Increased plasma levels of endothelin-1 and urotensin-II in patients with coronary heart disease
Increased plasma levels of endothelin-1 and urotensin-II in patients with coronary heart disease
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DOI：
10.1007/s00380-009-1178-6
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发表时间：
2010-03-01
影响因子：
1.5
通讯作者：
Tang, Chao Shu
中科院分区：
文献类型：
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作者：
Chai, San Bao;Li, Xue Min;Tang, Chao Shu
研究已确定血管收缩剂内皮素-1 (ET-1) 和尾加压素-II (U-II) 在动脉粥样硬化性心血管疾病的发展中发挥作用。我们旨在观察 2006 年 11 月至 2007 年 5 月接受经皮腔内冠状动脉成形术 (PTCA) 和支架治疗的冠心病 (CHD) 患者血浆 ET-1 和 U-II 水平的变化。我们通过放射免疫分析 (RIA) 检测了 40 名 CHD 患者和 40 名年龄匹配的健康受试者血浆 ET-1 和 U-II 水平。卡方检验、学生t检验和单向方差分析用于统计分析。通过简单线性回归分析测试变量之间的相关性。冠心病患者的ET-1和UII水平显着高于健康对照（分别为20.05 +/- 4.65 vs 8.16 +/- 3.38和71.90 +/- 11.61 vs 20.89 +/- 7.00 pg/ml，均P < 0.01）。重要的是，CHD 患者的血浆 U-II 和 ET-1 水平相关（r = 0.64，P = 0.01）。 PTCA和支架治疗后第1天，血浆ET-1和U-II水平较治疗前分别显着升高99%和25%（均P < 0.01）。治疗后第3天，ET-1水平较治疗前升高25%（P < 0.01），U-II水平迅速下降并接近基线水平（P > 0.05）。治疗后第7天，CHD患者ET-1和U-II水平显着低于治疗前（均P < 0.01）。由于冠心病患者血浆中ET-1和U-II水平可能升高，因此它们的激活对于冠心病患者的早期干预可能具有临床意义，特别是在PTCA和支架治疗后。
Research has identified the vasoconstrictors endothelin-1 (ET-1) and urotensin-II (U-II) as having a role in the development of atherosclerotic cardiovascular disease. We aimed to observe alterations in plasma levels of both ET-1 and U-II in patients with coronary heart disease (CHD) undergoing percutaneous transluminal coronary angioplasty (PTCA) and stent therapy from November 2006 through May 2007. We examined plasma levels of ET-1 and U-II in 40 patients with CHD and 40 age-matched healthy subjects by radioimmunoassay (RIA). Chi-square test, Student's t-test, and one-way analysis of variance were used for statistical analyses. Correlations between variables were tested by simple linear regression analysis. Coronary heart disease patients had significantly higher ET-1 and UII levels than healthy controls (20.05 +/- 4.65 vs 8.16 +/- 3.38 and 71.90 +/- 11.61 vs 20.89 +/- 7.00 pg/ml, respectively, all P < 0.01). Importantly, plasma levels of U-II and ET-1 were correlated in patients with CHD (r = 0.64, P = 0.01). On day 1 after PTCA and stent therapy, plasma levels of ET-1 and U-II were significantly higher, by 99% and 25%, respectively, than those before therapy (all P < 0.01). On day 3 after therapy, ET-1 levels were higher by 25% (P < 0.01) than before therapy, and U-II levels decreased rapidly and were close to baseline levels (P > 0.05). On day 7 after therapy, CHD patients had significantly lower ET-1 and U-II levels than before therapy (all P < 0.01). Since ET-1 and U-II levels may be increased in plasma of patients with CHD, their activation might have clinical significance in terms of early intervention in patients with CHD, especially after PTCA and stent therapy.