Death, Sudden, Cardiac ; Humans ; Reward

Objective:To prepare compound isosorbide mononitrate sustained-release capsules and study the drug release. Meth-ods:Isosorbide mononitrate pellets were prepared by the fluidized bed coating technology. The influencing factors in the preparation process were examined and the major factors were optimized by single factor experiments. The drug release was determined by HPLC. The best formula was screened by optimizing aspirin coating solution. Results:The compound isosorbide mononitrate sustained-release capsules were prepared by the best formula. Both the two drugs could achieve promising release, and in vitro release behavior of isosor-bide mononitrate was fitted Higuchi equation,which was similar to that of the imported preparations. The release of aspirin in acidic and alkaline media was in coincidence with the release requirements. Conclusion:The formula is reasonable and the preparation process is stable with promising sustained release property.

Objective To inquire into the correlation of cardiac AT 1 receptor,? 1 receptor with PKC/MAPKs(protein kinase C/mitogen-activated protein kinase) signal transduction pathway during myocardial remodeling.Methods Twenty-four Wistar rats were randomly divided into four groups-sham group,infarcted group,losartan group and betaloc group.Except sham group,left anterior descending coronary artery was ligated for 21 days.In the other three groups,expression changes of cardiac collagen subtype Ⅰ,Ⅲ,fibronectin(FN),c-fos,ERK 1 (extracellular signal-regulated kinase,ERK)and PKC proteins were studied with immunohistochemistry and computer image analysis. c-fos mRNA expression was tested by reverse transcription and polymerase chain reaction(RT-PCR).Results Expressions of collagen Ⅰ,collagen Ⅲ , FN,c-fos,ERK 1 and PKC proteins were significantly enhanced(P

Objective Mapping the sites of earliest activation in AF patients with rheumatic heart disease. Finding out the ratio of AF originate from the pulmonary veins. Methods There were 9 patients with valvular atrial fibrillation (1 male, 8 females age (42?13) years, histories of rheumatic heart disease (11?9) years, and mitral valve area 1.01?0.02 cm2) involved in the research. 3 patients had organized thrombus in left atrial appendage. 6 patients with persistent AF received anticoagulation therapy (warfarin 2 or 3 weeks) and drug cardioversion (amiodarone 400 mg, three times per day, for 7 days) before procedures, while other 3 patients with paroxysmal AF received neither anticoagulation therapy nor drug cardioversion. All patients received percutaneous balloon mitral valvotomy (PBMV). After finished PBMV, four multipolar electrode catheters were placed in the high right atrium (HRA), coronary sinus (CS), left atrium (LA) and pulmonary veins (PVs). S1S2 and S1S2S3 programmed stimuli were delivered in HRA, CS, LA and PVs respectively. For the patients who failed to induce AF, burst stimuli were used. Results 11 AF generating sites, which induced by S1S2 and S1S2S3 programmed stimuli, could be confirmed by identification of the earliest regions of atrial activation for the first AF cycle. However, 1 AF obtained by 260 ms RR interval burst stimuli, affirmed by shortest activation cycle length. All confirmed 12 AF original sites were original as following: RA (n=4), LA (n=1), CS (n=2); PVs (n=5). Among the 5 PVs original sites, 3 was from left superior pulmonary vein, while the other 2 were from right superior pulmonary vein and left inferior pulmonary respectively. Conclusion PVs could be the ectopic origin of valvular AF.

