الفهرس | Only 14 pages are availabe for public view |
Abstract Coronary artery ectasia (CAE) is an uncommon angiographic finding, the prevalence in most series ranges from 1.2% (Swanton et al., 1978). To 5.3% (Demopoules et al. 1997). The most accepted definition for CAE was provided by Hartnell et al. (1985) who defined CAE as arterial segment with a diameter of at least 1.5 times the diameter of adjacent normal coronary artery segment. CAE was classified to • Diffuse ectasia or localized ectasia. • Fusiform or Saccular ectasia • Atherosclerosis is the most common cause of CAE and there is a high association of CAE with stenotic coronary artery disease (Demeopoulos et al., 1997). • CAE is not an innocent condition even patient with pure ectasia with out stenosis may present by chronic stable angina pectoris, unstable angina, myocardial infarction and heart failure (Kruger et al., 1999). A well established medical therapy for CAE is not available but an appropriate regimen suggested by Sorrel et al. (1998) included oral anticoagulants, antiplatelets and calcium channel blockers therapy. Immune cells appear to be critical in development of atherosclerosis. High levels of neopterin was found in patient with chronic stable angina pectoris and acute coronary syndrome (Schumacher et al., 1997). Neopterin is a marker of immune system activation and can be used as a marker for activity of coronary artery disease (Garcia et al., 2002). Aim of the study Measurement and correlation of the levels of neopterin to the presence or absence of CAE in patients with stable coronary artery disease. |