Clinical and Angiographic Characteristics of Coronary Artery Ectasia and Its Correlation with High-Sensitivity C-Reactive Protein and Serum Uric Acid

Abstract

Introduction: The most plausible factor for coronary artery ectasia (CAE), a subset of coronary artery disease (CAD), is extensive inflammation. High-sensitivity C-reactive protein (hs-CRP) and serum uric acid (sUA) are well known markers of inflammation. Most of the previous studies (done in the Western population and of Middle East Asia) evaluated their role individually as a marker of inflammation in CAD. We aimed to investigate the possible association of isolated CAE with inflammation as assessed by the hs-CRP and sUA levels and check whether the inflammatory hypothesis holds good in the south Asian population. Materials and Methods: Patients admitted for coronary angiography with age ≥30 years were evaluated. Patients with both CAE and CAD were excluded. A total of 60 patients were studied. Patients with isolated CAE (30) were compared with an equal number of patients with obstructive CAD (30) and their clinical profile was studied. The hs-CRP, sUA, and novel inflammatory markers such as neutrophil–lymphocyte ratio (NLR), mean platelet volume (MPV), and red cell distribution width (RDW) were compared between the groups. Results: Of the 60 patients studied, males were 56% in the isolated CAE group and 50% in the obstructive CAD group. The hs-CRP (2.39 ± 0.41 vs. 1.41 ± 0.29, P < 0.001) and sUA levels (6.46 ± 0.58 vs. 5.36 ± 0.40, P < 0.001) were significantly elevated in the isolated CAE group compared to the obstructive CAD group. Among the novel inflammatory markers, the NLR (3.98 ± 0.42 vs. 2.91 ± 0.30, P < 0.001) and RDW (12.69 ± 0.27 vs. 12.13 ± 0.48, P < 0.001) were significantly higher in the CAE group compared to obstructive CAD group, whereas the MPV did not have a statistically significant difference (9.5 ± 0.98 vs. 9.6 ± 1.08, P = 0.525). Conclusion: The inflammatory etiology of CAE was supported by an elevated hs-CRP, sUA, and other novel inflammatory markers compared to the atherosclerotic obstructive CAD group.