Background Plaque erosion causes 30% of STEMI cases, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared to rupture in autopsy studies.

Objectives We hypothesised that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo.

Methods 40 STEMI patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct-related artery and a peripheral artery were analysed for expression of 102 cytokines using arrays: results were confirmed with ELISA. Thrombectomy samples were analysed for differential mRNA expression using RT-PCR.

Results 23 lesions were classified as RFC (58%), 15 as IFC (38%) and 2 were undefined (4%). 12% (12/102) of cytokines were differentially expressed in both coronary and peripheral plasma. CXCL11 was preferentially expressed in RFC (SAM adjusted p<0.001; ELISA IFC 10.2 vs RFC 10.8 log₂ pg/ml; p=0.042). IFC was associated with preferential expression of Epidermal Growth Factor (SAM adjusted p<0.001; ELISA IFC 7.42 vs RFC 6.63 log₂ pg/ml, p=0.036) and thrombospondin-1 (TSP-1) (SAM adjusted p=0.03; ELISA IFC 10.4 vs RFC 8.65 log₂ ng/ml, p=0.0041). Thrombectomy mRNA showed elevated CXCL11 in RFC (p=0.0007) EGF expression in IFC (p=0.0264) and, but no differences in expression of TSP-1.

Conclusions These results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated TSP-1 and EGF may play an aetiological role in erosion.