BACKGROUND: Despite restoration of blood flow to myocardial cells after ischemia, a large percentage of myocardial cells die after reperfusion. Oxidized phophatidylcholines (OxPC) are a group of molecules that are generated during reperfusion that have been shown to mediate inflammation, platelet aggregation, thrombosis and cell death, however their presence and role in STEMI remains unclear. METHODS: Blood and coronary thrombectomy samples were collected from 13 subjects with STEMI and 4 subjects with non-obstructive CAD prior to, and at completion of angioplasty/angiography respectively. The complete oxidative lipidomic profile at the onset of STEMI and after reperfusion was compared to control prior to and after diagnostic angiography. The oxidative lipidomic profile of each was established and compared using high-performance electrospray mass spectrometry of plasma and coronary thrombectomy samples. RESULTS: Thirteen STEMI subjects age 57 8years and 4 patients age 56 8 years who presented for clinically indicated coronary angiography/angioplasty were enrolled in this study. Seventy-nine distinct OxPC molecules were identified in human plasma. During ischemia, 22 OxPC molecules were significantly different compared to control subjects and following reperfusion, 40 OxPC molecules were significantly different compared to control subjects. Fragmented OxPC molecules in the control vs ischemia population went from 3.8 vs 20.6ng/mg of protein, (p 1⁄4 0.07) and with reperfusion increased to 1.8 vs 34.7ng/mg of protein, (p1⁄40.01) and was 54.8ng/mg of protein in the coronary thrombus sample, increased compared to reperfusion (p1⁄40.3). The increase in fragmented OxPCs in plasma during reperfusion was due to a significant increase in carboxylic acid OxPCs and aldehyde OxPCs. In coronary thrombus, the increase in fragmented OxPCs was due to a significant increase in aldehyde OxPCs only. In all, fragmented OxPCs increased by 5 fold with onset of ischemia, 19 fold with reperfusion. While coronary thrombus had the highest concentration of fragmented OxPCs, it did not correlate with plasma samples indicating that thrombus and reperfusion samples were independent of one another. CONCLUSION: We have shown for the first time that OxPC molecules are present in human STEMI subjects during ischemia, reperfusion and coronary thrombus. Consistent with reperfusion injury, OxPC levels undergo marked increases with reperfusion. Coronary thrombus contains high levels of OxPCs due to coronary plaque disruption and is independent of reperfusion. In light of our findings, attenuation of the biologic effects of OxPCs may be a novel therapeutic approach to reduce the deleterious effects of reperfusion injury.