0 05) 3 hours after myocardial infarction,and remarkably decreased (P

Objective To inquire into the effects of cardiac ? 1 -adrenergic receptor on myocardial remodeling and modulating calcium channel. Methods The models of myocardial remodeling after myocardial infarction in Wistar rats were used to study the expression changes of cardiac collagen subtype Ⅰ,Ⅲ,fibronectin (FN) with immunohistochemistry,and changes of T-type calcium channel,L-type calcium channel and ? 1 -adrenergic receptor mRNA expressions by reverse transcription and polymerase chain reaction(RT-PCR) and in situ hybridization. Cardiac total Ca 2+ was tested by atomic absorption/flame emission spectrophotometer. Results Cardiac collagenⅠ,collagen Ⅲ,FN protein expressions in betaloc group were remarkably decreased (P

Objective To investigate vagal effects on atrial fibrillation(AF)thresholds at different sites of pulmonary veins after autonomic denervation.Methods In 10 mongrel dogs,the cervical vagal trunks were isolated bilaterally and decentralized from Oct 2004 to May 2005.The ansae subclaviae were exposed bilaterally as they exited from the stellate ganglia,doubly ligated,and cut.Local rapid electrical stimulation(S1S1=80 ms,impulse duration 0.5 ms)was performed to right appendage(RAA)、left appendage(LAA)、left atrium(LA)and different sites of 4 pulmonary veins.AF threshold was determined at each site in the baseline state,during bilateral cervical vagal stimulation(VNS,12.5 Hz,impulse duration 0.5 ms,stimulation voltage 5～8 V)and during infusion of atropine.Results During VNS,a lower AF threshold was observed at all sites,especially at distal of 4 pulmonary veins(P0.05).Conclusion Vagal nerve not only contributes to the maintenance of AF originating from pulmonary veins,but also greatly promotes the initiation of AF.

Objective To study the electrophysiologic characteristics of atrial-ventricular reentrant tachycardia(AVRT)characterized by paroxysmal occurrence that slow atrioventricular accessory pathway participatesin.Methods Twenty-one cases were chosen from patients receiring radiofrequency ablation therapy in Peking University People's Hospital from July in 1999 to January of 2005.The patients with slow atrioventricular accessory pathways diagnosed correctly were divided into two groups with paroxysmal tachycardia and permanent tachycardia in terms of the occurrent frequence of AVRT.The electrophysiologic features of AVRT of two groups were contrastively analyzed.Results Compared with the group of permanent AVRT,it was found that antidromic refractory period of slow atrioventricular accessory pathways was longer[(359?46)ms vs (318?31)ms,P

Objective To inquire into T-type calcium channel effects on atrial electrical remodelling and its mechanisms during atrial fibrillation.Methods Animal experiment was performed in Peking University Pepole's Hospital from Feb.2002 to Oct.2006.Fifteen adult cross-bred dogs were used in the experiment.Ten dogs underwent continuous rapid atrial pacing(500 beats/min)for twenty-four weeks to create persistent atrial fibrillation.In five rapidly-paced dogs,50mg pure powder/day of mibefradil dihydrochloride was given from the second day after pacemaker implantation and continued until the twenty-fourth week.A group of size-matched dogs(n=5)without being given mibefradil was used as a pure atrial fibrillation group.Another group of size-matched dogs(n=5)without pacemaker implantation was used as a control group.Atrial fibrillation duration was determined by electrophysiological study.Canine atrial myocytes were isolated by enzymatic dissociation and intracellular Ca2+ cytosolic transient was studied with confocal imaging.Results (1)The preoperation atrial effective refractory period was 280/90~110 ms.In the twenty-fourth week after rapid atrial pacing,atrial effective refractory period was obviously extended(2000/1400~1700 ms)in the T-type Ca2+ channel blocker group compared with the preoperation one.In the twenty-fourth week,the induced rate of persistent atrial fibrillation was 75% in atrial fibrillation group,whereas the persistent atrial fibrillation occurred in only one case(20%)in the T-type Ca2+ channel blocker group.(2)Intracellular Ca2+ concentration of atrial myocytes was unremarkably changed in control group after blocking L-type Ca2+ channel(1.17?0.09 OD ratio),whereas the intracellular Ca2+ concentration was obviously enhanced(2.35?1.05 OD ratio)(P

1.9?V and 95% confidence interval was 1.52-2.41?V.There was significant differences among the groups(P