Discussion

SCAD is found in up to 10% of women younger than 50 years of age with acute coronary syndrome and could be present in up to 1.1% of patients undergoing angiography.1 Contrary to the earlier belief that SCAD mostly affected young women (younger than 50 years of age), contemporary studies reveal that the average age of diagnosis is the mid-40s to mid-50s, with Saw et al2 observing one of the largest cohort of patients with non-atherosclerotic SCAD containing 58% women aged 50 years or above. It has been reported that almost 80% of patients diagnosed with SCAD are women, with up to 25% diagnosed during the peripartum period,3 usually presenting within the first 2 weeks after delivery.4

In up to 56.5% of patients, possible predisposing conditions associated with the occurrence of SCAD are present, including FMD (which our patient had), pregnancy, postpartum state, multiparity, hormonal therapy, connective tissue disorders and systemic inflammatory diseases.2 SCAD can be precipitated by vigorous exercise, Valsalva manoeuver, parturition or recreational drugs with hypersympathetic response or extreme emotional stress, none of which were reported by our patient.2 A close association between FMD and SCAD has been described.3 ,5–7 As many as one-third of young women with non-ST elevation myocardial infarction and positive biomarkers may have FMD/SCAD.5 FMD is an idiopathic, segmental, non-inflammatory angiopathy without atherosclerosis that occurs mainly in young to middle-aged females. It can affect renal, carotid, vertebral and iliac as well as coronary arteries, leading to vascular stenosis and tissue ischaemia.5 Although not all patients with SCAD have FMD, it is important to subsequently evaluate as it can affect vital vascular territories in the body, as described above.5

There are three angiographic types of dissection without differences in prognosis: type 1, with multiple radiolucent lumens and arterial wall staining from contrast dye; type 2 (most common), with diffuse stenosis; and type 3, with resemblance to atherosclerotic lesions.8 Over time, the survival of patients with SCAD has dramatically improved from 50% to approximately 95%, likely owing to better diagnostic and treatment options, since coronary angiography, PCI and coronary artery bypass grafting (CABG) were not widely available before 1990.6 ,9

There is no consensus on treatment guidelines for SCAD. Conservative medical management is favoured in most cases, particularly if there is no evidence of ongoing cardiac ischaemia or haemodynamic instability. In a study published in 2012 by Alfonso et al, 45 patients with SCAD were included and followed for 6 years. Twenty-nine of the 45 patients (64%) were managed conservatively while 16 underwent revascularisation. The study concluded that conservative management of SCAD had excellent outcomes with favourable prognosis.10 Up to 10% of patients who are managed conservatively may, eventually, require coronary intervention, however, a 5-year revascularisation rate and recurrence of SCAD are not significantly different when compared with patients undergoing early intervention.11 Clinically, significant progression of dissection may occur in some medically managed patients, usually during the first week after the initial event.11 However, cases treated with stent placement can also pose risk of extension of dissection as well as displacement of intramural haematoma leading to worsening myocardial infarction. PCI failure, including total occlusion of the target vessel, may be as high as 53%, thus possibly making early conservative management more favourable.11

Medical management of SCAD is similar to the treatment of acute coronary syndrome, including the use of antiplatelet drugs, intravenous heparin and β-blockers. The medical regimen for conservative management is largely observational as there are no randomised controlled trials comparing different regimens.2 ,12 Anticoagulation with heparin, ACE inhibitors, β-blockers and dual antiplatelet therapy for up to 1 year is usually undertaken.8 ,12 Clopidogrel can be discontinued if healing of dissection is confirmed.2 Heparin can be discontinued if the cause of acute coronary syndrome is confirmed to be SCAD.13

The role of new P2Y12 antagonists is uncertain and IIb/IIIa antagonists should generally be avoided due to a potential for extending the dissection.12 ,13 Calcium channel blockers may be used in cases of coronary spasm,12 however, their use in SCAD has not been studied.2 The role of statins in non-atherosclerotic SCAD is not clear. Some experts recommend that statins should only be used if there is concomitant dyslipidaemia due to a small potential increase in risk of SCAD recurrence with the use of statins, however, this association is still under investigation.2 Thrombolytics are traditionally avoided due to the potential risk of extension of dissection and its accompanying haematoma, though one study did not find worsening outcomes with their use.14

