116 Atherosclerosis Supplements 12, no. 1 (2011) 13–184 Poster presentations 545 GRAFT STENOSIS IS ASSOCIATED WITH LIPOPROTEIN(A) C REACTIVE PROTEIN AND PLASMINOGEN ACTIVATOR INHIBITOR-1 IN PATIENTS UNDERGOING CORONARY ARTERY BYPASS SURGERY S.S. Habib, A.G.M. Abdel Gader, M.I. Kurdi, Z.A. Aseri. King Saud University, Riyadh, Saudi Arabia Objective: To assess the relationship between lipoprotein(a), High sensitivity C Reactive protein, markers of hemostasis and graft stenosis in coronary artery disease (CAD) patients after coronary artery bypass grafting. Materials and Methods: We studied 87 CAD patients patients who underwent CABG. Fasting venous blood samples were analyzed for Lipoprotein(a) [Lp(a)], high sensitivity C-reactive protein (hsCRP), fibrinogen, tissue-type plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), total and free tissue factor pathway inhibitor (TFPI-T, TFPI-F). The levels of these markers in those patients who did not have any history of a recurrent ischemic event after CABG (GroupA) were compared with levels in patients who had recurrent events of ischemia or infarction and had significant graft stenosis on angiography (GroupB). Results: GroupB patients had significantly higher BMI (p = 0.0402), Lp(a) (p = 0.0236) and hsCRP (p = 0.0416) than Group A.. Based on Gensini score GroupB had more severe CAD (85.05±56.27) compared to GroupA (54.46±33.25, p = 0.0058). Only PAI-1 levels were significantly higher in GroupB than GroupA (p = 0.0523). When the cutoff point for high risk level of Lp(a) was taken to be 20 mg/dl there was significantly higher prevalence of high risk levels of Lp(a) in GroupB (64.0%) than group A (38.6%, p = 0.0075). Similar comparison of hsCRP level between the two groups for different standard risk levels was found to be not remarkable. Conclusions: In middle aged men graft stenosis after CABG is associated with high lipoprotein(a) and CRP levels during the first year after coronary artery bypass grafting. However, PAI-1 was the only hemostatic marker which was significantly associated with grafts stenosis. 546 HIGH HEART RATE AS A RISK FACTOR FOR INCREASED ATHEROSCLEROSIS IN CORONARY ARTERY DISEASE (CAD) PATIENTS, STRONGLY RELATED TO NEW CARDIOVASCULAR EVENTS S. Radovanovic 1 , A. Djokovic 1 , D. Simic 2 , I. Zivanovic 1 , S. Jelic 1 , M. Krotin 1 . 1 University Hospital Bezanijska Kosa, 2 Clinical Center of Serbia, Belgrade, Serbia Objective: Although it was shown, that heart rate could promote atherosclerosis in monkeys, the link between cardiovascular diseases and heart rate remains largely unknown. Aim: To investigate the association between heart rate in CAD patients with biomarkers for endothelial dysfunction [soluble intercellular cell adhesion molecule 1 (s-ICAM-1), soluble vascular cell adhesion molecule 1 (s-VCAM-1)] and atherosclerosis, the intima-media thickness (IMT) of the common carotid artery. We also sought to determine prognostic significance of high heart rate in CAD patients in relation to new cardiac events. Methods: 120 consecutive patients, mean age, 59±7 years (74 men, 46 women) with angiographically demonstrated CAD were enrolled in this study. IMT was defined as maximum thickness of IMT in both left and right common carotid artery. All patients was done 24 h Holter electrocardiogram and the average heart rate correlated with carotid artery IMT and levels of s-ICAM-1 and s-VCAM-1 were spectrofotometricly. All patients were followed for 15±2 months, for cardiovascular ivents Results: Heart rate was significantly correlated with s-ICAM-1 (r = 0.24, p = 0.01) and s-VCAM-1 (r = 0.20, p = 0.03). Significant correlation was found between heart rate and IMT CCA sinistra (r = 0.20, p = 0.03) and CCA dextra (r = 0.19, p = 0.04). It was also found significantly correlation of IMT CCA with s-ICAM-1 (r = 0.54, p < 0.01) but not with s-VCAM-1.Correlation also existed between heart rate and repeted hospitalization for chronic heatr failure exarcerbation (r = 0.18, p < 0.04) and total number of cardiovascular events (r = 0.19, p < 0.03) during the one-year follow-up period. Conclusion: There was found linked heart rate with the markers of endothelial dysfunction and indices of atherosclerosis progression. High heart rate is strongly related with prognosis in CHF patients. 547 RED CELL DISTRIBUTION WIDTH AND INCIDENCE OF HEART FAILURE: A POPULATION-BASED COHORT STUDY Y. Born´ e, J.G. Smith, O. Melander, B. Hedblad, G. Engstr¨ om. Cardiovascular Epidemiology, Department of Clinical Sciences, Lund University, Skane University Hospital, Malm ¨ o, Sweden Background: Red cell distribution width (RDW) has been associated with cardiovascular disease (CVD), but the relation to incidence of heart failure (HF) is unclear. We investigated the association between RDW and incident HF in a population-based cohort. Methods: RDW was measured in 26,953 subjects (aged 45 to 73 years, 60% women), without history of myocardial infarction (MI), stroke or HF, who participated in the Malm ¨ o Diet and Cancer study during 1991–1996. Incidence of HF was identified from the national Swedish hospital discharge register during a mean follow-up of 15 