Objective To study the phosphorylation of AKT2 protein and autophagy activation in cardiac tissues of mice infected with coxsackievirus B3 (CVB3) for further analyzing the regulatory mecha-nism of PI3K/AKT2/mTOR signaling pathway on autophagy activation in viral myocarditis. Methods Thir-ty BALB/c mice were randomly divided into three groups (n=10): control group, myocarditis group and AKT activator-treated group. Those in the latter two groups were intraperitoneally injected with CVB3 to es-tablish the mouse model of acute viral myocarditis. Daily intraperitoneal injection of 0.04 mg/g of Akt acti-vator (SC79) was given to each mouse in the AKT activator-treated group 24 hours after CVB3 infection for 7 consecutive days,while the mice in the other two groups were given the same dose of normal saline. HE staining was used to observe the infiltration of inflammatory cells and tissue necrosis. Expression of CVB3 and inflammatory cytokines such as IL-1β and IL-6 in cardiac tissues at mRNA level was detected by q-PCR. Brain natriuretic peptide(BNP) and cardiac troponin I(cTnI) were measured by ELISA to evaluate myocardial injury. Changes in the expression of autophagy-related protein LC3 and Beclin1 at protein level as well as PI3K/AKT2/mTOR pathway were analyzed by Western blot assay. Results Compared with the con-trol group,massive inflammatory cell infiltration was observed in cardiac specimens of mice with myocarditis, but no obvious tissue necrosis was detected. Moreover,expression of CVB3 and inflammatory factors in car-diac tissues at mRNA level,levels of BNP and cTnI in blood,LC3Ⅱto LC3Ⅰratio as well as Beclin1 pro-tein level in cardiac tissues were significantly increased after CVB3 infection(P<0.05),whereas the activi-ty of PI3K/AKT2/mTOR signaling pathway was decreased. AKT activator not only down-regulated the LC3Ⅱ to LC3Ⅰratio and the expression of Beclin1 protein, but also enhanced the activation of PI3K/AKT2/mTOR signaling pathway in cardiac tissues of mice with myocarditis (P<0.05). Conclusion Enhanced autophagy and suppressed PI3K/AKT2/mTOR signaling pathway are observed in cardiac tissues of mice with myocarditis,indicating that the activation of autophagy may be regulated by PI3K/AKT2/mTOR signaling pathway.

Objective: To explore the electrocardiographic characteristics of patients with idiopathic ventricular arrhythmias (VAs) originating from different portions of distal great cardiac veins (DGCV). Methods: The study included 49 patients underwent successful RFCA of premature ventricular complex(PVCs)/ventricular tachycardia(VT) from different portions of the DGCV in our department from July 2009 to March 2016. The surface 12-lead electrocardiogram (ECG) and intraventricular ablation mapping features were analyzed. Patients were divided into four groups according to the mapping and ablation results: DGCV1(10 patients), DGCV2 (13 patients), proximalanterior interventricular vein (PAIV, 17 patients)and extend distal great cardiac vein (EDGCV, 9 patients). We analyzed the similarities and differences between surface 12-lead ECG of patients with PVCs/VT from different portions of DGCV, and compared with random chosen 290 patients with PVCs/VT from ventricular outflow tract and adjacent structure. Results: A positive R wave in inferior leads, a negative QS morphology in lead aVL and aVR were found among all groups. The different characteristics of surface 12-lead ECG of VAs originating from DGCV were as follows: (1)EDGCV patients demonstrated a positive R or r wave on lead Ⅰ(6/9) while a negative rS or qr wave was evidenced in other three groups (39/40). (2)A positive R pattern on lead V₁, V₅-V₆ (11/13) was presented in patients of DGCV2 group; R (without S or s) wave on V₁ (9/10), RS or Rs wave on V₅-V₆ were found in DGCV1 group; RS or rS wave was seen on lead V₁, R(without S)wave in lead V₅-V₆ (25/26) were found in EDGCV and PAIV group and the amplification of R wave in EDGCV was higher than V₁ of PAIV group.(3)Precordial lead transition zone was in front of V₁ for DGCV1 and DGCV2 groups (23/23), within V₁-V₃ for EDGCV group, but on V₂ or within V₂-V₃ for PAIV group.(4)Patients of DGCV1 and DGCV2 demonstrated a longer Pseudo delta wave time(PdW), intrinsicoid deflection time (IDT), significantly larger maximum deflection index (MDI) than those in PAIV and EDGCV groups (P<0.001). (5)The different characteristics of surface 12-lead ECG between VAs originating from DGCV and those from ventricular outflow tract and adjacent structure were as follows: ① The ECG features were similar between PVIA and LCC group, both demonstrated a rs wave on the lead Ⅰ, rS wave on V₁-V₂ and R wave on V₅-V₆; ②The ECG features were similar betweenEDGCV and RCC group, both presented with R or r wave on the lead Ⅰ, the QRS wave of precordial leads was similar as PAIV and LCC groups; ③A R wave on the lead V₁, V₅-V₆ was found in group DGCV2, and ILCC; ④Similar to the group Endo-MAA, patients in DGCV1 group also demonstrated a R wave on the lead V₁ and a Rs wave on V₅-V₆. Conclusion A positive R wave in inferior leads, a negative QS morphology in lead aVL and aVR are seen in all patients, but different electrocardiographic characteristics of PVC/VT originating from the different portions of the DGCV are presented on lead Ⅰ and V₁-V₆.