ABSTRACTS Heart, Lung and Circulation Abstracts S171 2007;16:S1–S201 420 Does a High-Fat Meal Acutely Alter Arterial Function and Wave Travel? J. Swampillai * , A. Williams, C.J. Jones, A.G. Fraser Wales Heart Research Institute, University Hospital of Wales, Cardiff, UK Background: High-fat meals and postprandial lipaemia are associated with atherosclerosis and coronary heart dis- ease. Arterial stiffness measurements are conventionally made following an overnight fast, but there are no pub- lished reports on acute effects of fat loading on arterial stiffness. We aimed to determine whether acute changes in arterial stiffness and wave intensity (WI) could be detected after fatty meal consumption. Methods: Thirteen subjects were studied using a high- resolution ultrasound system (Aloka SSD-5500, Tokyo) to measure diameter and flow in the common carotid artery. Blood pressure was measured in the right arm using sphygmomanometry. We derived instantaneous changes in WI (the product of pressure and velocity changes with respect to time), and in local arterial stiffness (beta and epsilon). After measuring fasting blood glucose, lipids and baseline WI, subjects consumed a standard fatty meal. Glucose, lipids and wave intensity scans were repeated 4 h later. Results: Glucose, total cholesterol and HDL cholesterol levels did not change 4 h after fatty meal ingestion. Triglycerides increased by 102.8 ± 67.5%, p < 0.01; and LDL cholesterol decreased by 12.6 ± 9.5%, p < 0.01. At baseline, beta correlated with total cholesterol (r = 0.59) and LDL cholesterol levels (r = 0.61), both p < 0.05. No changes in haemodynamic, wave intensity or arterial stiffness param- eters were observed. Conclusion: We found the expected changes in lipid pro- file after fatty meal ingestion, indicating an adequate fat load. This technique has not detected acute changes in arterial stiffness parameters or WI, suggesting that con- trary to current practice WI measurements do not need to be taken after an overnight fast. doi:10.1016/j.hlc.2007.06.425 421 Matrix Metalloproteinases are Independent Predictors of In-Stent Restenosis G. Tarr * , G.T. Jones, J. Chu, G. Wilkins, M.J.A. Williams Otago Medical School, Dunedin, New Zealand Background: Plasma matrix metalloproteinase (MMP) lev- els have previously been implicated in the cardiovascular mortality of patients with coronary artery disease (CAD). This study aimed to determine if MMP related markers were associated with a history of in-stent restenosis (ISR). The strength of any such associations was compared with that of other known demographic and clinical risk factors for ISR. Methods: The circulating levels of three MMP related markers (proMMP-9, active MMP-9 and TIMP-1) were assessed in 164 patients with in-stent restenosis and compared with 168 patients with no history of ISR. Multiple logistic regression was used to determine the independence of associations. Multiple receiver operat- ing characteristic (mROC) analysis was used to determine sensitivity and specificity of both individual and compos- ite risk markers. Results: Univariant analysis indicated that both active MMP-9 and TIMP-1 were significantly elevated in ISR patients. Active MMP-9 >2 ng/mL was associated with an adjusted odds ratio of 4.6 (95% confidence interval 2.4–9.1, p < 0.0001) for ISR. Analysis of conventional ISR risk fac- tors by mROC resulted in a c-statistic of 0.839. Addition of MMP related markers increased the c-statistic to 0.870, a 3.7% increase in the models discrimination. A cut down model, suitable for clinical risk prediction yielded a c- statistic of 0.858, with MMP related markers adding 5% to the model. Conclusion: Plasma MMP-related protein levels are ele- vated in patients with a history of ISR. Addition of MMP related proteins to currently accepted risk variables increase the overall predictive value for ISR. doi:10.1016/j.hlc.2007.06.426 422 The Negative Regulation of Peroxynitrite on Endothelial NO Production Wei-Zheng Zhang * , Charles Lang, David M. Kaye Wynn Department of Metabolic Cardiology, Baker Heart Research Institute, Melbourne, Australia Background: Under conditions of oxidative stress, nitric oxide (NO) generated from arginine can combine with superoxide radicals to form peroxynitrite (PN), which is subsequently able to nitrate protein tyrosine residues to form 3-nitrotyrosine. This process is known to involve ‘uncoupling’ of NO synthase, however the precise nature of the complex relationship between NO production, and oxidative stress in vivo is still unclear. Here, we sought to investigate how PN alters NO bioavailability Methods: The impact of PN on endothelial arginine transportation, intracellular arginine metabolism and membrane protein nitration were studied respectively by analysis of (a) cellular arginine uptake and efflux with [ 3 H]-arginine and cationic amino acid transporter 1 (CAT1) by RT-PCR, (b) characterisation of major arginine metabolites with HPLC, and (c) formation of 3- nitrotyrosine by HPLC and anti-3-nitrotyrosine antibody probing. Results: Significant reductions (p < 0.05) of 34%, 60% and 82%, respectively in endothelial arginine uptake were demonstrated after treated with 0.1, 0.25 and 0.5 mM PN in cell culture medium for 1 h, which was concurrent with up to three-fold increase of membrane 3-nitrotyrosine and reduced Km and V max , but was not associated with changes in the CAT1 mRNA level. In contrast, PN