Although low-grade inflammation has been linked to the prediction of atrial fibrillation (AF), evidence from some reports suggest that autoimmune activation might potentially be a relevant mechanism. We assessed the predictive value of inflammation and other markers for the risk of incident AF.
A score of age-controlled anthropometric, lipid, and nonlipid variables was compared in participants with recorded nonvalvular persistent/permanent AF (n = 110) to those of a nested cohort sample (n = 1126) of the Turkish Adult Risk Factor study. Available values preceding by 2 (±1) years the development of AF were used regarding incident AF (n = 87) in multivariable regression.
Comparing age-controlled inflammation and other markers across the 2 groups, low apolipoprotein (apo) B and total cholesterol levels differed highly significantly in each sex. Moreover, low-density lipoprotein (LDL)-cholesterol and fasting insulin concentrations were significantly lower, sex hormone binding globulin (SHBG), glucose and systolic blood pressure higher in women alone, while C-reactive protein levels were similar. A model of multivariable logistic regression analyses for overall AF and 2 models for incident AF demonstrated a consistent inverse predictive value for apoB in each gender [relative risk (RR) 0.44 (95% confidence interval (CI), 95% CI 0.30–0.66], along with age, as main determinants. SHBG in females and waist circumference in males were further significantly associated with initial AF. Never smoking (compared with ever smoking) tended to predict AF.
These findings, collectively, are highly consistent with an autoimmune process in which damaged epitope of apoB due to proinflammatory state emerge as a basic mechanism in the development of AF. ApoB level is likely only apparently reduced due to partial escape from assay.