P2-34 PROGNOSTIC SIGNIFICANCE OF ADIPOCYTOKINES AND EXTRACELLULAR MATRIX IN HEART FAILURE PATIENTS WITH HIGH BRAIN NATRIURETIC PEPTIDE

Abstract of the 16th Asian Pacific Congress of Cardiology, Taipei, Taiwan, 13–16 December, 2007 heterozygous for the adiponectin +276 G>T polymorphism to metabolic syndrome composing hypertension offspring (P=0.03). Furthermore, the significant association observed in sub-phenotypes of metabolic syndrome including HTN+ high triglyceride (HTG)+ obesity (p=0.034), HTN+HTG+ low HDL (P=0.01) and HTN+ obesity + low HDL (P=0.0196) respectively. The genotype relative risk were 4.42 (95% CI: 1.07–18.03) for +276 TT relative to +276 GT+GG for the sub-phenotype of HTN+ HTG + low HDL. The sub-phenotypes of HTN+ obesity + HTG and HTN + obesity + low HDL, subjects carrying +276 TT also tended to higher risk of transmission of subtype of metabolic syndrome (TT vs. GT+GG; odds ratio, 1.78; 95% CI: 0.7–4.52; odds ratio, 2.87; 95% CI: 0.89–9.29, respectively). Our data demonstrated the adiponectin gene was associated with simultaneous presence of both hypertension and other risk factors such as low HDL, high TG and obesity, suggesting the potential role of adiponectin gene in the context of simultaneously presence of hypertension and metabolic syndrome. Lower serum concentration of adipnectin in metabolic syndrome especially composing hypertension further suggested the causative role of the adiponectin gene in this subtype of metabolic syndrome.

P2-34 PROGNOSTIC SIGNIFICANCE OF ADIPOCYTOKINES AND EXTRACELLULAR MATRIX IN HEART FAILURE PATIENTS WITH HIGH BRAIN NATRIURETIC PEPTIDE

Yen-Hung Lin 1 , Yi-Lwun Ho 1,4 , Ron-Bin Hsu 2 , Chiou-Ping Chen 3 , Tse-Pin Hsu 3 , Chu-Yuan Lee 3 , Nai-Kuan Chou 2 , Chi-Ming Lee 1 , Shoei-Shen Wang 2 , Ming-Fong Chen 1 . 1 Division of Cardiology, Department of Internal Medicine, Departments of 2 Surgery and 3 Nursing, 4 Graduate Institute of Clinical Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan Objectives: The goal was to assess prognostic values of simultaneous measurement of adipocytokines and extracellular matrix in heart failure patients with high brain natriuretic peptide (BNP). Background: Increased BNP has been associated with poor prognosis of heart failure. However, using adipocytokines and extracellular matrix to do further risk stratification in heart failure patients with high BNP has not been reported. Methods: Patients with heart failure manifestations, left ventricular ejection fraction (LVEF) ≤ 45% and BNP level ≥1000pg/ml were enrolled in this study. Gender, age, medications, serum biochemical data, and outcome of heart failure were recorded. Adipocytokines including adiponectin, leptin, resistin, visfatin, and apelin were measured. Extracellular matrix including type I and III amioterminal propeptide of procollagen (PINP and PIIINP), matrix metalloproteinase-2 and 9 (MMP-2 and MMP-9), and tissue inhibitor of metalloproteinase 1 (TIMP-1) were analyzed. Results: A total of 131 (98 males and 33 females) patients were enrolled. The age was 61±16 years and mean LVEF was 38%. Follow-up duration was 240±174 days. The BNP was 2179±869 pg/ml. There were 12 patients died and 20 patients with heart failure related admission during follow-up. Mortality was associated with adiponectin (21.2±14.7 vs 13.3±10.1 ug/ml, p=0.03), resistin (38±38 vs 26±24 ng/ml; p=0.049), PIIINP (7.8±2.1 vs 6.5±3.0 ug/l; p=0.021), MMP-2 (357±91 vs 272±91 ng/ml; p=0.001), TIMP-1 (192±63 vs 143±63 ng/ml), and serum creatinine (1.7±0.5 vs 1.5±1.2 mg/dl; p=0.001). Heart-failure related admission was associated with apelin (0.19±0.14 vs 0.23±0.25ng/ml; p=0.01), and PIIINP (8.1±2.8 vs 6.3±2.9 ug/l; p=0.002). Adiponectin was associated significantly with atrial fibrillation (17.4±12.6 vs 12.6±10.0 ug/ml, p=0.038). Cox regression analysis showed mortality and heart-failure related admission were associated significantly with MMP-2 (p=0.008) and PIIINP (p=0.011), respectively. Using MMP-2 282 ng/ml as a cutoff point, significant difference in survival was noted from Kaplan-Meier survival curve (p=0.001). Conclusions: Extracellular matrix rather than adipocytokines could do further risk stratification for prognosis of patients with heart failure and high BNP.

