Infectious agents, protein electrophoresis and immunoglobulin levels in patients with coronary artery ectasia

Abstract Background Even the mechanism of coronary artery ectasia (CAE) shares the common pathophysiologic steps and risk factors with atherosclerosis which led to assume that CAE is a variant of atherosclerosis, there are certain discrepancies or aspects incompatible of atherosclerosis. Purpose We hypothesized that pathophysiology of CAE might differ from that of atherosclerosis in terms of inflammatory parameters, infectious agents. Therefore, we assessed and compared the levels of IgG antibody against Chlamydia pneumonia, and Helicobacter Pylori, components of serum protein electrophoresis and plasma levels of total Ig G and Ig E. Materials and methods Seventy patients with coronary artery disease (CAD) and 30 patients with CAD coexisted with CAE comprised the study populations. Blood samples were allowed to clot at room temperature then centrifuged at 1500 rpm for 5 minutes then serum kept at deep freeze (−20°C) to be used for the measurement of IgG antibodies against C. pneumoniae and H. Pylori, total IgE, IgG levels and protein electrophoresis. Results There were not statistically significant differences between patients with and without CAE regarding the clinical and laboratory parameters except hemoglobin levels (Figure I). IgE, Alpha 2 macroglobulin, Beta-1 globulin levels were found to be higher in patients with CAE+CAD than those of CAD alone (Figure IIa). There was no statistically significant correlation between the Gensini score, and IgG antibody against H. Pylori (r=0.048, p=0.66) and C. Pneumoniae (r=−0.12, p=0.27) regarding the whole study population. Additionally, logistic regression analysis by including variables IgE, hemoglobin, Alpha 2 macroglobulin, beta-1 globulin, and gender, revealed that Ig E and alpha 2 macroglobulin were independently and positively associated with the presence of CAE (Figure IIb). Conclusion Independent association of serum IgE levels and alpha2 globulins with the presence of CAE underlines the divergent features of pathophysiology of CAE compared with atherosclerosis or CAD alone. Funding Acknowledgement Type of funding sources: None. Figure IFigure II