Prognostic relevance of ventricular arrhythmias in surgical patients with gastrointestinal tumors

BACKGROUND Individuals diagnosed with gastrointestinal tumors are at an increased risk of developing cardiovascular diseases.Among which,ventricular arrhythmia is a prevalent clinical concern.This suggests that ventricular arrhythmias may have predictive value in the prognosis of patients with gastrointestinal tumors.AIM To explore the prognostic value of ventricular arrhythmias in patients with gastrointestinal tumors receiving surgery.METHODS We retrospectively analyzed data from 130 patients undergoing gastrointestinal tumor resection.These patients were evaluated by a 24-h ambulatory electrocardiogram(ECG)at the Sixth Affiliated Hospital of Sun Yat-sen University from January 2018 to June 2020.Additionally,41 general healthy age-matched and sexmatched controls were included.Patients were categorized into survival and non-survival groups.The primary endpoint was all-cause mortality,and secondary endpoints included major adverse cardiovascular events(MACEs).RESULTS Colorectal tumors comprised 90%of cases.Preoperative ambulatory ECG monitoring revealed that among the 130 patients with gastrointestinal tumors,100(76.92%)exhibited varying degrees of premature ventricular contractions(PVCs).Ten patients(7.69%)manifested non-sustained ventricular tachycardia(NSVT).The patients with gastrointestinal tumors exhibited higher PVCs compared to the healthy controls on both conventional ECG[27(21.3)vs 1(2.5),P=0.012]and 24-h ambulatory ECG[14(1.0,405)vs 1(0,6.5),P<0.001].Non-survivors had a higher PVC count than survivors[150.50(7.25,1690.50)vs 9(0,229.25),P=0.020].During the follow-up period,24 patients died and 11 patients experienced MACEs.Univariate analysis linked PVC>35/24 h to all-cause mortality,and NSVT was associated with MACE.However,neither PVC burden nor NSVT independently predicted outcomes according to multivariate analysis.CONCLUSION Patients with gastrointestinal tumors exhibited elevated PVCs.PVCs>35/24 h and NSVT detected by 24-h ambulatory ECG were prognostically significant but were not found to be independent predictors.

Analysis of the Efficacy of Low-Dose Betaloc Combined with Amiodarone in Treating Ventricular Arrhythmia

Objective:To explore and analyze the clinical effect of low-dose Betaloc combined with amiodarone in treating ventricular arrhythmia.Methods:70 patients with ventricular arrhythmia who were admitted to the Department of Cardiology of our hospital between August 2022 and August 2023 were selected as research subjects.They were divided into two groups using the coin-tossing method:the combination group(n=35)and the reference group(n=35).The combination group was treated with low-dose Betaloc and amiodarone,and the control group was treated with low-dose Betaloc alone.The treatment efficacy,cardiac function indicators,and related tested indicators of the two groups were compared.Results:The total efficacy of the treatment received by the combination group was much higher than that of the control group(P<0.05).Besides,after treatment,the cardiac function indicators such as left ventricular ejection fraction(LVEF),left ventricular end-systolic volume(LVESV),and cardiac index(CI)of the patients in the combination group were significantly better than those of the reference group(P<0.05).Furthermore,the high-sensitivity C-reactive protein(Hs-CRP),N-terminal prohormone of brain natriuretic peptide(NT-proBNP),adiponectin(APN),and other related test indicators of the patients in the combination group were significantly better than those of the reference group(P<0.05).Conclusion:Low-dose Betaloc combined with amiodarone has a noticeable effect in treating ventricular arrhythmia and deserves to be widely promoted.

Clinical Efficacy of Metoprolol Succinate Extended-Release Tablets in the Treatment of Post-Myocardial Infarction Ventricular Arrhythmias

Objective:To investigate the clinical efficacy of metoprolol succinate extended-release tablets in the treatment of post-myocardial infarction ventricular arrhythmias.Methods:The clinical data of 84 patients with post-myocardial infarction ventricular arrhythmia included in the study were collected and they were divided into Groups A and B with 42 cases each using the randomization method.Group A was treated with oral glucosamine hydrochloride,while Group B was administered oral metoprolol succinate extended-release tablets.Combined indicators were used to evaluate the improvement of clinical indicators,therapeutic effects,and the incidence of adverse reactions in the two groups.Results:The baseline data of the two groups of patients were not statistically significant(Pall>0.05);after treatment,the QT dispersion,corrected QT dispersion,and heart rate of Group B were lower than that of Group A(Pall=0.000<0.001);the 2 total clinical effectiveness of Group B was 95.24%,which was significantly higher than 80.95%in Group A(χ=4.087,P=0.043<0.05);the total incidence of adverse reactions in Group B was 4.76%,which was significantly lower than 219.04%in Group A(χ=4.087,P=0.043<0.05).Conclusion:In the treatment of post-myocardial infarction ventricular arrhythmia,the use of metoprolol succinate extended-release tablets can effectively correct the QT dispersion of patients,improve their heart rate,increase clinical effectiveness,and reduce the incidence of adverse reactions.

