Objective:To explore the influence of radiofrequency ablation (RFA)on P-wave dispersion (difference between maximum and minimum P-wave interval)in patients with paroxysmal atrial fibrillation (PAF).Methods:A total of 95 PAF patients underwent circumferential pulmonary vein isolation.The preoperative and postoperative 12-lead ECG were recorded for 24h,maximum P-wave interval (Pmax)and minimum P-wave interval (Pmin)were measured,and P-wave dispersion was calculated.Since three months after operation,patients received outpatient follow up and dynamic ECG every month for six months.The operation was judged for successful or not according to symptoms of atrial fibrillation and dynamic ECG results,and patients were divided into success group (n=70)and recurrence group (n=25).Results:Compared with before operation,there was significant reduction in P-wave dis-persion [(48.84±4.08)ms vs.(42.22±4.02)ms,P <0.01]in all PAF patients after RFA.Compared with be-fore operation,there was significant reduction in P-wave dispersion [(47.63±3.58)ms vs.(40.67±4.82)ms,P<0.01]in success group;and reduction in P-wave dispersion [(49.51±1.64)ms vs.(48.26±3.48)ms]in recur-rence group,but no significant difference (P =0.346).After circumferential pulmonary vein isolation,P-wave dis-persion in success group was significantly lower than that of recurrence group (P <0.01).Conclusion:Circumferen-tial pulmonary vein ablation can improve P-wave dispersion in patients with atrial fibrillation,and it's more signifi-cant for success group.P-wave dispersion can predict the recurrence of atrial fibrillation after circumferential pulmo-nary vein ablation.

Acute coronary artery syndrome (ACS) was confirmed by coronary arteriography in 398 patients,and 378 healthy persons served as the control group.Serum uric acid in ACS and control group showed normal distribution,and serum uric acid level in ACS group (322?107 )?mol/L was significantly higher than those in control group (302?77)?mol/L (P＜0.01 ).The prevalence of hyperuricemia (HUA) was 27.0% in male patients and 25.2% in female.Systolic blood pressure,diastolic blood pressure,fasting plasma glucose,total cholesterol,triglycerides,creatinine and blood urea nitrogen in ACS group were higher than those in control group (all P＜0.01 ).Muhivariable analyses adjusted for age and sex indicated that raised fasting plasma glucose,total cholesterol,uric acid and mean arterial pressure were risk factors for coronary artery stenosis in ACS,and HUA played a role in the pathogenesis of ACS.

OBJECTIVESTo observe the effects of renal ischemic postconditioning (RI-Post) on myocardial apoptosis in rabbits with acute myocardial ischemia and reperfusion.

METHODSAll rabbits were subjected to 60 minutes ischemia by left anterior descending coronary artery occlusion (LADO) and 6 hours reperfusion. The rabbits are randomly divided into 3 groups (n = 8 in each group): (1) Ischemia-reperfusion (IR): LADO and reperfusion without additional intervention; (2) RI-Post: after 60 minutes of LADO, the left renal artery was occluded for 30 seconds and reperfused for 30 seconds and repeated 3 times, then the coronary artery was reperfused for 6 hours; (3) Medication intervention (MI): 10 minutes before coronary reperfusion, rabbits were treated with PKC antagonist GF109203X (0.05 mg/kg, IV), followed by RI-Post treatment and 6 hours coronary reperfusion. Myocardial apoptosis was measured by TUNEL and the myocardial Bcl-2 and Bax protein expressions were assessed by immunohistochemistry.

RESULTSCompared with the IR group and the MI group, myocardial apoptosis was significantly reduced (P < 0.05) and the Bcl-2 protein expression increased (P < 0.01) while the Bax protein expression decreased (P < 0.05) in the RI-Post group.

CONCLUSIONSRemote renal postconditioning applied right before the onset of coronary artery reperfusion can reduce the myocardial apoptosis induced by myocardial ischemia and reperfusion and up-regulate Bcl-2 while down-regulate Bax expression possibly by activation of protein kinase C.

