Effect of fenofibrate and telmisartan on glucose and fatty acid metabolism in insulin-resistance rat in vivo

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Abstracts

percent (%). Predicted LV mass was calculated using Korean-specified equation. Nocturnal BP was expressed as mean systolic BP and dipping (%). Results: Age of the subjects was 56.5 ± 14.4, 47.5% were male patients. Average ambulatory BPs for 24 h, daytime, and night-time were 142.8 ± 12.9 mm Hg, 146.3 ± 13.2 mm Hg, and 131.1 ± 19.3 mm Hg, respectively. OPR was 118.6 ± 19.9(%) and the nocturnal dipping was 10.2 ± 11.3%. In multiple linear regression model, 24 h SBP (β = −0.123, p = 0.018) and nocturnal dipping (β = −0.126, p = 0.018) were independent determinant of OPR of LV as well as age (β = 0.113, p = 0.038), gender (β = −0.423, p = 0.0001), and body mass index (β = 0.390, p = 0.0001). Odds ratio for LVH was 2.79 for 24 h SBP (>143 mm Hg) and 4.95 for BMI (>25 kg/m2). Odds ratio for iLVM was 2.03 for non-dipper (p = 0.03), 4.70 for BMI (>25 kg/m2), and 1.17 for female gender. Conclusion: Nocturnal blood pressure or dipping is independently associated with inappropriately high LV mass in essential hypertension patients as well as obesity. doi:10.1016/j.ijcard.2009.09.267 HT000592 Effect of different dose of atorvastatin on cardial protection and inflammation in patients with stable angina after percutaneous coronary intervention GUANGLING CHEN, JINGZI SU The First Affiliated Hospital of Fujian Medical University, China Objective: To study the effects of atorvastatin for protection of myocardium and inflammatory factors after percutaneous coronary intervention (PCI). Methods: 82 patients with chronic stable angina without previous statin treatment at least 2 months before PCI were randomized to receive atorvastatin 10 mg/qn (group A n= 27), 20 mg/qn (group B n= 28) or 40 mg/qn (group C n= 27) treatment 3 days before PCI. cTnI, hsCRP, IL-6, and sICAM-1 were measured at baseline and at 8 and 24h after the procedure. Results: The peak levels of marks of cTnI were increased significantly in all three groups after PCI (P <0.05). Postprocedural peak levels of marks above the upper normal limit in group A, group B and group C were: 55.56%, 28.57% and 18.52% for cTnI. cTnI elevation >3 time upper normal limit was 44.44% in group A, 17.85% in group B and 11.11% in group C. Either above the upper normal limit or elevation >3 time upper normal limit of the mark of cTnI, there were significant differences in group A and group B (P<0.05) or in group A and group C (P <0.05), however there was no significant difference in group B and group C (P >0.05). The level of IL-6, sICAM-1 and hsCRP 8 h after PCI was higher than those before the PCI (P <0.05). There was significant difference of IL-6 and hsCRP among the three groups (P<0.05), but no significant difference about sICAM-1 (P>0.05). The level of hsCRP and sICAM-1 24 h after PCI was higher than those 8h after the PCI (P<0.05) in each group, but IL-6 significantly decreased (P <0.05). Conclusion: Even short term pretreatment with atorvastatin before PCI may reduce procedural myocardial injury in chronic stable angina patients, and increase the function as the increase of dose in the study extension. doi:10.1016/j.ijcard.2009.09.268 HT000624 Effect of fenofibrate and telmisartan on glucose and fatty acid metabolism in insulin-resistance rat in vivo ZHAO WEIHUA, HU JIAN Department of Cardiology, The First Affiliated Hospital of China Medical University, China Objective: Fenofibrate is a kind of peroxisome proliferator-activated receptor-alpha (PPARalpha) agonist that is used for treating hyper-

