Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction

Background. In acute myocardial infarction (AMI) treated with percutaneous coronary intervention (PCI), myocardial injury results from complex processes during both ischemia and reperfusion. Release of reactive oxygen species (ROS) may contribute to the accumulated myocardial damage. Aims: To examine by frequent sampling of peripheral blood oxidative stress and early inflammation inpatients undergoing primary PCI for AMI. Secondly, to assess whether a correlation exists between these parameters and the extent of myocardial damage. Methods: Sixteen patients undergoing primary PCI within 6 h of AMI onset were included. Peripheral blood was sampled at start of procedure (to) and repeatedly over 24 h following reperfusion. Main plasma analyses were: 8-iso-PGF(2 alpha) (oxidative stress), 15-keto-dihydro-PGF(2 alpha) (cyclooxygenase-mediated inflammation); and troponin-T (myocardial injury). Additional analyses included: total antioxidant status (TAS); vitamins; hsCRP and lipids. Results: 8-Iso-PGF(2 alpha) increased following restoration of blood flow, returned to to values after 3 h and was reduced below to the following day. TAS decreased significantly from to to the next day. There was no significant correlation between 8-iso-PGF(2 alpha) and troponin T values. 15-Keto-dihydro-PGF(2 alpha) was elevated during the first hour. There was a major rise in hsCRP after 24 h. Conclusion: Following reperfusion by primary PCI in AMI, oxidative stress and an inflammatory response are induced immediately. A rise in 8-iso-PGF(2 alpha) during ischemia indicate that ROS generation may also take place during severely reduced coronary blood flow and hypoxia. No direct relationship between 8-iso-PGF(2 alpha) or 15-keto-dihydro-PGF(2 alpha) and troponin T was evident. The present study adds to the increasingly complex pathophysiological roles of ROS acting both as signal molecules and as mediators of tissue injury.