years and studied in relation to RDW. Results: During follow-up, 786 subjects (55% men) were diagnosed with new- onset HF, of whom 168 had an MI before or concurrent with the HF. After adjustment for potential confounding factors (including age, sex, biological, lifestyle and socio-economic factors), the hazard ratios (HR) for HF were 1.31 (95% CI: 1.05–1.62) in the top compared to the bottom quartile of RWD (p for trend 0.008). In secondary analyses with censoring at incident MI, results were similar (HR: 1.45, 1.13–1.86). After additional adjustment for N-terminal pro-B-type natriuretic peptide and cystatin C in a randomly selected subcohort (n = 4,761), HR was 1.73 (CI: 0.97–3.10) comparing the top vs. bottom quartile of RWD. Conclusions: RDW was found to be associated with long-term incidence of HF among middle-aged subjects. 548 TYPE 2 DIABETES AND THE PROGRESSION OF VISUALIZED ATHEROSCLEROSIS TO CLINICAL CARDIOVASCULAR EVENTS C.H. Saely 1,2,3 , P. Rein 1,2,3 , A. Vonbank 1,2,3 , K. Huber 4 , H. Drexel 1,2,3,5 . 1 VIVIT Institute, 2 Internal Medicine, Academic Teaching Hospital Feldkirch, Feldkirch, Austria, 3 Private University of the Principality of Liechtenstein, Triesen, Liechtenstein, 4 Department of Cardiology, Wilheminen Spital, Vienna, Austria, 5 Drexel University College of Medicine, Philadelphia, PA, USA Background: We aimed at prospectively evaluating to what extent pre-existing coronary artery disease (CAD) accounts for the increased long-term vascular event risk of patients with type 2 diabetes (T2DM). We hypothesized that baseline CAD among patients with T2DM may account substantially for their increased cardiovascular risk. Methods: Over 8 years we recorded vascular events in 750 consecutive patients whose baseline CAD state was verified angiographically. Results: The prevalence rates of CAD (87.8% vs. 80.4%; p = 0.029) and of significant coronary stenoses 50% (69.5% vs. 58.4%; p = 0.010) as well as the extent of CAD, defined as the number of significant coronary stenoses (1.7±1.6 vs. 1.4±1.5; p = 0.014) were higher in patients with T2DM (n = 164) than in non- diabetic subjects. During follow-up, T2DM strongly predicted vascular events (n = 257) independently from the presence and extent of baseline CAD (hazard ratio (HR) 1.36 [1.03–1.81]; p = 0.032); conversely, the presence and extent of baseline CAD predicted vascular events independently from T2DM (HRs 3.29 [1.93–5.64]; p < 0.001 and 1.37 [1.23–1.53]; p < 0.001, respectively). The overall risk increase conferred by T2DM was driven by the extremely high 53.3% event rate of patients with both T2DM and significant CAD at baseline; individuals with T2DM who did not have significant CAD at baseline showed a significantly lower event rate (22.0%; p < 0.001). Conclusion: We conclude that T2DM and angiographically visualized coronary atherosclerosis are mutually independent predictors of vascular events. The overall risk increase conferred by T2DM is driven by accelerated progression of pre-existing atherosclerosis to clinical cardiovascular events. 549 YOUTH WHOSE PARENTS SMOKED HAVE REDUCED FLOW-MEDIATED DILATATION AS YOUNG ADULTS M. Juonala 1 , C.G. Magnussen 2,3 , A. Venn 4 , J.S.A. Viikari 1 , T. Dwyer 2 , O.T. Raitakari 5 . 1 Research Centre of Applied and Preventive Cardiovascular Medicine and Department of Medicine, University of Turku and Turku University Central Hospital, Turku, Finland, 2 Murdoch Childrens Research Institute, Melbourne, VIC, Australia, 3 Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland, 4 Menzies Research Institute, Hobart, TAS, Australia, 5 Research Centre of Applied and Preventive Cardiovascular Medicine and the Department of Clinical Physiology, University of Turku and Turku University Central Hospital, Turku, Finland Background: Passive smoking has been associated with endothelial dysfunction among healthy youth. Since other risk factors in youth have been shown to have a long-term impact on endothelial dysfunction in adulthood, we aimed to examine the effect of parental smoking status, a proxy for passive smoke exposure, in youth on flow-mediated dilatation (FMD) in adulthood. Methods: 2171 participants in the population-based, prospective, observational Cardiovascular Risk in Young Finns and Childhood Determinants of Adult Health studies who had conventional risk factors (lipids, blood pressure, adiposity) as well as self-report of parental smoking status measured when aged 3−18 years at baseline (1980−85) who were re-examined 19−27 years later (2004−07) when aged 28−45 years. Brachial artery FMD was ascertained at follow-up using B-mode ultrasound. Results: In analyses adjusting for age, sex, and childhood risk factors (lipids, blood pressure, adiposity, and parental education status), FMD was reduced among participants who had parents that smoked in youth compared to those whose parents did not smoke (Young Finns: 9.2% vs.8.6%, P = 0.001; CDAH: 7.4% vs.4.9%, P = 0.04). These effects remained after further adjustment for adult risk factors (lipids, blood pressure, adiposity, own education status, and own smoking status; Young Finns, P = 0.001; CDAH, P = 0.03). Father’s smoking