score. A weak positive correlation was detected between TO and Gensini score (r:0,165, p:0,036) and a weak negative correlation was detected between TS and Gensini score(r:-0,193, p:0,013).When HRV parameters of CAD and control groups were compared; SDNN, SDNN index and LFnu values were found significantly decreased in CAD group (SDNN: 116,3Æ36,3 msvs 131,8Æ39,7 ms, p:0,010; SDNN index: 44,8Æ15 msvs 51Æ16,7 ms, p:0,013; LFnu: 65,9Æ20,2 vs 71,6Æ14,6, p:0,041 in patients with CAD and control group respectively). Also negative correlation between SDNN, SDNN index and Gensini score were found (r:-0,356, p<0.001 and r:-0,270, p:0.001 respectively). Furthermore TO is negative correlated with LFnu, HFnu, and LF/HF ratio (r:-0,277; p<0,001, r:-0,243; p:0,002, r:-0,251, p: 0,001 respectively). TS is positive corelated with RMSSD and SDNN index (r:0,203; p:0,009, r:0,170, p:0,030 respectively). Conclusıons: Our data show that HRT and HRV variables are impaired in patients with CAD patients versus those with control group and weakly correlated with severity of CAD. PP-151 Association of the Factor V Leiden Mutation (1691G>A, Arg534Gln) with Ischemic Stroke in Nonvalvular Atrial Fibrillation in Turkish Population Atilla _ Içli 1 , Nilgün Erten 2 , Yasin Türker 3 , Salaheddin Akçay 4 , Habil Yücel 4 , Erdo gan Yas ¸ar 1 , Mehmet Koray Adalı 4 , Recep Sütçü 5 , Fatih Aksoy 4 1 Department of Cardiology, Ahi Evran University Education and Research Hospital, Kırsehir, 2 Department of Neurology, Giresun University, Giresun, 3 Department of Cardiology, Duzce University, Duzce, 4 Department of Cardiology, Suleyman Demirel University, Isparta, 5 Department of Biochemistry, Katip Celebi University, _ Izmir Background: Factor V Leiden is an inherited disorder of blood clotting. It is a variant of human factor V that causes a hypercoagulability disorder. In this disorder, the Leiden variant of factor V cannot be inactivated by activated protein C. The gene that codes the protein is referred to as facor V. Mutation of this gene a single nucleotide polymorphism (SNP) is located in exon 10. As a missense substitution it changes a protein's amino acid from arginine to glutamine. Factor V Leiden gene is present in 3% of the general population. People who carry the factor V Leiden gene have a fivefold greater risk of thrombosis than the rest of the population. Atrial fibrillation (AF) is the commonest sustained cardiac arrhythmia, which confers a high risk of mortality and morbidity from stroke and thromboembolism We wanted to investigate Factor V Leiden Mutation (1691G>A, Arg534Gln) in patients with AF who have had a stroke than in healthy controls. Methods: The factor V Leiden mutation was analysed in 70 patients with nonvalvuler AF who have had a stroke and 70 healthy individuals with no documented episode of AF matched for age, race and sex. The factor V Leiden mutation was identified by polymerase chain reaction method. Distribution of the factor V Leiden mutation alles (allel G, allel A) and genotypes (Normal (GG) genotype, heterozygous (GA) or homozygous (AA) mutant genotype) were identified in study population. Demo- graphic characteristics and risk factors for AF and stroke were evaluated in the study groups. Results: There was no significant difference with respect to age and gender between groups. Genotype distribution of AF patients who have had a stroke and control groups shown in the table. The frequency of GG normal genotype of the factor V Leiden was significantly lower in patients with AF patients who have had a stroke group compared with control group (57 (81.4%) vs 66 (94.3%), p¼0.02). The frequency of GA genotype heterozygous mutant genotype was significantly higher in AF patients who have had a stroke group than control (12 (17.1%) vs 4 (5.7%), p¼0.034). Between the two groups were compared according to the dominant genetic model (GA+AA vs. GG), The number of patients carrying at least one A mutant allele (GA + AA) was significantly higher in AF patients who have had a stroke group than control (14 (20%) vs 5 (7.1%), p¼0.026). Conclusıons: In this study, our data suggest that the factor V Leiden mutation (1691G>A, Arg534Gln) may be associated with AF patients who have had a stroke from other clinical risk factors, but this should be confirmed in a much larger series of patients. Screening for this mutation may help in identifying patients at risk and in deciding the antithrombotic strategy. PP-152 Effect of smoking on Tp-e interval, Tp-e/QT and Tp-e/QTc ratios as indices of ventricular