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Abstracts of the 17th Asian Pacific Congress of Cardiology
cause mortality was 7.4%. In Kaplan-Meier survival analysis, warfarin treatment was not associated with lower risk of MACE (p = 0.601) or mortality (p = 0.324). However, it was associated with increased risk of major bleeding (p = 0.011). Cox regression analysis showed that independent predictor of MACE was diabetes (p = 0.024). Conclusion: It is likely that the benefit of oral anticoagulation therapy after PCI in Asian AF patients is different from that in western population. P-253 Effect of Atorvastatin on Paraoxonase (PON) Gene Family and Oxidative Status in Hypercholesterolaemic Pateints Amar Nagila1 , Surrerut Porntadavity2 , T Permpongpaiboon2 , S Tantrarongroj2 , P Porapakkham3 . 1 Department of Biochemistry, School of Pharmaceutical and Biomedical Sciences, Pokhara University, Nepal, 2 Department of Clinical Chemistry, Faculty of Medical Technology, Mahidol University, Thailand, 3 Department of Cardiology, Chest Disease Institute, Thailand The paraoxonase (PON) gene family consists of three members, PON1, PON2 and PON3 and has been shown to play a role in anti-atherosclerosis. The aim of this study was to investigate the effects of atorvastatin treatment on PON activity and oxidative status, lipid peroxidation markers (malondialdehyde (MDA), conjugated diene (CD), total peroxides (TP)), total antioxidant substance (TAS) and oxidative stress index (OSI). Furthermore, we have also evaluated the influence of PON polymorphisms on the responses of PON activity and oxidative status to atorvastatin treatment in hypercholesterolaemic patients. Atorvastatin treatment significantly reduced the levels of TC (24.5%, P < 0.001), LDL (22.4%, P < 0.001), TG (24.4, P < 0.05), CD (4.4%, P < 0.05), MDA (15.2%, P < 0.01), TP (13.0%, P < 0.01) and OSI (24.0%, P < 0.001), and significantly increased the levels of TAS (27.3%, P < 0.001), serum PON1 activity towards paraoxon (13.4%, P < 0.05) and PON3 activity towards p-nitrophenyl butyrate (13.2%, P < 0.05). Atorvastatin did not have an effect on the PON2 activity in mononuclear cell after three months of treatment. Interestingly, the increased of PON1 activity towards paraoxon and PON3 activity as well as the reduction of oxidative stress in responding to atorvastatin treatment were influence by only PON1T-107C polymorphism. In summary, atorvastatin treatment reduced both plasma atherogenic lipids and oxidative stress may be via by increasing PON1 and PON3 activities and the interaction of gene-therapeutic response. P-254 Beneficial Effects of Daming Capsule (DMC) on Cardiovascular Diseases (CVD) Yong Zhang, Jing Ai, Hongli Shan, Chaoqian Xu, Benzhi Cai, Yanjie Lu, Zhiguo Wang, Baofeng Yang. Department of Pharmacology, Harbin Medical University, China Introduction: DMC is a herbal formula widely utilized as lipid-modulating Traditional Chinese Medicine. The present study was designed to investigate the mechanisms for DMC to treat CVD. Methods: Left anterior descending coronary artery was occluded. Biochemical index (TC, TG, LDL-C and HDL-C) were measured 6 weeks after the drug regimen. The protective effects of DMC were evaluated from changes of electrocardiogram (ECG), and the size of myocardial infarcted area. Resting membrane potential (RMP) and IK1 were measured using patch clamping technique. Kir2.1 was detected by Western-blotting.
Results: After treatment with DMC, the serum levels of TC and LDL-C were significantly decreased, with no changes in the TG and HDL-C levels. DMC significantly reduced the size of myocardial infarcted area, inhibited ST segment raise and decreased the arrhythmia score compared to MI group. RMP was significantly depolarized in MI group, and recovered in DMC treated rats. IK1 current was markedly decreased in MI group, and reversed by DMC, consistent with its protein level of Kir2.1. Conclusions: DMC had protective effects on CVD, regulation of IK1 /Kir2.1 may be one of the important mechanisms for DMC’s beneficial effects, indicating that DMC might be applied to treating CVD. P-255 Metaanalysis on the Effects of Vitamin E on Cardiovascular Outcomes in High Risk Patients, An Update Queenie Guinto Ngalob1 , Rodel N. Delgado1 , Geraldine Z. Racaza2 , Michael Joseph F. Agbayani1 , Gregory Ryan A. Ardena2 , Rommel R. Geronimo1 , Regina P. Berba1 . 1 Department of Medicine, University of the Philippines Philippine General Hospital, Philippines, 2 Department of Medicine University of the Philippines-Philippine General Hospital, Philippines Background: Vitamin E is a drug marketed for cardiovascular benefits. However, recent randomized trials do not show consistent benefit in cardiovascular outcomes. A metaanalysis conducted three years ago concluded no benefit in high risk patients. Conflicting researches are still ongoing, hence the need for an update. Objective: This meta-analysis aims to update the investigation on whether vitamin E in high risk patients causes significant risk reductions in non-fatal myocardial infarction, stroke, cardiovascular death and all-cause mortality. Methods: A computerized search was done on the Medline database using PubMed. Randomized controlled trials involving high-risk patients with a vitamin E treatment arm and non-supplemental arm that tested for the specified cardiovascular outcomes were included. After quality appraisal and validity assessment, data were extrapolated and entered into RevMan 4.2.3. Results: Eight randomized controlled trials were included in the study. No significant reductions in all-cause mortality (OR 1.02, 95% CI [0.98 1.07]), cardiovascular death (OR 1.00, 95% CI [0.95 1.06]), stroke events (OR, 0.97, 95% CI [0.89 1.07]) or non-fatal myocardial infarction (OR 0.93, 95% CI [0.83 1.04]). Moreover, for non-fatal MI outcomes, statistical heterogeneity was present (Chi2 13.46, df 3, p 0.004, I2 77.7%). Conclusion: We found no significant reduction in risk for cardiovascular outcomes with Vitamin E supplementation in high risk patients. This allows us to conclude that Vitamin E should not be routinely recommended for high-risk patients.