Patients with spontaneous coronary artery dissection (SCAD) who are discharged on oral anticoagulation (OAC) or dual antiplatelet therapy (DAPT) that combines aspirin plus ticagrelor have a higher risk of major adverse cardiovascular events (MACE), according to an Australian-New Zealand cohort study published March 7 in the European Heart Journal.

Quan M. Dang, MD, PhD, et al., looked at prospective and retrospective data from the Australian-New Zealand SCAD (ANZ-SCAD) Registry, which included patients aged ≥18 years with a diagnosis of acute coronary syndrome secondary to SCAD (nonatherosclerotic and noniatrogenic) from 23 hospital sites in Australia and New Zealand. The primary endpoint was occurrence of MACE, defined as all-cause death, nonfatal myocardial infarction (MI), nonfatal stroke, heart failure or coronary revascularization. SCAD recurrence was a secondary endpoint.

Of 586 patients screened for inclusion, SCAD was confirmed by the core laboratory in 505 patients (150 recruited prospectively at hospital admission for SCAD and 355 retrospectively using medical record data of SCAD diagnosed from 2010 to 2024).

Results showed that over the median 21 months of follow-up, a MACE event occurred in 8.6% of patients, mostly due to nonfatal MI, and SCAD recurred in 3.6% of patients. Nine patients died, five during the index SCAD hospitalization and four during follow-up.

Factors independently associated with MACE were oral anticoagulation on discharge (adjusted hazard ratio [aHR], 3.8), ticagrelor plus aspirin (aHR, 1.8), fibromuscular dysplasia (aHR, 2.2) and a history of stroke (aHR, 3.8). Researchers found that factors associated with a higher risk of SCAD recurrence were fibromuscular dysplasia (aHR, 3.9), ticagrelor plus aspirin (aHR, 2.6) and a history of stroke (aHR, 6.2).

Notably, use of DAPT combining aspirin and ticagrelor – but not the less potent drug clopidogrel – was associated with a higher risk of MACE. The authors write, "These findings add to the hypothesis that SCAD may be primarily caused by intramural bleeding (the outside-in mechanism), with the harmful association of more potent antiplatelet therapy with adverse cardiovascular events requiring further study."

In an accompanying editorial comment, Marysia S. Tweet, MD, FACC, and Jason C. Kovacic, MBBS, PhD, FACC, write that "a broader grasp of genetic predisposition, mechanisms, predictors, and treatment strategies" will aid in "reducing and ultimately preventing adverse outcomes, thereby creating a safer and more certain future for SCAD patients and their families."