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P2-35 BNP REDUCTION BY BETA BLOCKERS AND CALCIUM ANTAGONISTS AFTER ACUTE MYOCARDIAL INFARCTION

Atsushi Namiki, Kaoru Sugi, Junichi Yamazaki. Toho University School of Medicine, Tokyo, Japan Background: Because Japanese patients with acute myocardial infarction (AMI) have a greater incidence of coronary spasm than Caucasians, calcium antagonists are prescribed generally in Japan. A multicenter clinical trial in Japan (The Japanese Beta Blockers and Calcium Antagonists in Myocardial Infarction Study: JBCMI) revealed that beta blockers increased heart failure events compared with calcium antagonists in patients with AMI. The objective of this study was to compare brain natriuretic peptide (BNP) between patients administered with a beta blocker and a calcium antagonist after AMI. Methods: We investigated 26 patients with AMI who underwent successful percutaneous coronary intervention. Thirteen patients (Group B) were administered with carvedilol, a beta blocker, and 13 (Group C) were prescribed with amlodipine, a calcium antagonist. BNP levels before, 3 and 6 months after medication and BNP reduction rate at 3 and 6 months after medication were compared in both groups. Results: BNP levels before medication showed no difference between 2 groups (138 and 122 pg/ml in Group B and C). At 3 months after starting carvedilol or amlodipine, BNP level was 101 and 36 pg/ml (p<0.05), and 101 and 31 pg/ml (p<0.01) at 6 months in Group B and C. BNP reduction rate compared with that before medication was 32 and 64% at 3 months (p<0.05), 32 and 69% at 6 months (p<0.05) after starting medication in Group B and C. Conclusion: BNP reduction in patients after AMI who underwent emergent successful percutaneous coronary intervention is more augmented by calcium antagonist than by beta blocker.

P2-36 EFFICACY AND SAFETY OF LERCANIDIPINE VERSUS AMLODIPINE FOR TREATING HYPERTENSIVE OUTPATIENTS

Nakarin Sansanayudh, Supakit Wongwiwatthananukit, Siriluck Veerayuthvilai. Phramongkutklao Hospital, Thailand Objectives: To compare the incidence of peripheral edema, other adverse events and efficacy of lercanidipine and amlodipine in patients with hypertension Methods: This is a randomized, open-labeled, parallel design study in hypertensive outpatients. Eighty patients, who had indication for anti-hypertensive medication and had no previous history of edema, were randomized using block randomization into two groups (40 patients in each group). The control group received amlodipine 5 mg/d and the study group received lercanidipine 10 mg/d. Patients were assessed for (1) incidence of peripheral edema (2) incidence of other adverse events and (3) efficacy of treatment after 4 and 8 weeks of treatment. After 4 weeks of treatment, the dose was doubled in patients who did not achieved blood pressure goal according to JNC VII. Results: Baseline patient’s characteristics were similar in both groups. All side effects occurred within 4 weeks of treatment in both groups and there was no additional edema or other side effects reported between week 4 and week 8. After 4 weeks of treatment, seven of forty patients in control group (17.5%) developed peripheral edema compared to none of study group (0%); p=0.012. All seven patients who developed edema were female. There was a trend towards higher incidence of all adverse side effects in the control group (22.5% vs. 5%, p=0.051) and higher incidence of severe side effects causing withdrawal of treatment in the control group (12.5% vs. 0%, p=0.055). The baseline systolic blood pressure (SBP) and diastolic blood pressures (DBP) were 159.69±10.47 mmHg and 93.10±10.18 mmHg in study group and 159.15±12.33 mmHg and 92.10±9.55 mmHg in control group, p>0.05. After 4 weeks, lercanidipine significantly reduced SBP (−22.19±12.61 mmHg, p<0.001) and DBP (−10.62±10.60 mmHg, p<0.001). Amlodipine also reduced SBP (−23.35±16.13 mmHg, p<0.001) and DBP (−12.00±9.32 mmHg, p<0.001) significantly from baseline. There was no difference in both SBP and DBP between lercanidipine and amlodipine groups at week 4 and week 8 and the percentage of patients who achieved BP goal was also not significantly difference between two groups at week 4 and week 8. Conclusions: Both lercanidipine and amlodipine were effective for treating hypertensive outpatients. Lercanidipine had lower incidence of peripheral edema