O. Çelik, B. Çabuk, E. Demirci, M. Kalçık, L. Bekar, M. Yetim, T. Doğan
{"title":"Assessment of serum asymmetric dimethyl arginine levels in patients with coronary artery ectasia","authors":"O. Çelik, B. Çabuk, E. Demirci, M. Kalçık, L. Bekar, M. Yetim, T. Doğan","doi":"10.15761/jic.1000270","DOIUrl":null,"url":null,"abstract":"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","PeriodicalId":91545,"journal":{"name":"Journal of integrative cardiology","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of integrative cardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15761/jic.1000270","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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