Prevalence of Inflammatory Gene Polymorphisms in Nonvalvular Atrial Fibrillation Patients

Abstract number: P1723

Gori¹ AM, Gensini² F, Cecchi¹ E, Brogi¹ D, Michelucci¹ A, Padeletti¹ L, Porciani¹ MC, Prisco¹ D, Abbate¹ R, Gensini¹ GF

¹¹Department of Medical and Surgical Critical Care, Thrombosis Centre, University of Florence; Azienda Ospedaliero-Universitaria Careggi, Florence, Italy ²²Department of Clinical Pathophysiology, Unit of Medical Genetics, University of Florence, Italy

Nonvalvular atrial fibrillation (NVAF) is the most common arrhythmia in clinical practice and is a potential cause of thromboembolic events. Recently, the involvement of inflammatory processes in NVAF has been suggested, but no data are available on genetic polymorphisms of the inflammatory markers in NVAF. We investigated the prevalence of C-Reactive Protein (CRP) 1059G/C, Interleukin 6 (IL-6) -174G/C, and Interleukin 1Beta (IL-1Beta) -511 C/T promoter polymorphisms in 195 patients with AF (mean age 73 ± 8; 107M / 88F) and in 390 apparently healthy subjects. One hundred and six NVAF patients had history of ischemic event(s): ischemic stroke (n= 67), and transient ischemic attack (TIA) (n= 39). In 89 NVAF patients no history of arterial ischemia was registered. CRP 1059G/C, IL-6 -174G/C and IL-1Beta -511 C/T polymorphisms were analyzed by PCR and by microarray technology using electronic chip (Nanogen technology). Both in patients with NVAF and in control subjects the analyzed genotype distributions were in Hardy-Weinberg equilibrium. The analysis of CRP 1059G/C and IL-6 -174G/C polymorphisms showed no significant differences in genotype distribution between NVAF patients and control subjects. The prevalence of IL-1Beta -511 TT and CT genotypes in NVAF patients was lower (62.0%) but not significantly (P= 0.051) different than that found in control subjects (69.2%). No significance differences in genotype distribution of CRP 1059G/C, IL-6 -174G/C and IL-1Beta -511 C/T polymorphisms between NVAF patients with history of ischemic events and NVAF patients without history of arterial ischemia were observed. Similarly, the genotype distribution of the inflammatory gene polymorphisms did not differ between patients with chronic (n= 142) or paroxysmal (n= 53) NVAF. The percentage of AF patients with more than two rare variants of inflammatory genes was significantly (P < 0.05) lower (44.6%) than that found in control subjects (55.2%). In conclusion, our data showed a trend towards a significant difference in genotype distribution of the IL-1Beta polymorphism in relation to AF.