Abstract 14288: Differential Cytokine Expression in Plaque Erosion and Rupture in ST Segment Elevation Myocardial Infarction
Introduction: ST Segment Elevation Myocardial Infarction (STEMI) is largely due to plaque rupture (60-70% of cases) and plaque erosion (30-40%). Coronary inflammation plays a pivotal role in rupture, but the pathophysiology of erosion is unknown. Autopsy studies have shown that inflammatory infiltrates are much less abundant in erosion compared to rupture. We explored the hypothesis that differences in intracoronary cytokines can be demonstrated in vivo in the early phase of STEMI in patients undergoing primary percutaneous coronary intervention (PPCI).
Methods: We recruited 40 STEMI patients undergoing PPCI with in less than 6 hours of chest pain in a single-centre observational study. Blood samples were taken from the infarct-related artery using thrombus aspiration. Culprit plaques were imaged using optical coherence tomography (OCT) before PCI and classified by two blinded observers. The expression profiles of 102 cytokines were measured using an array, and comparisons of the two pathological groups performed using the ‘significance analysis of microarray’ (SAM) methodology. Significant findings were validated with enzyme-linked immunosorbent assays (ELISA) and Wilcoxon rank-sum tests.
Results: Mean age of patients was 63.7 years and 33% were female. Twenty-three lesions were classified as plaque rupture (58%), fifteen as plaque erosion (38%) and two were undefined (4%). Erosion was associated with preferential expression of Thrombospondin-1 (TSP-1) (SAM adjusted P = 0.03; ELISA erosion median 10.4 versus rupture median 8.65 log2 ng/ml: P = 0.004) and Epidermal Growth Factor (EGF) (SAM adjusted P < 0.001; ELISA erosion median 7.42 versus rupture median 6.63 log2 pg/ml: P = 0.036). Interferon-inducible T-cell alpha chemo-attractant was preferentially expressed in plaque rupture (SAM adjusted P <0.001: ELISA rupture median 10.8 versus erosion median 10.2 log2 pg/ml: P = 0.042).
Conclusions: These results provide novel evidence for differential expression of cytokines in plaque rupture and erosion in STEMI. TSP-1 has been linked to endothelial cell apoptosis, whilst EGF may be a marker of a more fibrous plaque phenotype. Further work is needed to understand if these molecules play an etiological role in erosion.
- Myocardial infarction, STEMI
- Plaque rupture
- Percutaneous coronary intervention (PCI)
Author Disclosures: S.S. Chandran: None. J. Watkins: None. A. Abdul-Aziz: None. P. Calvert: None. S. Rushworth: None. K. Bowles: None. M. Flather: None. A. Ryding: None.
- © 2016 by American Heart Association, Inc.