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Deletion polymorphism of the angiotensin I converting enzyme gene is a potent risk factor for coronary artery ectasia
  1. S Gülec1,
  2. Ö Aras2,
  3. Y Atmaca1,
  4. Ö Akyürek1,
  5. N Q Hanson2,
  6. T Sayin1,
  7. M Y Tsai2,
  8. N Akar1,
  9. D Oral1
  1. 1Department of Cardiology, Medical School of Ankara University, Ankara, Turkey
  2. 2Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, Minnesota, USA
  1. Correspondence to:
    Ömer Aras, MD, Department of Medicine, Division of Hematology, Oncology and Transplantation, 420 Delaware St. SE, Mayo Mail Code 480, Minneapolis, MN 55455-0374, USA;

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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 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.1,2 In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone3 and the development of aneurysms.4 Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE.


We prospectively evaluated 3427 consecutive patients undergoing coronary angiography for the evidence of CAE. Coronary diameters and percent stenosis were measured by using computerised quantitative angiography in a biplane mode (Philips DCI, Eindhoven, Netherlands). CAE was defined as an arterial segment with a diameter of at least 1.5 times the diameter of the adjacent normal coronary artery. If no adjacent normal segment could be identified, the mean diameters of coronary segments in a control group without coronary disease (n = 81) served as normal values.

ACE ID genotype was determined in two groups of patients. Group 1 consisted of 152 patients who were …

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