title: The role of angiotensin converting enzyme genotype in coronary artery ectasia.
abstract: Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.
authors.affiliation: Department of Cardiology, Siyami Ersek Cardiovascular and Thoracic Surgery Center, Istanbul, Turkey.
authors.forename: Huseyin
authors.initials: H
authors.lastname: Uyarel
authors.forename: Ertan
authors.initials: E
authors.lastname: Okmen
authors.forename: Zeynep
authors.initials: Z
authors.lastname: Tartan
authors.forename: Hülya
authors.initials: H
authors.lastname: Kasikcioglu
authors.forename: Sennur Unal
authors.initials: SU
authors.lastname: Dayi
authors.forename: Ahmet
authors.initials: A
authors.lastname: Karabulut
authors.forename: Bülent
authors.initials: B
authors.lastname: Uzunlar
authors.forename: Hasan
authors.initials: H
authors.lastname: Samur
authors.forename: Nese
authors.initials: N
authors.lastname: Cam
mesh_terms: D016022:Case-Control Studies; D017023:Coronary Angiography; D003327:Coronary Disease / Q000235:genetics* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D004108:Dilatation, Pathologic / Q000235:genetics / Q000473:pathology; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D012307:Risk Factors
chemical_list: D007703:Peptidyl-Dipeptidase A