ArticleIndian heart journal
Infectious agents, protein electrophoresis and immunoglobulin levels in patients with coronary artery ectasia.
Article in Indian heart journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
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6 authors.
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Abstract
backgroundAlthough the mechanism of coronary artery ectasia (CAE) shares the common pathophysiologic steps resembling those of atherosclerosis, there are certain discrepancies or aspects incompatible with atherosclerosis. Therefore, we hypothesize that the pathophysiology of CAE might differ from that of atherosclerosis in terms of inflammatory parameters, infectious agents and the read out of protein electrophoresis. MATERIALS AND
methodsSeventy patients with coronary artery disease (CAD) and 30 patients with both CAD and CAE comprised the study populations. Blood samples were centrifuged for the measurement of IgG antibodies against C.pneumoniae and H.Pylori, alongside with total IgE, IgG levels and protein electrophoresis.
resultsThere were not statistically significant differences between patients with and without CAE regarding the complete blood counting and routine biochemical laboratory parameters except hemoglobin levels. Among other studied laboratory parameters, IgE, Alpha 2 macroglobulin, Beta-1 globulin levels were found to be higher in patients with CAE + CAD than those of CAD alone. Logistic regression analysis by including the variables IgE, Hb, Alpha 2 macroglobulin, beta-1 globulin, and gender, revealed that Ig E (Odd ratio:1.004 85 % CI: 1.000-1.008, p = 0.01) and alpha 2 macroglobulin (Odds ratio: 9.41, 95 %CI: 1.69-52.28, p = 0.028) were independently and positively associated with the presence of CAE.
conclusionIndependent 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. Comparable activity of humoral immunity measured by IgG antibody against C.Pneumoniae, and H. Pylori has suggested that these infectious agents do not play an additional role in the pathogenesis of CAE.
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