Culprit plaque morphology determines inflammatory risk and clinical outcomes in acute coronary syndrome
Authors' conclusion
This study demonstrates a distinct inflammatory response and a lower risk of MACE+ following IFC-ACS.
Study context
- Population
- Consecutive acute coronary syndromes (ACS) patients characterised by culprit lesion phenotype (OPTICO-ACS study programme)62% RFC-ACS, 25% IFC-ACS
- Participants
- 398 patients
- Exposure
- IFC-ACS vs RFC-ACS
- Outcome
- MACE+:
- Cardiac death
- Recurrent ACS
- Hospitalization for unstable angina
- Target vessel revascularization
- Follow-up
- 2 years
Methodological detailstranslational, consecutive patients, Inflammatory profiling at baseline and after 90 days
- Translational
- Consecutive patients
- Inflammatory profiling at baseline and after 90 days
Main finding
As reported in the abstract
MACE+
P = 0.02
Observational data: associations, not effects.
Further findings
Inflammatory proteome expression (368-plex proteomics)
- Lower inflammatory proteome expression with IFC-ACS vs RFC-ACS, including interleukin-6 and proteins associated with the response to interleukin-1β
Plasma interleukin-1β, baseline to 3 months
- Decreased following IFC-ACS
- P < 0.001
- Remained stable following RFC-ACS
- P = 0.25
Interleukin-6 levels in RFC-ACS, by MACE+ (subgroup)
- Decreased in RFC-ACS patients free of MACE+
- P = 0.01
- Persisted high in those with MACE+
Original publication
Culprit plaque morphology determines inflammatory risk and clinical outcomes in acute coronary syndrome. Eur Heart J. Published 29 June 2023. doi:10.
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