Animals ; Apoptosis ; Female ; Ischemia ; metabolism ; Ischemic Preconditioning ; Kidney Diseases ; metabolism ; Male ; Myocardial Reperfusion Injury ; metabolism ; Myocardium ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rabbits ; bcl-2-Associated X Protein ; metabolism

Objective :To explore influence of serum uric acid (UA) on platelet function in patients with coronary heart disease (CHD) and influence of low dose aspirin (100mg) on serum UA level .Methods : A total of 117 CHD patients hospitalized in our hospital from Apr 2017 to Sep 2017 were selected .According to serum UA level ,they were divided into non-hyperuricemia group (n＝69) and hyperuricemia group (n＝48).They all received aspirin an-tiplatelet therapy after admission .Their arachidonic acid (AA ) induced platelet inhibition rate were detected by thrombelastography (TEG) on the seventh day after admission .The change of serum UA level after taking aspirin for three months were followed up .Results : After treatment ,AA induced platelet inhibition rate in hyperuricemia group is significantly lower than that in non-hyperuricemia group [(65.00 ± 19.39)% vs.(85.41 ± 22.83)%,P＝0.001]. Compared with the first day after admission ,there were significant rise in serum UA level in hyperuricemia group [(471.72 ± 53.46) μmol/L vs.(499.72 ± 54.98) μmol/L] and non-hyperuricemia group [ (319.43 ± 57.11) μmol/L vs.(338.46 ± 58.97) μmol/L] after taking aspirin for three months ,P＜0.05 both .Compared with non-hyperuricemia group ,there was a significant rise in serum UA level [(338.46 ± 58.97) μmol/L vs.(499.72 ± 54.98) μmol/L ,P＝0.001] in hyperu-ricemia group .Conclusion : In CHD patients complicated hyperuricemia ,their arachidonic acid induced platelet inhibition rate are significantly lower than that in non-hyperuricemia group .Small dose aspirin leads to serum UA level rise and its in-creasing amplitude in hyperuricemia group is significantly higher than that in non-hyperuricemia group .So , clinicians should monitor serum UA level of those patients in clinical work .

AIM:To investigate whether ellagic acid (EA) attenuates hypoxic-ischemic encephalopathy (HIE) by down-regulating autophagy.METHODS:In vivo, Sprague-Dawley rats (n=17) were randomly divided into 3groups:5 rats for sham group, 6 rats for HIE group and 6 rats for HIE+EA pretreatment group.The rats in HIE+EA pretreatment group were treated with EA (10 mg/kg, 10 m L/kg, suspended in corn oil, ig).After 24 h of operation, the rats from each group were sacrificed and their brains were collected.TTC staining and HE staining were used to define the infarct areas and brain structure.The autophagy-related proteins beclin-1, P62, LC3-II/-I and Atg5 in the cortex in each group were compared by Western blot.In vitro, PC12 cells were divided into 3 groups:control group, Coand CoEA pretreatment group.Co800μmol/L was added to the PC12 cells to induce an anoxic environment.The PC12 cells were pretreated with EA at 8μmol/L and the cell viability was measured by CCK-8 assay.The production of reactive oxidative species (ROS) in the cells was detected by flow cytometry with DCFH-DA staining.MDC staining and TM-RE staining were applied to reflect the extent of autophagy and the state of apoptosis, respectively.The autophagy-related proteins in PC12 cells were also investigated.RESULTS:In HIE group, 7-day-old rats were given the operations and the their large infarct areas in the hemisphere were observed by TTC staining.HE staining displayed the injured hemispheres which contained few neurons, and exhibited edema status and serious structural damage.EA pretreatment decreased the infarct area and alleviated the damage to hemisphere with more visible neurons, compared with HIE group.Compared with sham group, the levels of autophagy-related proteins Atg5, beclin-1 and LC3-II/-I in the cortex were increased (P<0.01) , and P62 protein expression was decreased (P<0.01) in HIE group.Compared with HIE group, the protein expression of Atg5, beclin-1 and LC3-II/-I was decreased (P<0.01) and P62 protein expression was increased in HIE+EA pretreatment group (P<0.01).In vitro, compared with CoPC12 cells in CoEA pretreatment group showed a lower ROS level.Moreover, the cells in CoEA pretreatment group exhibited higher mitochondrial membrane potential than that in CoMDC staining in Coshowed high value of fluorescence and increased number of autophagosomes.EA pretreatment reduced the number of autophagosomes and the extent of autophagy to protect PC12cells.Furthermore, the protein levels of Atg5, beclin-1 and LC3-II/-I in Cowere higher (P<0.01) , and the protein expression of P62 was lower (P<0.01) than those in control group.In CoEA pretreatment group, the protein levels of Atg5, beclin-1 and LC3-II/-I were decreased (P<0.01) and the protein expression of P62 was increased as compared with Co (P<0.01).CONCLUSION:EA pretreatment attenuates autophagy to protect the neurons against HIE injury.

