Demir Bulent, Caglar Ilker Murat, Tureli Hande Oktay, Pirhan Osman, Aciksari Gonul, Gedikbasi Asuman, Zorkun Cafer, Demir Esra, Karakaya Osman
Clin Lab. 2014;60(11):1909-20. doi: 10.7754/clin.lab.2014.140316.
The aim of this study was to evaluate the serum soluble CD40 ligand (sCD40L) levels, serum uroten- sin II levels, and serum leptin levels as an indirect indicator of endothelial dysfunction, inflammation, and atherosclerosis at the microvascular level, and the comparison of those values with those of the control group with a nor- mal coronary flow pattern.
The study included 35 consecutive patients (17 women, 18 men; average age: 51.20 ± 10.93 years) in our hospital who underwent coronary angiography due to objective myocardial ischemia and in whom slow coronary flow was detected. The control group included 34 consecutive patients with normal coronary flow pattern (18 women, 16 men; average age: 54.59 ± 12.40 years). The coronary flow rates of all patients and control subjects were documented by the thrombolysis in myocardial infarction (TIMI) frame count. Serum sCD40L concentrations, serum urotensin II concentrations and serum leptin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available kits.
The corrected TIMI frame count for LAD, Cx, RCA, and mean TIMI frame count were significantly higher in patients with slow coronary flow (SCF), compared to subjects with normal coronary flow (43.8 ± 1.7 vs. 17.7 ± 4.7, p < 0.001; 27.9 ± 6.9 vs. 11.9 ± 4.8, p < 0.001; 25.4 ± 8.4 vs. 11.1 ± 3.1, p < 0.001; and 32.3 ± 6.4 vs. 13.7 ± 5, p < 0.001, respectively). The serum soluble CD40 ligand and serum urotensin II levels were significantly higher in the slow coronary flow group compared to the control group (12.00 ± 5.43 ng/mL--6.49 ± 5.03 ng/mL, p < 0.001; and 50.94 ± 34.28 pg/mL--26.91 ± 11.52 pg/mL, p < 0.001, respectively). In addition, there was no statistically significant difference between the slow coronary flow group and the control group with regard to serum leptin levels and hs-CRP levels (both p > 0.05).
This study suggests that soluble CD40 ligand and urotensin II likely play a role in the pathogenesis of slow coronary flow.
本研究旨在评估血清可溶性CD40配体（sCD40L）水平、血清尾加压素II水平和血清瘦素水平，以此作为微血管水平内皮功能障碍、炎症和动脉粥样硬化的间接指标，并将这些值与具有正常冠状动脉血流模式的对照组进行比较。
本研究纳入了我院35例因客观心肌缺血接受冠状动脉造影且检测到冠状动脉血流缓慢的连续患者（17例女性，18例男性；平均年龄：51.20±10.93岁）。对照组包括34例具有正常冠状动脉血流模式的连续患者（18例女性，16例男性；平均年龄：54.59±12.40岁）。所有患者和对照者的冠状动脉血流速率通过心肌梗死溶栓（TIMI）帧数记录。血清sCD40L浓度、血清尾加压素II浓度和血清瘦素浓度采用酶联免疫吸附测定法，使用市售试剂盒进行测量。
与冠状动脉血流正常的受试者相比，冠状动脉血流缓慢（SCF）患者的左前降支（LAD）、回旋支（Cx）、右冠状动脉（RCA）校正TIMI帧数和平均TIMI帧数显著更高（分别为43.8±1.7对17.7±4.7，p<0.001；27.9±6.9对11.9±4.8，p<0.001；25.4±8.4对11.1±3.1，p<0.001；以及32.3±6.4对13.7±5，p<0.001）。冠状动脉血流缓慢组的血清可溶性CD40配体和血清尾加压素II水平显著高于对照组（分别为12.00±5.43 ng/mL对6.49±5.03 ng/mL，p<0.001；以及50.94±34.28 pg/mL对26.91±11.52 pg/mL，p<0.001）。此外，冠状动脉血流缓慢组与对照组在血清瘦素水平和高敏C反应蛋白（hs-CRP）水平方面无统计学显著差异（p均>0.05）。
本研究表明可溶性CD40配体和尾加压素II可能在冠状动脉血流缓慢的发病机制中起作用。