arrhythmogenesis Hakan Tas ¸olar 1 , Mehmet Ballı 1 , Mustafa Çetin 1 , Burak Altun 2 , Musa Çakıcı 1 , Adil Bayramo glu 3 , Ömür Otlu 3 , Hasan Pekdemir 3 1 Adiyaman University Training and Research Hospital, Department of Cardiology, Adiyaman, 2 18 Mart University, Faculty of Medicine, Department of Cardiology, Canakkale, 3 Inonu University Faculty of Medicine, Turgut Ozal Medical Center, Department of Cardiology, Malatya Background: Smoking may lead to ventricular arrhythmias and sudden cardiac death via altering ventricular recovery time dispersion indices such as QT interval and QT dispersion (QTd). Tp-e/QT ratio and Tp-e/QTc ratio are also known as predictors of ventricular arrhythmogenesis. The aim of our study was to assess effect of smoking on ventricular arrhythmogenesis using Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratios. Methods: 45 chronic smokers and 30 age- and sex-matched non-smoker controls were included in our study. Tp-e interval and Tp-e/QT ratio were measured by 12-lead electrocardiogram, and the Tp-e interval corrected for heart rate. Results: QTd and corrected QT (QTc) were significantly higher in smokers group compared to controls (29.7 Æ 5.6 vs 26.1 Æ 4.4 and 36.1 Æ 8.4 vs 31.1 Æ 4.8 ms, P¼0.008 and P<0.007, respectively). cTp-e interval, Tp-e/QT and Tp-e/QTc ratios were also significantly higher smokers (88.1 Æ 8.5 vs 71.1 Æ 6.8 and 0.24 Æ 0.03 vs 0.17 Æ 0.02 ms, P<0.001 for all). In smoker group, the amount of smoking was correlated both cTp-e interval and Tp-e/QTc ratio (r¼0.72, P<0.001 and r¼0.55, P<0.001, respectively). Conclusıon: We found in our study that cTp-e interval, Tp-e/QT and Tp-e/QTc ratios were increased in smokers and significantly correlated to the amount of smoking. PP-153 Decreased transepicardial dispersion of repolarisation in hypertrabeculation/ noncompaction cardiomyopathy patients Hatice Betül Erer 1 , Tolga Sinan Güvenç 1 , Servet Altay 1 , Elif _ Iclal Çekirdekçi 1 , Nazmiye Özbilgin 1 , Nurten Sayar 1 , Dilaver Öz 1 , Ahmet Ekmekçi 1 , Aycan Zencirci 1 , Gönül Zeren 2 , Osman S ¸ahin 3 , Ahmet Lütfü Orhan 4 , Mehmet Eren 1 1 Dr.Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Center, Department of Cardiology, Istanbul, 2 Ordu State Hospital, Department of Cardiology, Ordu, 3 Seydis ¸ehir State Hospital, Department of Cardiology, Konya, 4 Faculty of Medicine, Medeniyet University, Department of Cardiology, _ Istanbul Purpose: We aimed to evaluate the changes in the TpeakÆTend interval (an index of transmural dispersion of repolarisation) with other traditional electrocardiographic indices of electrical dispersion in patients with hypertrabeculation/noncompaction (HT/NC) cardiomyopathy. Methods: We enrolled 55 (38 men and 17 women; mean age 33Æ15 years) HT/NC cardiomyopathy patients (mean LVEF 44Æ16%) and 18 controls (mean age 31Æ11). Exclusion criteria were as follows: valvular heart disease, other congenital heart diseases, documented coronary artery disease, pulmonary hypertension, chronic renal failure, diabetic neuropathy and patients using digoxin or antiarrhythmic drugs at the time of admission. Twelve-lead ECGs were recorded at a tape speed of 50 mm s-1. QT interval duration and corrected QT interval duration (according to the Bazett's formula) were measured manually after twofold magnification. The following parameters were analysed: QTp interval dura- tion (from the onset of the QRS complex to the peak of the T wave); QTe interval duration (from the onset of the QRS complex to the end of the T wave); TpÆTe interval duration (from the peak to the end of the T wave); QT dispersion was measured from all 12 leads (I-V 6). Differences between groups were compared by using Mann Whitney-U test. Results: Corrected values of the QTp, QTe and TpÆTe intervals in the controls and HT/NC cardiomyopathy patients are listed in Table. We found that minimum QT interval was significantly lower in the patient group than the controls (p¼0.016). T wave negativity was more frequent in the HT/NC patients (p¼0.01). Conclusıon: In HT/NC cardiomyopathy patients the transmural dispersion of repo- larization is decreased and it may be associated with increased arrhythmias. Factor V Leiden Mutation (1691G>A, Arg534Gln) genotype frequencies AF patients with stroke (n:70) Control (n:70) P n: % n: % GG genotype 57 81.4 66 94.3 0.020 GA genotype 12 17.1 4 5.7 0.034 AA genotype 1 1.4 0 0 0.316 GA + AA genotypes (Dominant genetic model) 14 20 5 7.1 0.026 C140 JACC Vol 62/18/Suppl C j October 26–29, 2013 j TSC Abstracts/POSTERS POSTERS