Canadian Spontaneous Coronary Artery Dissection Cohort Study: 3-Year Outcomes.

Background: Spontaneous coronary artery dissection (SCAD) is an important cause of myocardial infarction (MI) in young to middle-aged women.
Objectives: We aim to define the long-term natural history of SCAD.
Methods: We performed a multicenter, prospective, observational study of patients with nonatherosclerotic SCAD presenting acutely from 22 North American centers. We recorded baseline demographics, in-hospital characteristics, precipitating and predisposing conditions, angiographic features (adjudicated), in-hospital and 3-year major adverse cardiovascular events (MACE). Cox regression multivariable analysis was performed.
Results: We prospectively enrolled 750 consecutive patients with SCAD from June 2014 to June 2018. Mean age was 51.7 ± 10.5 years, 88.5% were women (55.0% postmenopausal); 31.3% presented with ST-segment elevation myocardial infarction, and 68.3% with non-ST-segment elevation myocardial infarction. Precipitating emotional stressor was reported in 50.3%, and physical stressor in 28.9%. Predisposing conditions included fibromuscular dysplasia in 42.9% (56.4% in those with complete screening), peripartum state 4.5%, and genetic disorders 1.6%. Most patients were treated conservatively (84.3%); 14.1% underwent percutaneous coronary intervention (PCI), 0.7% coronary artery bypass graft. At 3.0-year median follow-up, mortality was 0.8%, recurrent MI 9.9% (extension of previous SCAD 3.5%, de novo recurrent SCAD 2.4%, iatrogenic dissection 1.9%), with overall MACE 14.0%. Presence of genetic disorders, peripartum SCAD, and extracoronary fibromuscular dysplasia were independent predictors of 3-year MACE. Patients who underwent PCI at index hospitalization had similar postdischarge MACE compared with no PCI. At 3 years, 80.0% remained on aspirin and 73.5% on beta-blockade.
Conclusions: Long-term mortality and de novo recurrent SCAD was low in our contemporary large SCAD cohort that included low revascularization rate and high use of beta-blockade and aspirin. Genetic disorders, extracoronary fibromuscular dysplasia, and peripartum SCAD were independent predictors of long-term MACE.
Competing Interests: Funding Support and Author Disclosures This study was funded by the Canadian Institutes of Health Research, Abbott Vascular, AstraZeneca, St Jude Medical, and Servier. Dr Saw has received unrestricted research grant support from the Canadian Institutes of Health Research, Heart & Stroke Foundation of Canada, National Institutes of Health, University of British Columbia Division of Cardiology, AstraZeneca, Abbott, St Jude Medical, Boston Scientific, and Servier; has received salary support from Michael Smith Foundation of Health Research; has received speaker honoraria from AstraZeneca, Abbott, Boston Scientific, and Sunovion; has received consultancy and advisory board honoraria from AstraZeneca, St Jude Medical, Abbott, Boston Scientific, Baylis, Gore, and FEops; and has received proctorship honoraria from Abbott, St Jude Medical, and Boston Scientific. Dr So has received unrestricted research grant supports from the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, National Institutes of Health, Eli Lilly, Spartan Biosciences, Roche Diagnostics, and Aggredyne; and has received speaker honoraria and advisory board honoraria from AstraZeneca and Bayer. Dr Gornik has received research support from CVR Global; has received equity and intellectual property from Flexlife Health; and is on the advisory board of FMD Society of America. Dr Lavoie has received speaking honoraria from Boehringer Ingelheim, Pfizer, BMS Sanofi, Novartis, Servier, and Bayer. Dr Ganesh has received research grants from the National Heart, Lung, and Blood Institute (HL139672), NIH, Doris Duke Charitable Foundation, and the Frankel Cardiovascular Center at the University of Michigan; and is on advisory boards of FMD Society of America and SCAD Alliance. Dr Ko is supported by the Jack Tu Chair in Cardiovascular Outcomes, Sunnybrook Hospital, and University of Toronto. Dr Madan is supported by the Heart & Stroke Foundation Polo Chair in Cardiology at the University of Toronto; and has received advisory board honoraria from Medtronic Canada, HLS therapeutics, JAMP Pharma, Novartis Canada, and Pendopharm Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2022. Published by Elsevier Inc.)