ABSTRACTS Heart, Lung and Circulation Abstracts S25 2007;16:S1–S201 Conclusions: Heparin increases plasma MPO levels in patients with STEMI presumably due to liberation of MPO from the coronary endothelium. MPO levels did not increase after bilvalirudin and may reflect a decreased anti-inflammatory effect of bilvalirudin. Further studies are required to investigate these findings. doi:10.1016/j.hlc.2007.06.064 60 Plasma Myeloperoxidase Levels are Highest in the Infarct- Related Artery (IRA) in Patients with ST Elevation MI Mark Nallaratnam 1 , Tessa Mocatta 2 , Anthony J. Kettle 2 , David Smyth 1 , Christine Winterbourn 2 , John Elliott 1 , Mark Richards 1 , Dougal McClean 1 1 Cardiology Department, Christchurch Hospital, New Zealand; 2 Free Radical Research Group, Christchurch School of Medicine, Christchurch, New Zealand Background: Rupture of unstable coronary plaque involves activation of inflammatory cells, leading to forma- tion of occlusive thrombus and ST-elevation myocardial infarction (STEMI). Myeloperoxidase (MPO) is a heme- enzyme released by degranulating neutrophils, resulting in production of free radicals and decreased nitric oxide bioavailability. We hypothesise that plasma MPO levels are raised in the coronary circulation at the time of STEMI. Methods: We enrolled 10 patients presenting with STEMIs and undergoing primary PCI within 12 h from the onset of chest pain. Samples were taken from the femoral artery, aorta, IRA (pre- and post-stenting), and the coronary sinus using a special aspiration catheter. Samples were analysed for plasma MPO using an ELISA assay and compared with healthy controls. Results: Of the 10 patients, 8 were male. The mean age was 64 years (range 42–85). The mean time to the lab from onset of chest pain was 300 min (range 75–600). Five of the STEMIs were anterior. All patients were TIMI grade 0 or 1 at initial angiography. As shown in graph 1, plasma MPO levels at time of STEMI were higher than healthy controls ((mean ± S.E.M.), p < 0.01), and were significantly higher in the IRA pre-stenting, compared to other sites in the circulation (p < 0.05). Conclusions: We conclude that plasma MPO levels are highest in the IRA at the site of plaque rupture in patients undergoing STEMI. This suggests that MPO release may be implicated in the pathogenesis of plaque rupture lead- ing to occlusive thrombus formation and ST elevation MI. Further studies are required to validate this finding. doi:10.1016/j.hlc.2007.06.065 61 Natriuretic Peptides Stimulate the Cardiac Sodium Pump via NPR-C Coupled NOS Activation M. William, G.A. Figtree, E.J. Hamilton, A. Garcia, H.H. Rasmussen Department of Cardiology, Royal North Shore Hospital, Australia Natriuretic peptides (NP) and their receptors (NPR) are expressed in the heart but their effects on myocyte function are poorly understood. Because NPRs are coupled to syn- thesis of cGMP, an activator of the sarcolemmal Na + –K + pump we examined if atrial natriuretic peptide (ANP) reg- ulates the pump. We voltage clamped rabbit ventricular myocytes and identified electrogenic Na + –K + pump cur- rent (I p ) as the shift in membrane current induced by 100 mol/L ouabain. ANP stimulated the Na + –K + pump when the intracellular compartment was perfused with pipette solutions containing 10 mmol/L Na + , but had no effect when the pump was at near maximal activation with 80 mmol/L Na + in the pipette solution. Stimulation was abolished by inhibition of cGMP-activated protein kinase with KT-5823, nitric oxide (NO) activated guanylyl cyclase with ODQ, or NO synthase (NOS) with L-NAME. Since synthesis of cGMP by NPR-A and NPR-B is not NO-dependent or ODQ sensitive we exposed myocytes to ANP (4–23), a peptide that selectively binds to the NPR-C “clearance” receptor. ANP (4–23) stimulated the Na + –K + pump. To examine whole cell NO production, we loaded myocytes with the NO-sensitive fluorescent dye diacetylated DAF-2 and examined them by confocal microscopy. ANP (4–23) induced a significant increase in DAF-fluorescence which was abolished by L-NAME. We