Coronary microevaginations characterize culprit plaques and their inflammatory microenvironment in a subtype of acute coronary syndrome with intact fibrous cap: results from the prospective translational OPTICO-ACS study
Authors' conclusion
This study provides novel evidence for a pathophysiological involvement of CME in the development of IFC-ACS and provides first evidence for a distinct pathophysiological pathway for IFC-ICB, driven by CME-derived flow disturbances and inflammatory activation involving the innate immune system.
Study context
- Population
- Patients with acute coronary syndrome (ACS) undergoing optical coherence tomography of the culprit vessel and immunophenotyping of the culprit lesion (OPTICO-ACS)
- Participants
- 557 patients
- Exposure
- Culprit vs non-culprit lesions; IFC-ACS vs RFC-ACS; IFC-ICB vs IFC-ACB
- Ruptured fibrous cap (RFC)n = 258reference
- Intact fibrous cap (IFC)n = 100
- Outcome
- Frequency of CMEs as a feature of plaque vulnerability
Main finding
As reported in the abstract
CME frequency
P < 0.001
- Coronary microevaginations (CMEs) in culprit vs non-culprit lesions
- 25 vs. 4%, P < 0.001
Observational data: associations, not effects.
Further findings
CME frequency, IFC-ICB vs IFC-ACB
P = 0.030
CME as predictor of IFC-ICB (multivariable regression)
| RR (95% CI) | P value | ||
|---|---|---|---|
| CMEStrongest independent predictor | 3.36 (1.67–6.76) | P = 0.001 | |
| 0.10.31310Relative risk (log scale) |
Monocytes in aspirated culprit thrombi
P = 0.017
| Outcome | IFC-ICB | IFC-ACB | P value |
|---|---|---|---|
| Monocyte culprit ratio (culprit blood) | 1.1 ± 0.2 | 0.9 ± 0.2 | P = 0.048 |
Monocytes in aspirated culprit thrombi
- IFC-ACB showed accumulation of CD4+ T cells
Original publication
Coronary microevaginations characterize culprit plaques and their inflammatory microenvironment in a subtype of acute coronary syndrome with intact fibrous cap: results from the prospective translational OPTICO-ACS study. Eur Heart J Cardiovasc Imaging. Published 3 July 2023. doi:10.
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