During the 7-day acute admission, she remained asymptomatic from a cardiac perspective with normal telemetry. The obstetric team reviewed at least daily, both as a routine and for any maternal pregnancy concerns. Investigations for fetal wellbeing included a Kleihauer test and fetal growth ultrasound, both of which were normal. The estimated foetal weight (EFW) was on the 40^th centile, with a normal amniotic fluid index (AFI) and doppler studies. A multidisciplinary team (MDT) meeting was undertaken to discuss the antenatal, intrapartum and postpartum management for this patient. The consensus management was for elective birth at 37 weeks gestation, with either a vaginal birth with a modified second stage or caesarean section considered appropriate, with early regional anaesthesia in either event. It was considered that for the intervening weeks, aspirin alone would be suitable anticoagulation, and so the enoxaparin ceased. Given the increased concern regarding SCAD in the post-partum period, a planned 2 week elective admission postpartum in conjunction with telemetry monitoring for the first 48 hours was recommended.

The patient was discharged at 34 weeks gestation on 150mg aspirin daily. She was required to stay within 30 minutes of the hospital and present if she had any concerns. A further MDT with patient involvement was undertaken to plan the mode of delivery. After counselling that the modified second stage would involve an early epidural, telemetry, no active pushing and a forceps delivery, the patient decided on an elective caesarean section, for which she was consented and planned for at 37+1 weeks.

An uncomplicated caesarean section was conducted at 37+1 weeks, resulting in an uncomplicated delivery of a 2.8kg baby with APGARS of 7 and 7 under combined spinal-epidural (CSE) anaesthetic. She was commenced on 47.5mg of extended-release metoprolol and 150mg of aspirin once daily and remained well for the 2-week admission post-delivery. On discharge, she completed the metoprolol for a further 4 weeks and the aspirin for a total 12 weeks. Due to the high risk of iatrogenic dissection with an angiogram, a CTCA and CTA of carotid, vertebral, subclavian, renal and iliac arteries were conducted to exclude aneurysm and resolution of the SCAD. This showed normal vessels and SCAD resolution at 3 months post-partum.

Spontaneous coronary artery dissection (SCAD) is an ischaemic event that occurs with an expanding intramural haematoma between the tunica media and intima of an artery resulting in separation of the intima-media complex. This creates a false lumen which in turn compresses the true lumen of the vessel resulting in ischemia and therefore an acute coronary syndrome (ACS)³. Amongst the general population, there is great variation in type of primary presenting ACS being STEMI, NSTEMI and unstable angina^4,5,6. The vast majority of SCAD presentations (87-95%) occur in women at a mean age of 41 years old, slightly lower than the 45 year mean for SCAD in males, yet most of these women do not have typical cardiovascular risk factors^7,8. Patients with SCAD are grouped into three subsets; coronary artherosclerotic disease (CAD), females in the peripartum period and idiopathic SCAD⁹.

SCAD is responsible for 25% of myocardial infarctions (MI) antenatally and 50% of MI’s in the peri- and postpartum periods¹⁰. Patients with pregnancy associated spontaneous coronary artery dissection (p-SCAD) generally present with a more severe clinical manifestations when compared with SCAD not associated with pregnancy. SCAD antepartum is very rare but is associated with high maternal and fetal morbidity^11,12. As per the Mayo SCAD Registry, SCAD in pregnancy is more likely to occur postpartum, most likely to be associated with STEMI, and significantly correlated to multiparity, infertility treatment and pre-ecclampsia^11,13. SCAD can be associated with connective tissue disorders, vasculitis polycystic kidney disease and use of particular drugs. Its pathophysiology in pregnancy is multifactorial, likely due to a combination of sexual hormones and an increase in shearing force from a hyperdynamic circulation.

