Abstract 16872: Increased Production of Oxidized Phosphatidylcholine Molecules in Patients Presenting With ST Elevation Myocardial Infarction (STEMI)
Introduction: Despite restoration of blood flow to myocardium after ischemia, a large percentage of myocardial cells die after reperfusion. This phenomenon is termed ischemia/reperfusion injury (I/R). Oxidized phosphatidylcholines (OxPC) are generated in the presence of reactive oxygen species, which are abundant during I/R. We aimed to determine the change in OxPC in patients presenting with STEMI who undergo primary Percutaneous Coronary Intervention (PCI).
Methods: Blood samples were collected from subjects with STEMI (n=27) and subjects with non-obstructive CAD (n=20) prior to, and at completion of PCI/angiography respectively. The complete oxidative lipidomic profile at the onset of STEMI and after PCI was compared to control prior to and after diagnostic angiography. The oxidative lipidomic profile was established and compared using high-performance electrospray mass spectrometry.
Results: Seventy nine distinct OxPCs were identified in human plasma which included fragmented OxPCs, terminal furans, isoprostanes and long-chain products. There were 17 compounds that showed a significant increase in the STEMI population when compared to control. The largest changes seen overall were in the fragmented OxPCs. Fragmented OxPCs in control vs pre PCI STEMI had a significant rise from 8.9 vs 21.8 ng/ml of plasma, (p = 0.0001) and STEMI post PCI increased to 8.9 vs 29.7 ng/ml of plasma, (p = 7.1x10-5). When organizing molecules by functional group, fragmented carboxylic acid OxPCs were the most abundant in plasma with pre vs post PCI levels increasing from 12.8 to 22.2 ng/ml of plasma (p= 0.03).
Conclusion: We have shown for the first time that OxPC molecules are present in patients with STEMI and are increased when compared to control patients. There is also a significant increase in OxPC levels after PCI in the STEMI population. These changes represent increases in OxPC during ischemia and a further increase after reperfusion injury. Given the potent biological activity of OxPCs, the attenuation of their activity may be a novel therapeutic approach to reduce the deleterious effects of I/R.
Author Disclosures: R. Searle: None. D. Allen: None. D. Hasanally: None. R. Chaudhary: None. A. Ravandi: None.
- © 2015 by American Heart Association, Inc.