冠状动脉扩张患者血清不对称二甲基精氨酸水平的评估

O. Çelik, B. Çabuk, E. Demirci, M. Kalçık, L. Bekar, M. Yetim, T. Doğan
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引用次数: 0

摘要

背景:先前的研究表明,不对称二甲基精氨酸(ADMA)水平与心血管疾病(包括内皮功能障碍和动脉粥样硬化)密切相关。冠状动脉扩张(CAE)的特征是心外膜冠状动脉局部或弥漫性非阻塞性病变,其管腔扩张超过正常邻近段或血管直径的1.5倍。冠状动脉扩大的发病机制尚不清楚,其临床意义也尚不清楚。在本研究中,我们旨在探讨血清ADMA水平在CAE发病机制中的作用。方法:27例CAE患者(女性占51.9%;平均年龄:60.2±7.4岁),对照组29例(女性:55.2%;平均年龄59.3±6.9岁,冠状动脉血流正常。根据CAE的范围和涉及的血管数量进行分类(Markis分类)。采用静脉血样品的酶法测定血清ADMA水平。结果:CAE患者与对照组在人口学参数方面无显著差异。CAE组血清ADMA水平较高,但差异无统计学意义(1.22±0.13∶1.16±0.12 μM/L;p = 0.091)。在亚组分析中,弥漫性CAE患者血清ADMA水平显著高于对照组(1.25±0.11∶1.16±0.12 μM/L;p = 0.024)。结论:ADMA水平升高可能在弥漫性CAE发病机制中起重要作用。需要进一步的大规模研究来确定ADMA水平与CAE之间的关系。这些发现提示ADMA水平升高可能与内皮功能障碍相关,从而导致CAE的发生。*通讯:土耳其希提特大学医学院心脏病学系Macit Kalcik, Çorum,电话:(90)536 4921789,电子邮件:macitkalcik@yahoo.com
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Assessment of serum asymmetric dimethyl arginine levels in patients with coronary artery ectasia
Background: Previous studies have demonstrated that asymmetric dimethyl arginine (ADMA) levels were strongly associated with cardiovascular diseases including endothelial dysfunction and atherosclerosis. Coronary artery ectasia (CAE) has been characterized as a localized or diffuse non-obstructive lesion of the epicardial coronary arteries with a luminal dilation exceeding 1.5-fold the normal adjacent segment or vessel diameter. The etiopathogenesis of this coronary enlargement is completely unknown, and its clinical significance also remains poorly understood. In this study, we aimed to investigate the role of serum ADMA levels in the pathogenesis of CAE. Methods: Twenty-seven patients with CAE (female: 51.9% ; mean age: 60.2 ± 7.4 years) and 29 controls (female: 55.2% ; mean age: 59.3 ± 6.9 years) with normal coronary flow were included in this study. CAE was classified according to its extent and number of vessels involved (Markis classification). Serum ADMA levels were determined by using enzymatic assays from venous blood samples. Results: There was no significant difference in terms of demographic parameters between the patients with CAE and the controls. Serum ADMA levels were higher in the CAE group, however this was not statistically significant (1.22 ± 0.13 vs. 1.16 ± 0.12 μM/L; p=0.091). In subgroup analysis, serum ADMA levels were significantly higher in patients with diffuse CAE as compared to controls (1.25 ± 0.11 vs. 1.16 ± 0.12 μM/L; p=0.024). Conclusion: Increased ADMA levels may play an important role in the pathogenesis of diffuse CAE. Further large-scale studies are required to determine the relationship between ADMA levels and CAE. These findings suggest that increased ADMA level may be associated with endothelial dysfunction leading to the development of CAE. *Correspondence to: Macit Kalcik, Department of Cardiology, Hitit University Faculty of Medicine, Çorum, Turkey, Tel: (90)536 4921789, E-mail: macitkalcik@yahoo.com
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