For those presenting with typical or atypical symptoms consistent with an ACS, investigation typically starts with standard pathology such as serial troponin levels in addition to serial electrocardiography (ECG) and echocardiogram. SCAD must be considered among the diagnostic differentials. This is followed by the diagnostic modality of invasive coronary angiography for which there is usually significant concern surrounding fetal radiation. It is estimated that procedural exposure contributes to approximately 1 in 8000 of childhood cancer cases¹⁴. Unlike classic atherogenic myocardial infarction, percutaneous intervention (PCI) is not routinely recommended in SCAD. This is mainly due to the unpredictable nature of PCI and the high risk of haematoma propagation along the vessel (occurs in approximately one third of cases)¹⁵. Other modalities such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT) are fast becoming beneficial in vessel morphology, however, are typically reserved for cases where the diagnosis is unclear or where intervention of the lesion may be required¹⁵.

The vast majority of antenatal SCAD cases occur in the post-partum period, therefore data on delivery planning in the context of antenatal SCAD is very limited. A retrospective cohort study of 54 women showed that only 4 were diagnosed with SCAD antenatally; only 1 of these women chose to undergo elective termination, while the other 3 women had emergency caesarean sections, though the indication for caesarean delivery was not reported¹⁶. Another large case analysis compiling 120 cases of SCAD in pregnancy in contemporary literature showed that only 17.5% presented in the 3^rd trimester, and 6% in the 2nd trimester¹⁶.

Currently, the preferred treatment for antenatal SCAD is conservative, however, intervention may be required in the circumstances such as ongoing or recurrent clinical or ECG-demonstrated ischaemia, cardiogenic shock requiring support, sustained VT or VF, or a left main coronary artery dissection¹⁷. There is evidence that suggests any surgical intervention required to stabilise the female patient with a SCAD in pregnancy, such as PCI and CABG, are best performed postnatally, and as such if surgical intervention is required then emergent pre-procedure birth of the baby should be strongly considered¹⁶. Havakuk et.al. found that of the 4 women who underwent CABG antenatally, 50% experienced intrauterine fetal loss and the other 50% experienced significant fetal complications. While there is limited published research on the specifics of delivery planning and intrapartum management of SCAD in pregnancy, it is a known ischaemic cardiac event, and therefore principles applied to other ischaemic cardiac conditions in pregnancy can be extrapolated to SCAD in pregnancy. In order to achieve rate control, ß1-adrenergic blockers are the preferred treatment option, in addition to being widely used in other pregnancy conditions such as hypertension, arrhythmias, mitral stenosis and Marfan Syndrome¹⁰. It is, however, prudent to consider fetal effects such as bradycardia, hypoglycaemia and apnoea of the newborn.

It is proposed that the hormonal milieu associated with the pregnant and post-partum state are partially responsible for p-SCAD. In particular, high levels of progesterone may contribute to changes in protein composition, degradation of reticulin, collagen and elastic fibres and hypertrophy of smooth muscle of the vessel wall¹⁸. This, in combination with the other cardiac haemodynamic changes of pregnancy, such as increased cardiac output/intravascular volume and decreased peripheral vascular resistance (which are estrogen mediated), can ultimately increase the risk of rupture of a weakened vessel wall¹⁶.

It is unclear if the female sex hormones used for contraception increase the risk of SCAD in a similar way to pregnancy, as they are likely to only be only part of the mechanism. However, there are at least 7 published cases of women who experienced SCAD in the context of oral contraceptive pill use, suggesting a possible association^18,19,20. As well as this, other hyperestrogenic states have been associated with SCAD, such as hepatic cirrhosis²¹. Havakuk et al. showed that when compared to SCAD, women with p-SCAD had a higher risk of persistence and often progression of SCAD. This was demonstrated in one third of their population¹⁶. This ongoing fragility of the vessel wall steers the authors to advocate for an individualised discussion which takes into consideration the possible risk of SCAD recurrence with contraceptive use and that associated with repeat pregnancy. Further research into this area would be helpful for this patient cohort.

This case highlights the diagnostic and management dilemmas of SCAD in pregnancy. It can be a difficult clinical scenario to balance patient autonomy and safety, particularly on the background of a small evidence base with limited recommendations for optimal investigations and delivery modality. This case contributes valuable demographic data to the rare condition of SCAD intrapartum. Further research into this unique pregnancy-associated cardiac condition would provide a valuable contribution to the evidence base for clinicians faced with this scenario in future.