Comparison between High SensitiveC-Reactive Protein, Interleukin-6 Levels and White Blood Cell Count in Patients with Coronary Artery Ectasia, Obstructive Coronary Artery Disease and Normal Epicardial Coronary Arteries

Document Type : Original Article


1 Department of Cardiology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, IR Iran.

2 Department of Biostatics, School of Public Health, Hamedan University of Medical Sciences, Hamedan, IR Iran.


Background-Coronary artery ectasia (CAE) is a clinical entity characterized by localized or
diffused dilatation of at least 1.5 times that of the normal adjacent segments of the vessel. It
was once thought of as a variant of atherosclerosis. The role of inflammation in
atherosclerosis is increasingly well known; however, the association between inflammation
and CAE has been controversial. The aim of this study was to investigate the possible
relationship between leukocyte count and other leukocyte subtypes, the plasma levels of high
sensitive C-reactive protein (CRP), and interleukin-6 (IL-6) and the coronary ecstatic process
and compare these markers between obstructive coronary artery disease (CAD) patients and
normal controls.
Methods- We enrolled 29 patients with CAE and non-obstructive CAD, 29 with obstructive CAD,
and 30 normal epicardial coronary according to coronary angiography results. The peripheral
blood was taken, and white blood cell count (WBCC) as well as leukocyte subtypes, including
neutrophils, lymphocytes, and monocytes cell count, was measured. The plasma levels of high
sensitive CRP and IL-6 were determined using the ELISA as well.
Results- A higher number of neutrophils and monocytes were found in the patients with CAE as
well as obstructive CAD compared with the normal controls (p value = 0.021). Moreover,
levels of plasma high sensitive CRP and IL-6 were also significantly higher in the patients
with CAE and in the patients with obstructive CAD than those without CAD (p value <
Conclusion- This study demonstrated and expanded prior limited findings showing that significant
chronic inflammation may have a relationship with the pathogenesis of CAE, which was
associated with not only increased inflammatory markers but also inflammatory cells in the
patients with CAE (Iranian Heart Journal 2013; 14 (1):11-17).


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