Haematologica 2004;89: supplement no. 8 - Supplements ...

50Oral Communicationsthe Table, as% of stimulated controls (PMA). Theinhibitory effect by rosiglitazone was completelyreverted by the PPARγ antagonist bisphenol A diglycydilether (BADGE; 50 mmol/L) which, in the sameexperimental conditions, did not affect the PMAmediatedinduction of COX-2. In parallel, only rosiglitazonereduced the release of MMP-9 without affectingthe activity of other MMPs investigated (MMP-1and 2 and 3) at gelatin zimography and enzymeimmunoassay. Rosiglitazone reduces the inducedexpression of COX-2 as well as the stimulated releaseof MMP-9 in HUVEC. This effect occurs through aPPARγ-dependent mechanism since it is completelyreverted in the presence of BADGE. These antiinflammatoryand anti-angiogenic effects may contributeto vasculoprotection by PPARγ agonists invivo.CO-058PREVALENCE OF INFLAMMATORY GENE POLYMORPHISMS INNONVALVULAR ATRIAL FIBRILLATION PATIENTSGori AM, Gensini F, # Cecchi E, Innocenti D, Poli D,°Sticchi E, # Michelucci A, Padeletti L, Porciani MC,Prisco D, Abbate R, Gensini GFDepartment of Medical and Surgical Critical Area,University of Florence; °Dipartimento Cardiologicoe dei Vasi, Azienda Ospedaliera Universitaria, Florence;# Department of Clinical Pathophysiology,University of Florence, ItalyNonvalvular atrial fibrillation (NVAF) is the mostcommon arrhythmia in clinical practice and is apotential cause of thromboembolic events. Recently,the involvement of inflammatory processes inNVAF has been suggested, but no data are availableon genetic polymorphisms of the inflammatorymarkers in NVAF. We investigated the prevalence ofC-Reactive Protein (CRP) 1059G/C polymorphism,Interleukin 6 (IL-6) -174G/C promoter polymorphism,and Interleukin 1β (IL-1β) -511 C/T promoter polymorphismin 195 patients with AF (mean age 73±8;107 males and 88 females) and in 390 apparentlyhealthy subjects. One hundred and six NVAF patientshad history of ischemic event(s): ischemic stroke(n=67), and transient ischemic attack (TIA) (n=39). In89 NVAF patients no history of arterial ischemia wasregistered. CRP 1059G/C, IL-6 -174G/C and IL-1β -511 C/T polymorphisms were analyzed by PCR and bymicroarray technology using electronic chip (Nanogentechnology). Both in patients with NVAF and incontrol subjects the analyzed genotype distributionswere in Hardy-Weinberg equilibrium. The analysis ofCRP 1059G/C and IL-6 -174G/C polymorphismsshowed no significant differences in genotype distributionbetween NVAF patients and control subjects.The prevalence of IL-1Beta -511 TT and CTgenotypes in NVAF patients was lower (62.0%) butnot significantly (p=0.051) different than that foundin control subjects (69.2%). No significance differencesin genotype distribution of CRP 1059G/C, IL-6-174 G/C and IL-1β -511 C/T polymorphismsbetween NVAF patients with history of ischemicevents and NVAF patients without history of arterialischemia were observed. Similarly, the genotypedistribution of the inflammatory gene polymorphismsdid not differ between patients with chronic(n=142) or paroxysmal (n=53) NVAF. The percentageof AF patients with more than two rare variantsof inflammatory genes was significantly (p