Jung Ah Kwon | Search PubMed

PubMed2006

Decrease in plasma adiponectin concentrations in patients with variant angina pectoris.

BACKGROUND: Plasma adiponectin is decreased in patients with coronary artery diseases, especially in patients with acute coronary syndrome (ACS). However, the correlation between plasma adiponectin and variant angina pectoris (VAP) has not been verified. Plasma adiponectin concentrations between VAP and other coronary artery diseases was compared in the present study. The association between plasma adiponectin concentration and VAP was also investigated. METHODS AND RESULTS: Plasma adiponectin concentrations in the VAP group (n=101) were compared with those of the ACS group (n=117), the stable angina pectoris group (n=108), and the normal coronary group (n=81). Plasma adiponectin concentrations in VAP and ACS were significantly lower than that of the normal coronary group (6.6+/-5.4 vs 5.2+/-4.0 vs 9.0 +/-6.2 microg/ml, p<0.001, respectively). Multivariate analysis indicated that plasma adiponectin (odds ratio (OR) 0.735, 95% confidence interval (CI) 0.621-0.855, p=0.011), smoking (OR 2.012, 95% CI 1.210-3.880, p=0.020), and age (OR 0.976, 95% CI 0.957-0.997, p=0.022) correlated independently with the development of VAP. CONCLUSIONS: Our results suggest that a decrease in plasma adiponectin concentration might be associated with the development of VAP.

Adiponectin↗

PubMed2004

Effects of cilostazol on platelet activation in coronary stenting patients who already treated with aspirin and clopidogrel.

BACKGROUND: A recent study has shown that triple anti-platelet therapy (cilostazol+clopidogrel+aspirin) resulted in a significantly lower restenosis rate after coronary stenting than did conventional therapy (clopidogrel+aspirin). However, the anti-platelet effects of cilostazol, when combined with clopidogrel and aspirin, have not been evaluated. METHODS: Low dose cilostazol (50 mg/BID) was given to 47 patients who had already been taking clopidogrel (75 mg/day) and aspirin (100 mg/day) for more than 1 month subsequent to coronary stenting due to AMI and unstable angina. Markers of platelet activation, P-selectin and activated GPIIb/IIIa on platelets, were measured at baseline and 2 weeks after cilostazol treatment. We empirically divided patients into tertiles (low, n =16; moderate, n = 14; high group, n = 17), according to the baseline P-selectin expression. We then performed a comparative assessment of the anti-platelet effects of cilostazol at baseline and after 2 weeks of cilosatzol administration. RESULTS: P-selectin was significantly decreased after 2 weeks of cilostazol treatment in total patients (n = 47, 3.2 +/- 2.4% to 2.0 +/- 1.9%, p = 0.03). This inhibition of P-selectin expression was mainly achieved in the moderate and high P-selectin groups (low group; 1.4 +/- 0.5 to 1.9 +/- 1.3%, p > 0.05, moderate group; 2.5 +/- 0.3 to 1.3 +/- 0.3%, p < 0.05, high group; 5.4 +/- 2.7 to 2.7 +/- 2.8%, p < 0.05). Activated GPIIb/IIIa was not significantly changed (13.5% to 17.6%, p > 0.05). Underying disease, cardiovascular risk factors, concomitant medication including statin, and hsCRP were not related to the degree of P-selectin expression. CONCLUSION: Our data demonstrated that cilostazol treatment in addition to conventional anti-platelet therapy provides more effective suppression of platelet P-selectin expression in patients with relatively high platelet activity.

Aspirin↗