Association of Inflammation With Markers of Atherogenicity in Subjects With New-Onset Atria Fibrillation in a Nigerian Community

Abstract

Abstract Objectives The evidence supporting the role of circulating markers of inflammation in the pathogenesis of atria fibrillation remains controversial. This study investigated the levels of serum lipids, C-reactive proteins, erythrocyte sedimentation rate, prothrombin time, and platelet count in subjects with new-onset atria fibrillation (NAF), but with no established cardiac disease, in a Nigerian community. Methods The case control study involved a total of 200 subjects: 110 subjects with NAF and 90 apparently healthy subjects without AF, as control. AF was confirmed by a 12-lead electrocardiogram (ECG), while excluding subjects with high risk. Blood samples from the subjects were analyzed for the following parameters: C-reactive proteins using ELISA method and serum lipids using an enzymatic, colorimetric method; erythrocyte sedimentation rate, by Westergreen method; platelet count using a Midray hematology auto analyzer; and the prothrombin time using a tissue thromboplastin method. Data collected from the result were analyzed using SPSS version 15. Results There was a significant increase in the levels of C-reactive proteins and ESR in subjects with NAF when compared with the control subjects. A significant increase was observed in the mean values of total cholesterol and low-density lipoproteins in subjects with NAF, while that of high-density lipoproteins was lower in NAF than in controls. There was no significant difference in the mean values of triglyceride in NAF and the control. Results also showed significantly reduced prothrombin time, with more platelet count in subjects with NAF. The result demonstrated that females (56.3%) had greater risk of developing AF than males (45.8%), while incidence of AF was observed to increase with age. Conclusion The results of the markers assayed suggest marked dyslipidemia, inflammation, and thrombogenesis in subjects with new-onset AF. Hence dyslipidemia and inflammation play critical roles in the pathogenesis of atria fibrillation.