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| Effect of tirofiban on vascular endothelial dysfunction in patients with acute coronary syndrome |
| YAO Hongying1,YAN Songbiao2,ZHANG Yuchen2,LIU Huiliang1,YANG Shengli1,and MA Dongxing1 |
1. Department of Cardiovascular Diseases, General Hospital of the Chinese People’s Armed Police Forces, Beijing 100039, China;
2. Department of Cardiovascular Diseases, Beijing Friendship Hospital, Beijing 100050, China |
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Abstract Objective To study the effect of tirofiban on endothelial dysfunction in patients with acute coronary syndrome. Methods Eighty-six consecutive patients diagnosed as having acute coronary syndrome were recruited. They were randomly divided into two groups: tirofiban group ( n=40) and control group ( n=46). Tirofiban was administered with a loading dose of 10 μg/( kg·min) for 3 minutes, followed by infusion of 0.15 μg/( kg·min) for 48-72 hours. And the patients in control group were given physiological saline. The blood samples of the patients were obtained immediately after enrollment. The serum levels of ET and NO were measured. After 24 hours, the above-mentioned tests were repeated and the baseline diameter of brachial artery, the reactive hyperemia diameter and the diameter after sublingual nitroglycerin were examined respectively by high-resolution ultrasonic transducer. The FMD and NMD were calculated. The parameters were respectively compared in two groups and between groups. Results Compared with control group, the FMD was obviously better in tirofiban group ( 6.2%±3.0% vs 4.6%±2.1%, P=0.008). But no significant difference of FMD was observed between the two groups. And tirofiban significantly increased the level of NO [( 38.63±16.42) μmol/L vs( 44.74±2.77) μmol/L, P=0.017] and decreased the level of ET [( 117.61±14.25) pg/ml vs( 107.57±16.45)pg/ml, P=0.006]. Conclusions For the patients of ACS, the therapy of tirofiban can improve the FMD, and significantly decrease the levels of ET and increase the density of NO, indicating that tirofiban can protect the vascular endothelial cells and improve the vascular endothelium dysfunction.
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Received: 22 May 2013
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2013, Vol. 24 
