Copeptin level in coronary artery ectasia

Coronary heart disease is an important cause of mortality and morbidity. Coronary artery ectasia (CAE), is localized or diffuse enlargement of coronary artery more than 1.5 times in diameter in comparison with adjacent normal coronary artery. Etiology and pathophysiology of CAE is not fully elucidated. CAE caused by atherosclerosis, congenital, inflammatory, or connective tissue diseases is usually asymptomatic but may cause myocardial ischemia and infarction. Plasma concentrations of copeptin are correlated with AVP plasma concentrations. It is more reflective for endogenous stress than the cortisol. In cardiovascular diseases, stroke, sepsis and shock a rapid rise in plasma copeptin is seen. This increase have diagnostic and prognostic value. In the literature, there are no studies evaluating the copeptin levels in serum in patients with CAE. In this study, we aimed to investigate whether copeptinin has a role in coronary artery ectasia etiopathogenesis. Between October 2012-March 2013 in Firat School of Medicine, Department of Cardiology Catheter Laboratory we evaluated randomly 44 patients with a diagnosis of CAE and 44 normal coronary anatomy (NCA) with a total of 88 cases prospectively. Blood samples obtained from patients were stored at -70 º C and copeptin levels in sera were measured by ELISA method. Other necessary biochemical parameters were measured with autoanalyzer. Copeptin levels in CAE group were higher than other groups but were not statistically significant (700.00 ± 190.09 versus, 632.36 ± 217.6, p = 0.81). In subgroup analysis mean copeptin level of the diffuse CAE (Type I, II, III) was 239.08 ± 66.35 pg / mland in Type IV CAE (segmental ectasia) group was 906.62 ± 266.19 pg / ml. Although it did not reach to statistical significance level in patients with CAE high copeptin levels were found. In segmental ectasia (Type IV CAE) group copeptin levels were higher than diffuse CAE (Type I, II, III) and NCA so atherosclerosis is thoght to play a major role in the etiopathogenesis of especially diffuse CAE. For more effective treatment protocols in patients with CAE, more comprehensive studies to demonstrate CAE pathophysiology is needed. Our study is one of the pioneers in this field and will shed light for further studies. Key words: Coronary artery ectasia, copeptin, coronary artery disease