Spontaneous coronary artery dissection (SCAD) is increasingly recognised as an important cause of myocardial infarction (MI), especially in younger women. It is defined as a non-traumatic and non-iatrogenic separation of the coronary artery wall, which creates a false lumen that may or may not be in continuity with the true lumen. Although conventionally SCAD may be atherosclerotic or non-atherosclerotic in origin, contemporary series have focused on the non-atherosclerotic variant, since the pathophysiology, management, and outcomes are distinct from atherosclerotic coronary artery disease (which causes atherosclerotic SCAD). As such, contemporary usage of the term ‘SCAD’ is typically synonymous with non-atherosclerotic SCAD.
SCAD may be a result of an intimal-medial tear that can manifest as multiple radiolucent lumen on angiography, or it may result from spontaneous haemorrhage into the arterial wall that can be angiographically subtle. In fact, <30 % of SCAD have angiographic type 1 appearance (pathognomonic contrast stain of arterial wall with multiple radiolucent lumen) in the author’s large contemporary series.1 Thus, intracoronary imaging with optical coherence tomography (OCT) or intravascular ultrasound (IVUS) play important roles in the diagnosis of non-type 1 angiographic variant of SCAD. These type 2 and 3 variants have angiographic appearance of diffuse smooth stenosis or mimic atherosclerosis, respectively.2 The diagnosis of SCAD on OCT or IVUS requires presence of intramural haematoma and/or separation of the intimomedial membrane creating double lumen.3 In the author’s largest reported intracoronary imaging SCAD series of 22 patients, the lengths of these dissections on angiography are long, especially the type 2 forms (mean length ~58 mm).3 These angiographic variants were previously poorly recognised, resulting in missed and misdiagnosis of SCAD. Thus, there is a great emphasis on angiographers to become familiar with these non-pathognomonic angiographic SCAD variants to improve diagnosis.
The etiology of SCAD is not fully understood, but recent large series suggest that the majority of patients have potential underlying predisposing arteriopathy, such as fibromuscular dysplasia (FMD), connective tissue disorder and systemic inflammatory conditions, or the condition may be pregnancy-related.1 Less than 20 % may be idiopathic, where no predisposing arteriopathy is identified after vascular screening or detailed questionnaires for these disorders. The most dominant association with SCAD is FMD. Since the author’s discovery of the strong association and publication of the first case series of concomitant SCAD and FMD in 2012,4 the author and others subsequently reported that non-coronary FMD was present in up to 86 % of patients with SCAD.1,5,6 On the other hand, pregnancy-related SCAD (previously thought to be a major cause of SCAD) has a much lower reported frequency (<5 %) as a predisposing cause in contemporary series.7 Additional precipitating stressors, such as intense emotional stress, physical activities, hormone therapy, sympathomimetic drugs and intense Valsalva-like activities (e.g. vaginal delivery, coughing, retching, vomiting, bowel movement) have been reported to precipitate SCAD,1 especially in patients with underlying predisposing arteriopathy.