BACKGROUND: Coronary artery ectasia (CAE) has been defined as localized or diffuse dilatation of epicardial coronary arteries. The elevation of levels of inflammatory marker, such as C-reactive protein (CRP), has been associated with an increased risk for cardiovascular disease. In addition, inflammation has been reported to be an important component of vascular aneurysm formation. The relation between CAE and plasma CRP levels has not been investigated previously. METHODS: The study population was selected from a series of 2,200 consecutive patients who underwent coronary angiography. Clinical, angiographic results, and hsCRP were analyzed in patients with isolated CAE (Group I: n=15). During the same period, we randomly selected 30 patients with coronary stenosis form the atherosclerotic control group (Group II: n=30) and 30 control subjects with angiographically normal coronary arteries to form the healthy control (Group III, n=30). All patients had typical angina and positive or equivocal results of noninvasive stress tests. RESULTS : Baseline clinical characteristics such as age, sex, clinical diagnosis, medication, atherosclerotic risk factor were similar between the 3 groups. Among the CAE group, the extent of CAE were 1 vessel (20%), 2 vessel (33.3%), and 3 vessel (46.7%). Plasma hs-CRP levels were found significantly higher in group I ( isolated CAE) compared with group II (2.05짹0.78 vs 1.43짹0.59 mg/L, respectively, p<0.01) and group III (2.05짹0.78 vs 0.46짹0.29 mg/L, respectively, p<0.01). Group II patients had significantly higher levels of hs-CRP compared with group III subjects (1.43짹0.59 vs 0.46짹0.29 mg/L, respectively, p<0.01). Patients with multivessel CAE had significantly higher hs-CRP levels compared with single vessel CAE (2.35짹0.88 vs 1.33짹0.61 mg/L, respectively, p<0.01). Positive correlation was detected between the presence of CAE and levels of hs-CRP (r=0.6, p<0.01). CONCLUSION: This study showed that CAE have significantly higher hsCRP levels than patients with coronary stenosis and normal subjects. This findings suggest that aggessive inflammation may be involved in the pathogenesis of CAE.