Cohort study
The Australian-New Zealand spontaneous coronary artery dissection cohort study: predictors of major adverse cardiovascular events and recurrence
- Multicentre cohort study
- 23 Australian and New Zealand sites
- prospective and retrospective
Authors' conclusion
The findings support the hypothesis that SCAD is primarily caused by intramural bleeding, with a harmful association of more potent antiplatelet therapy and anticoagulation with adverse cardiovascular outcomes.
Study context
- Population
- Adults (≥18 years) with acute coronary syndrome (ACS) due to spontaneous coronary artery dissection (SCAD) confirmed on core laboratory adjudication505 with core-lab-confirmed SCAD
- Participants
- 586 adults
- Outcome
- MACE
- Follow-up
- Median 21 months
Main finding
As reported in the abstract
MACE (predictors)
Adjusted hazard ratio (95% CI)P value
Oral anticoagulation on discharge
3.8(1.6–9.3)
P = 0.003Ticagrelor combined with aspirin
1.8(1.04–3.2)
P = 0.037Fibromuscular dysplasia
2.2(1.05–4.5)
P = 0.037History of stroke
3.8(1.2–12.2)
P = 0.03- MACE
- 8.6%
Observational data: associations, not effects.
Further findings
Predictors of SCAD recurrence · median 21 months
| Comparison | aHR (95% CI) | P value | |
|---|---|---|---|
| Fibromuscular dysplasia | 3.9 (1.5–26.5) | P = 0.01 | |
| Ticagrelor + aspirin | 2.6 (2.1–5.3) | P = 0.01 | |
| History of stroke | 6.2 (1.8–9.5) | P = 0.01 | |
| 0.050.21520Adjusted hazard ratio (log scale) |
- Predictors of SCAD recurrence — SCAD recurrence incidence
- 3.6%
Original publication
The Australian-New Zealand spontaneous coronary artery dissection cohort study: predictors of major adverse cardiovascular events and recurrence. Eur Heart J. Published 7 March 2025. doi:10.1093/eurheartj/ehaf097
Summarised from the published abstract; every number is checked against it