Evaluation of the Serum Levels of Uric Acid and C-reactive Protein in Isolated Coronary Artery Ectasia

Abstract

Introduction: Isolated coronary artery ectasia (CAE) is defined as the arterial enlargement of 1.5 times or more compared to the adjacent normal arterial portion without significant coronary artery stenosis. Although the exact cause is not clearly known, increased inflammation is the most responsible factor in pathogenesis of CAE. Serum uric acid (SUA) and C-reactive protein (CRP) are the most widely used markers of inflammation. In this study, we aimed to investigate the possible association of isolated CAE with SUA and CRP levels.Patients and Methods: In this study, 4.600 patients undergoing coronary angiography in our hospital due to a known or suspected ischemic heart disease between January 2011 and August 2012 were retrospectively evaluated. Following the exclusion criteria, our study population consisted of 110 (63.6% males, mean age: 58.1±9.5 years) isolated CAE patients, 110 patients (63.6% males, mean age: 55.2.4±2.3 years) with coronary artery diseases (CAD) who were matched with this group in age, gender and cardiovascular risk factors (body mass index, hypertension, diabetes, hyperlipidemia and smoking status) and 100 patients with angiographically normal coronary arteries (51.0% males; mean age: 57.6±10.1 years). Basal SUA and CRP are routinely measured in our clinic before the coronary angiography.Results: Serum level of uric acid did not show a significant difference between CAE and CAD groups (6.5±0.5 mg/dL and 6.4±0.5 mg/dL; p>0.05), while this value was found significantly higher in both groups compared to the controls (5.1±0.5 mg/dL; p<0.001). Similarly, there was not a significant difference between CAE and CAD groups in terms of the serum level of CRP (1.8±0.0 mg/dL and 1.7±0.3 mg/dL; p>0.05), while CRP values were significantly higher in both groups compared to the controls (1.1±0.4 mg/dL; p<0.001).Conclusion: We found that levels of SUA and CRP were higher in the patients with CAE than in subjects with normal coronary artery, but no significant different was found compared to patients with CAD. These data suggest that both CAE and CAD shared common pathophysiological mechanisms.