BACKGROUNDAngiotensin II (Ang II) is a major contributor to the development of heart failure. However, the molecular and cellular mechanisms that underlie this process remain elusive. Inadequate angiogenesis in the myocardium leads to a transition from cardiac hypertrophy to dysfunction, and our previous study showed that Ang II significantly impaired the angiogenesis response. The current study was designed to examine the role of Jagged1-Notch signaling in the effect of Ang II during impaired angiogenesis and cardiac hypertrophy.

METHODSAng II was subcutaneously infused into 8-week-old male C57BL/6 mice at a dose of 200 ng·kg-1·min-1 for 2 weeks using Alzet micro-osmotic pumps. N-[N-(3, 5-difluorophenacetyl)-L-alanyl]-S-phenylglycine tert-butyl ester (DAPT), a γ-secretase inhibitor, was injected subcutaneously during Ang II infusion at a dose of 10.0 mg·kg-1·d-1. Forty mice were divided into four groups (n = 10 per group): control group; Ang II group, treated with Ang II; DAPT group, treated with DAPT; and Ang II + DAPT group, treated with both Ang II and DAPT. At the end of experiments, myocardial (left ventricle [LV]) tissue from each experimental group was evaluated using immunohistochemistry, Western blotting, and real-time polymerase chain reaction. Data were analyzed using one-way analysis of variance test followed by the least significant difference method or independent samples t-test.

RESULTSAng II treatment significantly induced cardiac hypertrophy and impaired the angiogenesis response compared to controls, as shown by hematoxylin and eosin (HE) staining and immunohistochemistry for CD31, a vascular marker (P < 0.05 for both). Meanwhile, Jagged1 protein was significantly increased, but gene expression for both Jag1 and Hey1 was decreased in the LV following Ang II treatment, compared to that in controls (relative ratio for Jag1 gene: 0.45 ± 0.13 vs. 0.84 ± 0.15; relative ratio for Hey1 gene: 0.51 ± 0.08 vs. 0.91 ± 0.09; P < 0.05). All these cellular and molecular effects induced by Ang II in the hearts of mice were reduced by DAPT treatment. Interestingly, Ang II stimulated Hey1, a known Notch target, but did not affect the expression of Hey2, another Notch target gene.

CONCLUSIONSA Jagged1-Hey1 signal might mediate the impairment of angiogenesis induced by Ang II during cardiac hypertrophy.

Animals ; Cardiomegaly ; chemically induced ; metabolism ; Cell Cycle Proteins ; metabolism ; Immunohistochemistry ; Jagged-1 Protein ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium ; metabolism ; Neovascularization, Physiologic ; drug effects ; Signal Transduction ; drug effects

BACKGROUNDHigh cost of imported pacemakers is a main obstacle for Chinese patients suffering from bradyarrhythmia, and a domestically developed pacemaker will help lower the burden. This study aimed to evaluate the safety and efficacy of Qinming8631 DR (Qinming Medical, Baoji, China), the first domestically developed dual-chamber pacemaker of China, compared with a commercially available pacemaker Talos DR (Biotronik, Berlin, Germany) in Chinese patients.

METHODSA prospective randomized trial was conducted at 14 centers in China. Participants were randomized into trial (Qinming8631 DR) and control (Talos DR) groups. Parameters of the pacing systems were collected immediately after device implantation and during follow-ups. The effective pacing rate at 6-month follow-up was recorded as the primary end point. Electrical properties, magnet response, single- and double-pole polarity conversion, rate response function, and adverse events of the pacing system were analyzed. The Cochran-Mantel-Haenszel Chi-square test, paired t-test, and Wilcoxon signed-rank test were used for measuring primary qualitative outcomes and comparing normally and abnormally distributed measurement data.

RESULTSA total of 225 patients with a diagnosis of bradyarrhythmia and eligible for this study were randomly enrolled into the trial (n = 113) and control (n = 112) groups. They underwent successful pacemaker implantation with acceptable postoperative pacing threshold and sensitivity. Effective pacing rates of trial and control groups were comparable both in the full analysis set and the per protocol set (81.4% vs. 79.5%, P = 0.712 and 95.4% vs. 89.5%, P = 0.143, respectively). In both data sets, noninferiority of the trial group was above the predefined noninferiority limit(-9.5%).

CONCLUSIONSThis study established the noninferiority of Qinming8631 DR to Talos DR. The safety and efficacy of Qinming8631 DR pacemaker were comparable to those of Talos DR in treating patients with cardiac bradyarrhythmia.

Aged ; Bradycardia ; therapy ; Cardiac Pacing, Artificial ; methods ; China ; Female ; Humans ; Male ; Middle Aged ; Pacemaker, Artificial ; adverse effects ; Prospective Studies