins showing 99% stenosis of the left anterior descending artery (arrowheads).

In view of preserved distal flow, hemodynamic stability, and absence of ongoing ischemic symptoms, the patient was managed conservatively without percutaneous coronary intervention. Medical therapy that was commenced included bisoprolol, enalapril, and dual antiplatelet therapy (DAPT) consisting of aspirin and clopidogrel. Shared decision was made for discontinuation of breastfeeding. The patient was monitored for 4 days and discharged with a plan for close outpatient follow-up.

Outpatient CT angiography of the carotid and renal arteries demonstrated no radiographic features suggestive of fibromuscular dysplasia. Interval CT Coronary Angiography (CTCA) at 6 months demonstrated complete resolution of the SCAD with widely patent coronary arteries (Figure 2). Medications including antiplatelets were subsequently discontinued given resolution of SCAD and patient’s preference to resume breastfeeding. Repeat TTE at 12 months demonstrated recovery of LVEF to 62% with no residual hypokinesis. She remained asymptomatic and had returned to normal physical activities.

Figure 2.

(a–c): Follow up CT coronary angiography at 6 months, demonstrating complete resolution of the spontaneous coronary artery dissection.

Discussion

Differential diagnosis of chest pain in younger females

Chest pain in younger females with raised troponins warrants considerations beyond the usual differentials of acute myocardial infarction, pulmonary embolism or aortic dissection. Unique differentials to this cohort, who often lack traditional cardiovascular risk factors, include SCAD and peripartum cardiomyopathy. SCAD is of particular relevance in pregnant or postpartum females, as it is a non-atherosclerotic cause of acute coronary syndrome (ACS). ¹

Epidemiology, pathophysiology and classification of SCAD

SCAD involves a spontaneous tear in the intimal layer of a coronary artery or a rupture of the vasa vasorum resulting in the development of an intramural haematoma. This causes luminal compression, which can lead to myocardial ischaemia and infarction. It is classified angiographically into 3 groups:

• Type 1: Visible dissection flap with dual lumens

• Type 2: Diffuse stenosis without a visible flap (most common)

• Type 3: Mimicking atherosclerosis with focal stenosis

SCAD accounts for approximately 1% to 4% of all acute coronary syndrome cases.^2,3 It predominantly affects women, with reports suggesting 70–90% of such cases,^2,4 and is responsible for up to 35% of myocardial infarctions in women ≤50 years of age.^3–5 Notably, SCAD is the most common cause of pregnancy-associated myocardial infarction, accounting for 43% of such cases. ¹

Pregnancy-associated SCAD (P-SCAD) has variable definitions, ranging from the third trimester of pregnancy up to several months postpartum, typically in women still breastfeeding.^6,7 Hormonal changes of pregnancy leading to weakening of the arterial wall have been implicated. Women with pregnancy-associated SCAD seem to have a poorer prognosis than women with SCAD unrelated to pregnancy, with frequent involvement of the left main or left anterior descending artery. ⁸

SCAD is also linked to connective tissue disorders like fibromuscular dysplasia (FMD), ⁹ which may increase susceptibility to arterial dissection. Emotional or physical stress, such as intense exercise or trauma, have been reported as potential triggers for SCAD events.

Management of SCAD

In contrast to atherosclerosis-related thrombotic occlusion where revascularization with percutaneous coronary angioplasty is recommended, conservative management is generally recommended for patients with SCAD who are hemodynamically stable and have no ongoing ischaemia or complete coronary occlusion. This allows for spontaneous healing of dissected segments. ¹⁰ Observational studies have demonstrated increased coronary complications and lower success rate with percutaneous coronary intervention, due to risk of iatrogenic dissection and propagation of the false lumen. ¹¹ However, in cases of refractory ischemia, left main coronary artery involvement, or hemodynamic instability, revascularization should be considered. ⁸

Evidence surrounding optimal medical therapy remains limited, with mainly observational studies formulating current treatment recommendations due to low incidence. The role and duration of antithrombotic agents in particular, remain debatable, although there are certain intracoronary features that support its use including grade of stenosis and presence of luminal thrombus. ¹² Medical management of SCAD with left ventricular (LV) dysfunction includes renin-angiotensin-aldosterone system (RAAS) inhibitors, beta blockade (BB) and mineralocorticoid antagonists (MRA), although the evidence for these medications for patients with no significant LV dysfunction remains uncertain. On the basis of extrapolation from studies in myocardial infarction and aortic dissection in patients with concomitant hypertension, beta blockade and RAAS inhibitors are theorized to reduce arterial shear stress, facilitate healing and reduce long-term recurrence. ⁸ In contrast to atherosclerotic disease, there is less evidence for statins in SCAD.

Given this, the selection of medications requires careful consideration in pregnant or breastfeeding individuals and shared decision making. While the safety of aspirin and labetalol in breastfeeding patients is better described, there is a paucity of data for others drugs. ⁸ In our case, decision was made after discussion with the patient to stop breastfeeding to avoid potential adverse drug effects on the infant.

Prognosis and follow-up of SCAD

The long-term prognosis of SCAD is favourable. Registries^13,14 report a 3-year recurrence rate of approximately 2%, and major adverse cardiac events (MACE) rate of 10–15%, both of which are lower than those observed in general acute coronary syndrome cohorts. Follow-up to monitor recovery and cardiac function is warranted for all patients with SCAD. CTCA has emerged as a valuable non-invasive modality for assessing vessel healing following SCAD, ¹⁵ particularly in cases involving proximal segments or large-calibre coronary arteries. Lifestyle modifications, including stress management, are emphasized. Screening for FMD is recommended in every patient. ⁸ Notably, postpartum SCAD carries a higher risk of recurrence with future pregnancies, and hence this group necessitates counselling on the risk of future pregnancies and its potential cardiovascular implications. ¹⁶

Conclusion

Prompt recognition of SCAD as a differential in young female patients, especially in the postpartum population, presenting with typical chest pain should be considered in the setting of raised troponins due to unique investigation and management considerations, which differ substantially from typical cases of ACS.