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

70Oral Communicationsdata strenghten the possibility that HcV infectionfacilitates the occurrence of carotid atheroscleroticlesions, independently from the major risk factors foratherosclerosis, possibly by potentiating lipid oxidation.allele increased in the patient genotype (VV=13.8±4.9; VL=10.8±3.0; LL=7.0±0.1; p=0.001). Finally,Kaplan-Meier and log rank were used to comparesurvivals among FXIIIA genotype (Figure).CO-096FXIII-A V34L AND FXIII-B H95R GENE POLYMORPHISMS:EFFECTS ON THE EFFICACY OF THROMBOLYTIC THERAPYIN ACUTE MYOCARDIAL INFARCTIONGemmati D, Tognazzo S, Serino Ml, Catozzi L,Ferrara R,* Campo G,* Ferrari R,* Scapoli GLCenter Study Haemostasis & Thrombosis andDepartment of Cardiology,* University of Ferrara,Ferrara, ItalyThrombolysis (TBL) is the most efficacious pharmacologicaltreatment in patients with ST-elevationacute myocardial infarction (AMI). The efficacy ofTBL relies on the capability to achieve a rapid reperfusionof the infracted myocardial area, minimizingthe occlusion time of the culprit coronary artery bythrombus dissolution and by prevention of arteryreocclusion. However, approximately half of treatedpatients fails to achieve an optimal tissue reperfusion.The aim of our study was to evaluate theeffects, if any, of two common FXIII gene polymorphismson non-invasive parameters of myocardialreperfusion and on 1-year event-free survival inpatients undergoing systemic TBL. The most readilyuseful tool for assessing reperfusion is the extent ofST-segment reduction from the baseline electrocardiogram:a reduction ≥50% within the first 60-180minutes after therapy is a validate marker of successfulreperfusion. Factor XIII plays a crucial role inthrombus organization and its variants have beendescribed affecting XL-fibrin structure. Therefore, weevaluated in 318 consecutive patients with AMI andin 440 healthy controls the gene distribution of twocommon FXIII polymorphisms (FXIII-A V34L and FXI-II-B H95R). The FXIIIA-L34 allele was underrepresentedin cases (20% vs 25%; p=0.03) whereas theFXIIIB-R95 allele was underrepresented in controls(10% vs 6.2%; p=0.014). Among the whole group ofAMI, those eligible for TBL therapy were 31.4%(n=100). The effects of the thrombolytic agent used(rt-PA, Actilyse, Boehringer) were analyzed by evaluatingthe extent of reduction of ST-segment (≥50%in 90 min) and monitoring an early CPK peak appearance(≤12h). Data retrospectively stratified by FXIIIgenotypes showed a significant higher number ofcases with ST-segment reduction (≥50%) in the FXI-IIA-L34 carriers with respect to the VV subgroup(93.6% vs 70.1%; p=0.01) and an earlier achievement(h) of the CPK peak as the number of the L34The incidence for adverse cardiac thrombotic eventsat 365 days was 52.3% and 14.3% respectively for theVV and the L-carrier subgroup (p=0.001). No significativedifferences were obtained computing the FXI-IIB polymorphism data. Our results suggest a key roleof the FXIIIA-L34 allele in modulating the effect ofcoronary TBL, achieving an optimal reperfusion aftertherapy and significantly reducing the incidence ofmajor adverse cardiac events.CO-097SOLUBLE CD40 LIGAND AND STROKE IN PATIENTS WITHNONVALVULAR ATRIAL FIBRILLATIONDi Lecce VN,* Fimognari F, Ferro D, Loffredo L,Del Ben M, Milite MT,^ Sbrighi P, Alessandri C,Violi FDivisione IV Clinica Medica, Policlinico Umberto I,Università “La Sapienza” Rome, Italy, *U.O.C. MedicinaInterna, Ospedale L. Parodi-Delfino, ASL RM G,Colleferro, Italy; ^Servizio di Patologia dell’Emostatsi,Ospedale L. Parodi-Delfino, ASL RM G, Colleferro,ItalyAim. Among patients with nonvalvular atrial fibrillation(NVAF) several clinical characteristics identifypatients at high risk for stroke, but no plasmamarkers have yet been shown to predict stroke. Theobjective of this study was to assess whether solubleCD40 ligand (sCD40L), a marker of platelet activationwith proimflammatory and prothromboticactivity, is associated with ischemic stroke in patientswith NVAF. Methods and Results: One hundred andfifty-nine consecutive patients with NVAF, admittedto our division were evaluated between March 2000and July 2003; forty five NVAF patients (28.3% of159 patients) had a clinical history of previousischemic stroke. Thirty healthy volunteers matchedfor age were used as controls. Compared to controls,haematologica vol. 89(suppl. n. 8):september 2004