The following is the introductory section of an article summarising the current literature on SCAD...
Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndromes. The increasing use of early angiography in the primary percutaneous coronary intervention (PPCI) era has led to earlier identification of patients with SCAD and may encourage an increased use of percutaneous revascularisation strategies in this population. However, the pathophysiology of SCAD is distinct from the usually stenotic atherosclerotic plaque rupture events responsible for most ST-elevation and non ST-elevation myocardial infarctions but our approach to managing these patients utilises largely the same medical and revascularisation therapies used in conventional acute coronary syndromes. This review examines the literature on SCAD and contemporary management issues.
Epidemiology and pathophysiology
SCAD is characterised by the presence of blood or thrombus in a false lumen usually occurring in the outer third of the vessel media. This false lumen extends for a variable distance down the coronary artery and may be circumferential or take a spiral passage as it extends down and around the coronary lumen within the vessel wall. Compression of the coronary lumen by the false lumen or by a dissection flap may obstruct or restrict flow within the true lumen causing myocardial ischaemia or infarction (Figure 1). SCAD is reported to occur most commonly in the left anterior descending coronary artery. The population incidence is difficult to quantify but is reported from angiographic series as between 0.1 and 1.1%. Some cases are not diagnosed until post mortum and angiographic appearances may be atypical and unrecognised unless there is a high index of clinical suspicion or use of intracoronary imaging (with intravascular ultrasound (IVUS) or optical coherence tomography (OCT).
The initial pathophysiological events in SCAD are debated. Although the most obvious potential source is a bleed into the vessel wall from the lumen itself, it seems increasingly likely that the process is initiated in the media and adventitia Haematoma within the wall of the vessel alters the tolerance of the endothelium to shear stress resulting in an intimal tear. This process is akin to the process of intramural haematoma which can precede aortic dissection. Patients can present with coronary haematoma alone with no evidence of an intimal flap. In these cases the haematoma causes luminal compression which may then limit antegrade flow.
SCAD affects a younger and predominantly female population, particularly in the peri and post partum period (although the commonest cause of acute coronary syndromes in pregnancy remains conventional atherosclerotic disease). There may be an association with situations of increased sheer stress such as following exercise or sneezing, in association with cocaine abuse or in high output states such as pregnancy although there is no clear association with hypertension. SCAD has been described in association with heritable connective tissue disorders such as Marfan’s syndrome and Eherlos-Danlos. Inflammatory conditions including autoimmune connective tissue disorders and vasculitides may be associated and the presence of an eosinophilic infiltrate has been described in some idiopathic and peri-partum cases (although this is not a universal finding). Cystic medial necrosis has been reported in some post mortum cases of SCAD. It may be that either an inflammatory, a pregnancy related or a hereditary molecular abnormality contributes to a weakening of the integrity of the vessel wall and/or vasa vasorum increasing the risk of SCAD.