Para-Hisian accessory pathway (AP) means the AP locate about 0. 5cm above or under the His bundle. To identify the AP location,the big tip catheter mapping must be under sinus rhythm,ventricular pacing and inducing SVT in order to avoid injury of His bundle. During ablation process, the surface morphology and juctional escape rhythm must be observed. If RF must be done under ventricular pacing, once ablating effect is confirmed,the pacing would be stopped and escape rhythm can be observed. If ante-grade condution are always through AP in SVT and endocardial mapping are confirmed multipe APs and AVN are bystander in SVT, we do not exclude abmormal growth in AVN. It can be ablated retrograde AP to treat SVT and should be avoided to ablate antigrade AP.

Aim To study the influence of rosuvastatin on toll-like receptor 4 ( TLR4 ) , and its downstream nu-clear transcription factor NF-kappa B p65, IκBα, in-flammation factors TNF alpha in rats with myocardial hypertrophy induced by pressure overload .Methods Myocardial hypertrophy was induced by abdominal aor-tic constriction ( AAC ) .Male Wistar rats were divided into 3 groups(n=10):① sham-operated rats(S);②AAC rats(M);③AAC+rosuvastatin(10 mg· kg -1· d-1 ) rats.From 1 week pre-opertion to 4 weeks post-operation, three groups were performed by gavage ad-ministration with equal volume of rosuvastatin and vehi-cle.The rats underwent cardiac color Doppler exami-nation.The level of ANP,TLR4, NF-κB p65,IκBα, TNF-αmRNA and protein expression in myocardium were detected by real-time PCR, Western blot, immu-nohistochemical and ELISA respectively .Results The sizes of heart and cardiomyocytes and the expression of ANP mRNA and TLR4 signaling molecules were signif-icantly increased in group M , which could be blocked by rosuvastatin .TLR4 protein was positively related to ANP, NF-κB p65 and TNF-αrespectively .Conclusion Rosuvastatin prevents cardiac hypertrophy induced by pressure overload , which is associated with its inhi-bition of TLR4, NF-κB and TNF-αin myocardium ex-pression .

Objective To investigate the association of T help (Th) lymphocyte and heart rate variability (HRV) in congestive heart failure (CHF) patients. Methods Ninety-six patients with CHF and thirty healthy persons were enrolled in the study. Time-domain HRV analysis was performed based on 24 hour Holter Electrocardiogram (ECG) monitoring. Interferon-γ (IFN-γ) was used as markers for the differentiation of Th1 subsets and interleukin-10 (IL-10) for the Th2 subsets. IFN-γand IL-10 in CD4 + T lymphocytes were quantified by 3-color flow cytometry. Results The frequency of IL-10-Producing T Cells in the CHF group was significantly lower than those in the healthy control ( ( 16.4 ± 5.8 ) % vs. ( 26.8 ± 3.7 ) %, t = 9. 243, P ＜ 0. 001 ). The frequency of IFN-γ in the CHF group ( ( 18.4 ± 7.3 )% ) was significantly lower than that in the healthy controls ( (7.3 ±4.6) % ,t =7. 917, P ＜ 0. 001 ). The following index of HRV in the CHF groups were all significantly lower than those in the healthy controls: (98. 6 ± 21.3) ms vs. ( 145. 1 ± 42. 6) ms for SDNN, (83. 9 ± 22.4) ms vs.(136.5 ±39.6)ms for SDANN, (40.6 ± 14.5) ms vs. (55.8 ± 17.9) ms for SDNNI, (20. 7 ± 12.9) ms vs.(29.1 ± 12.6) ms for RMSSD, (5.6 ± 3.7 ) % vs. ( 11.8 ± 4.4) % for PNN50 ( Ps ＜ 0.05 ). In CHF patients, the frequency of IL-10 were positively associated with SDNN, SDANN, SDNNI, RMSSD and PNN50 ( r = 0. 49,0. 57,0. 58,0.47 and 0. 52 ,respectively,Ps ＜ 0.01 ). In the CHF patients, the frequency of IFN-γand IFN-γ/IL-10 ratio were negatively associated with SDNN ,SDANN ,SDNNI, RMSSD and PNN50 ( r = - 0. 49, - 0. 54, - 0. 57, - 0.52,- 0.53, - 0. 52, - 0.64, - 0.57, - 0. 58, - 0. 67, Ps ＜ 0. 01 ). Conclusions Autonomic nervous system is involved in the regulation of the balance of Th1/Th2 in patients with CHF. Sympathetic nerve system enhances the effect of Th1 ,whereas parasympathetic nervous system enhances the effect of Th2.

Objective To study the protective effect of fluvastatin on cardiac remodeling and cardiac function, and to investigate its effect on Von Willebrand factor (VWF). Methods The rat model of cardiac heart failure (CHF) was in-duced by isoproterenol injection (170 mg/kg) via subcutaneous. Eighteen model rats were randomly divided into fluvastatin (20 mg ·kg-1·d-1) group, placebo group and control group. Rats were treated with normal saline in placebo group and control group. After 6-week treatment, the structure and function of hearts were measured by echocardiography in three groups. The ventricular weight index, the serum levels of VWF and B-type natriuretic peptide (BNP) were measured by ELISA assay. The levels of VWF mRNA in cardiac muscle were measured by RT-PCR. Results Compared with control group, the val-ues of left ventricular end-diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) were significantly increased in placebo group and fluvastatin group, while values of left ventricular ejection fraction (LVEF) and left ventricular ejection fraction shortening (LVFS) were significantly decreased (P＜0.05). The values of left ventricular wet weight/body weight (LVRW) and right ventricular wet weight/body weight (RVRW) were increased in placebo group and fluvastatin group. The expression of VWF mRNA in cardiac tissues was enhanced significantly (P＜0.01). Compared with placebo group, the values of LVEDD, LVRW and RVRW were significantly decreased in fluvastatin group. The expression of VWF mRNA in cardiac tissues was significantly decreased (P＜0.01), and the values of LVEF and LVFS were significant increased in fluvas-tatin group (P＜0.05). The level of VWF was positively corrected with BNP(r=0.996). Conclusion Fluvastatin could im-prove the cardiac function and cardiac remodeling, which may be by reducing the level of VWF and improving endothelial function.