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Background:Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of myocardial infarction (MI). Chronic systemic inflammatory diseases (CIDs) are common amongst SCAD patients. Whether they contribute to the cause of SCAD or were simply bystanders remain unknown.Methods:We compared the baseline demographics, presentation characteristics and cardiovascular outcomes between patients with and without CIDs in the Canadian SCAD Study. CIDs included systemic inflammatory disorders as well as autoimmune diseases. Patients completed questionnaires along with detailed history of CIDs. Blood biomarkers for inflammation (e.g. C-reactive protein [CRP], erythrocyte sedimentation rate [ESR], white blood cell counts) were obtained at the discretion of the treating physicians. Major adverse cardiovascular events (MACE) were defined as the composite of all-cause mortality, stroke or transient ischemic attack, MI, hospitalization for heart failure and unplanned revascularization.Results:Of 1225 patients with SCAD, 96 (7.8%) had a history of CIDs. Patients with CIDs were of similar age (52.5 vs.51.8 yrs, p=0.51), but were more likely to be women (96.9% vs 89.2%, p=0.02). There were no significant differences in baseline demographics, ECG, or angiographic findings between CID or non-CID cohorts. Among patients with biomarkers performed, there was no difference in CRP (9.6 vs. 12.9mg/L, p=0.54), ESR (10 vs. 13.9, p=0.42), white cell count (12.6 vs. 11.3, p=0.80), neutrophil count (5.1 vs. 5.6, p=0.70), or lymphocyte count (1.7 vs. 2.0, p=0.41), in CID versus non-CID groups, respectively. The proportion of patients treated conservatively or with revascularization were not different between groups. At median follow up of 3.0yrs (IQR 2.0-3.8), in hospital and overall MACE were not significantly different between CID and non-CID patients (8.4% vs. 6.1%, p=0.38) and (23% vs. 16.8%, p=0.12), respectively.Conclusion:In our large SCAD cohort, there were no significant differences in presentation or outcomes in SCAD patients with or without CID. Importantly, there was no difference in levels of inflammatory biomarkers, supporting the hypothesis that active inflammation was not an important contributor of SCAD.