Spontaneous coronary artery dissection (SCAD) is an infrequent but increasingly recognised cause of acute coronary syndrome (ACS) that predominantly affects relatively young women aged 45–52 years and may even occur in association with pregnancy, where it is the most common cause of a myocardial infarction.1 2 In contrast to ACS due to atherosclerotic disease, SCAD sufferers have few traditional risk factors apart from hypertension,3 and the pathophysiology involves impaired coronary flow, not due to plaque rupture, plaque erosion or thrombus formation associated with a calcific nodule, as is the case for atherosclerotic disease,4 but to the spontaneous formation of an intramural haematoma (IMH) that causes dissection of the vessel wall medial layer. The IHM is likely due to vasa vasorum rupture with or without an intimal tear. As the IMH expands, it compresses the ipsilateral coronary artery wall against the contralateral wall, thereby occluding the coronary lumen and results in ischaemia or infarction of the subtended myocardium. While much has been learnt about the clinical presentation and sequelae of SCAD from studies of retrospective and ambispective registries, meta-analyses and prospective cohorts, major gaps in our understanding of disease mechanisms, management and outcomes persist, with little prospective data from large cohorts and lack of data from randomised control studies.

Garcia-Guimaraes and colleagues5 report on the treatment and clinical outcomes of SCAD determined in a cohort of 389 patients assembled from The Spanish Registry on SCAD involving subjects from 34 hospitals. Although the study uses a non-randomised observational design, particular strengths are its prospective nature, the reasonably large size of the cohort assembled, its careful documentation of SCAD diagnosis by a central angiography reading group and …