triglyceridemia and low high-density lipoprotein hyperlipidemia. The paper discusses the mechanism and effects of combined therapy of fenofibrate and telmisartan on insulin resistance rat. Methods: 1. Animal preparation. 2.1 Measurement index. 2.1.1 Evaluation insulin resistance. 2.1.2 Analyzing fasting blood glucose: 1.1.3 Blood pressure, 1.1.4 Serum index, 1.1.5 The expression of PPARγ, HSL, Ap2R, esistin and adiponectin by Reversal Transcription Polymerase Chain Resction (RT-PCR), and 1.1.6 Measurement of PPARαprotein and PPARγ protein by Western blot analysis. Results: 1 The result between control group and high fat group: the weight of the high fat group increases than the control group, and the blood glucose, insulin concentration, free fatty acid, triglyceride and GIR of high fat group are significantly higher than the control group, p < 0.01. 2 The result of serum index: comparison with the high fat group, the weight of the three groups by drugs treatment is markedly reduced, p < 0.01 and GIR improved significantly, p < 0.01. 3 The result of PCR: the high fat group decreased significantly than the control group, P < 0.01. Conclusions: 1 High fat feeding can establish the metabolic syndrome rat model. 2 Both telmisartan and fenofibrate can improve the insulin resistance, and combined therapy can improve the abnormal metabolism further. 3 Fenofibrate can increase the blood pressure of rats but telmisartan can inhibit this effect, combined therapy has a beneficial impact. 4 Both telmisartan and fenofibrate can regulate the cytokines, such as combined therapy can increase the level of adiponectin. 5 Insulin resistance can decrease the expression of PPARα and PPARγ mRNA mRNA, but fenofibrate can increase the expression of PPARα mRNA and telmisartan can increase the expression of PPARγ mRNA. 6 Telmisartan and fenofibrate regulate their target gene t. doi:10.1016/j.ijcard.2009.09.269

HT000691 Left ventricular hypertrophy in obese hypertensive men BRANKO JAKOVLJEVIĆa, VESNA STOJANOVb, GORAN BELOJEVIĆa, DANICA CVETKOVIĆ MATIĆb, DRAGAN LOVIĆc a Institute of Hygiene and Medical Ecology, School of Medicine, Serbia b Clinical Centre of Serbia, Belgrade, Serbia c Private Internal Medicine Clinic “Lovic”, Serbia Objectives: Both obesity and arterial hypertension cause left ventricular (LV) hypertrophy. The aim of this study was to assess the influence of obesity on the occurrence of LV hypertrophy in hypertensive men. Design and methods: Altogether 56 hypertensive men aged 57.3± 10.8 years took part in the study. Body Mass Index (BMI) was calculated as kg/m2. Obesity was defined as BMI equal or over 30 kg/m2, overweight as BMI between 25 and 29.9 kg/m2. LV hypertrophy was assessed by echocardiography criteria — LV mass LVM (g), left ventricular mass index LVMI (g/m2), left ventricular end diastolic diameter LVEDD (cm), and interventricular septum IVS (cm). Results: Obesity was present in 35 men (62.5%), overweight in 18 men (32.1%), and normal weight was reported in only 3 (5.4%) hypertensive men. LV hypertrophy was diagnosed in 41 men (73.2%), according to LVM; in 46 (82.1%) men, when LVEDD was used as a criterion. Obese men had higher LVM (367.44±66.23) compared to overweight men (352.38±71.60; p <0.001). Obese men had higher LVEDD (6.11 ± 0.35) compared to overweight men (5.68 ± 0.54; p < 0.001). Obese men had higher LVMI (188.68 ± 35.24) than normalweight men (159.19 ± 31.75; p = 0.004), as well as higher IVS (1.19 ± 0.13) than men with normal weight (1.07 ± 0.17; p < 0.001), but were comparable to overweight men. All echocardiography parameters of left ventricle were strongly correlated to BMI. Logistic regression model identified obesity (OR = 3.12, 95%CI = 1.26–4.38) and overweight (OR = 2.54, 95%CI = 1.17–3.01) as significant predictors of LV hypertrophy (assessed by LVM), independent from age and blood pressure. Conclusion: LV hypertrophy is present in more than two thirds of all hypertensive men. Obesity and overweight are present