Advocates of early coronary intervention argue that patient survival is improved with an aggressive revascularisation strategy compared with conservative medical management. Shamloo et al concluded that early intervention with either CABG or PCI following the diagnosis of SCAD leads to better outcomes, longer symptom-free intervals and, consequently, less need for future intervention. Their study sample comprised of 440 patients who were treated with early intervention (PCI or CABG) and followed for a period of up to 400 days.9 They reported that 21.2% of the patients originally treated conservatively ultimately required CABG or PCI compared with 2.5% for whom an early revascularisation approach was pursued (p=0.001).9 Of note, the study characteristics were different from that conducted by Alfonso et al,10 with more female study participants (70% vs 58%), greater number of pregnancy-related cases (26% vs 4%), higher number of critically ill patients with at least two-vessel dissection (16.1% vs 11%), higher incidence of ST elevation myocardial infarction (64.9% vs 40%) and left main dissection (6.1% vs 2%).9 It is noteworthy that the Shamloo et al study covered a period from 1931 to 2008, a time when coronary diagnostic and treatment modalities, both invasive and medical therapy, were undergoing tremendous transformation. This broad timeframe may influence the findings of Shamloo et al,9 including the fact that 21.5% of their cases were diagnosed during autopsy examination. To the contrary, other contemporary studies, including Alfonso et al,10 included SCAD cases, and were all diagnosed premortem by coronary angiography or by other newer tomographic imaging techniques (optical coherence tomography, multislice CT, intravascular ultrasound, etc).

In light of current evidence, the management approach should be individualised for each case, based on patient stability, location of dissection (coronary segment involved) and TIMI flow. Many researchers use a Bypass Angioplasty Revascularisation Investigation (BARI) classification to describe the location of dissection. Lettieri et al15 found that distal location of the dissection (based on BARI classification) and TIMI flow 2–3 are more likely to be managed conservatively compared with proximal or mid-vessel location and TIMI flow 0–1, respectively. Furthermore, they also found that the inpatient cardiovascular complication rate was higher for surgical treatment (16.1% vs 3.8%; p 0.028) but long-term outcome was similar for medical and surgical approaches over a mean follow-up of 31 months. Therefore, patients with TIMI flow 0–1 or clinical instability may benefit from early coronary revascularisation and inpatient monitoring for 5–7 days.7 ,11 PCI and stenting may be preferable in proximal vessel dissection with significant reduction in coronary perfusion whereas conservative management can be chosen in mid-to-distal dissection involving only a single vessel.3 ,14 The more distal lesions, usually, do not require any intervention.16 Watchful waiting also seems prudent in stable patients, to avoid the risk of PCI guide wire being passed into false lumen thereby extending dissection.17

The majority of medically managed cases tend to result in natural healing of dissection, which should be reassessed with repeat angiogram in 4–6 weeks with the understanding that a minority of these patients may still end up requiring coronary revascularisation. Late angiographic follow-up can be carried out to assess for progression of dissection. Alfonso et al10 conducted late follow-up angiographies with a median of 262 days (range 175–284 days). They found that 2 of the 10 patient managed conservatively who underwent late angiography showed progression of the dissection requiring late revascularisation.

Delayed PCI may allow better visualisation of vessel lumen and thus more accurate stent placement to completely exclude the dissection.3 ,17 CABG is usually reserved for patients with failed PCI or cases involving left main or multiple vessel dissection, though stenting of spontaneous left main dissection may be appropriate in emergent situations.3 ,6 ,14 Further screening for FMD should be considered in all cases of SCAD, especially in women. This usually includes abdominal angiography to evaluate renal and iliac arteries, and CT angiogram of the head to investigate carotid vessels.5