Cardiac-targeted PIASy gene silencing mediates deSUMOylation of caveolin-3 and prevents ischemia/reperfusion-induced Na_(v)1.5 downregulation and ventricular arrhythmias

Background:Abnormal myocardial voltage-gated sodium channel 1.5(Nav1.5)expression and function cause lethal ventricular arrhythmias during myocardial ischemia–reperfusion(I/R).Protein inhibitor of activated STAT Y(PIASy)-mediated caveolin-3(Cav-3)small ubiquitin-related modifier(SUMO)modification affects Cav-3 binding to the Nav1.5.PIASy activity is increased after myocardial I/R,but it is unclear whether this is attributable to plasma membrane Nav1.5 downregulation and ventricular arrhythmias.Methods:Using recombinant adeno-associated virus subtype 9(AAV9),rat cardiac PIASy was silenced using intraventricular injection of PIASy short hairpin RNA(shRNA).After two weeks,rat hearts were subjected to I/R and electrocardiography was performed to assess malignant arrhythmias.Tissues from peri-infarct areas of the left ventricle were collected for molecular biological measurements.Results:PIASy was upregulated by I/R(P<0.01),with increased SUMO2/3 modification of Cav-3 and reduced membrane Nav1.5 density(P<0.01).AAV9-PIASy shRNA intraventricular injection into the rat heart down-regulated PIASy after I/R,at both mRNA and protein levels(P<0.05 vs.Scramble-shRNA+I/R group),decreased SUMO-modified Cav-3 levels,enhanced Cav-3 binding to Nav1.5,and prevented I/R-induced decrease of Nav1.5 and Cav-3co-localization in the intercalated disc and lateral membrane.PIASy silencing in rat hearts reduced I/R-induced fatal arrhythmias,which was reflected by a modest decrease in the duration of ventricular fibrillation(VF;P<0.05 vs.Scramble-shRNA+I/R group)and a significantly reduced arrhythmia score(P<0.01 vs.Scramble-shRNA+I/R group).The anti-arrhythmic effects of PIASy silencing were also evidenced by decreased episodes of ventricular tachycardia(VT),sustained VT and VF,especially at the time 5–10 min after ischemia(P<0.05 vs.Scramble-shRNA+IR group).Using in vitro human embryonic kidney 293 T(HEK293T)cells and isolated adult rat cardiomyocyte models exposed to hypoxia/reoxygenation(H/R),we confirmed that increased PIASy promoted Cav-3 modification by SUMO2/3 and Nav1.5/Cav-3 dissociation after H/R.Mutation of SUMO consensus lysine sites in Cav-3(K38R or K144R)altered the membrane expression levels of Nav1.5 and Cav-3 before and after H/R in HEK293T cells.Conclusions:I/R-induced cardiac PIASy activation increased Cav-3 SUMOylation by SUMO2/3 and dysregulated Nav1.5-related ventricular arrhythmias.Cardiac-targeted PIASy silencing mediated Cav-3 deSUMOylation and partially prevented I/R-induced Nav1.5 downregulation in the plasma membrane of cardiomyocytes,and subsequent ventricular arrhythmias in rats.PIASy was identified as a potential therapeutic target for life-threatening arrhythmias in patients with ischemic heart diseases.

Clinical Effect Analysis of Small and Medium Doses of Betaloc Combined with Amiodarone in the Treatment of Ventricular Arrhythmia

Objective:To explore and analyze the clinical effect of small and medium doses of Betaloc combined with amiodarone in the treatment of ventricular arrhythmia.Methods:60 patients with ventricular arrhythmia that were treated in the Department of Cardiology of our hospital from May 2018-May 2023 were selected for this study,and they were divided into a research group(n=30)and a reference group(n=30).The study group was treated with small doses of Betaloc and amiodarone,while the reference group was treated with conventional treatment.The total efficacy of medication,QRS interval,standard deviation of normal-to-normal(NN)intervals(SDNN),root mean square of successive differences between normal heartbeats(RMSSD),standard deviation of the average NN intervals(SDANN),and incidence of adverse reactions were compared between the groups.Results:The effectiveness of medication in the study group was significantly higher than that in the reference group(P<0.05).Besides,there was no statistically significant difference(P>0.05)in the QRS interval and SDNN between the two groups before treatment.After treatment,the QRS interval and SDNN of the study group were significantly lower than those of the reference group(P<0.05).Before treatment,there was no significant difference in RMSSD and SDANN between groups(P>0.05).After treatment,RMSSD and SDANN in the study group were significantly better than those in the reference group(P<0.05),and the difference was statistically significant.The incidence of adverse reactions in the study group was significantly lower than that in the reference group(P<0.05),and the difference was statistically significant.Conclusion:Small doses of Betoprolol and amiodarone is more effective in the treatment of ventricular arrhythmia,which has the value of popularization and application.

I-123 metaiodobenzylguanidine imaging for predicting ventricular arrhythmia in heart failure patients

Compared to antiarrhythmic drugs, implantable cardioverter defibrillator （ICD） leads to a more significant im- provement in preventing ventricular arrhythmia in heart failure patients. However, an important question has been raised that how to select appropriate patients for ICD therapy. 1-123 metaiodobenzylguanidine （MIBG） planar and SPECT imaging have shown great potentials to predict ventricular arrhythmia in heart failure patients by as- sessing the abnormalities of the sympathetic nervous system. Clinical trials demonstrated that several parameters measured from 1-123 MIBG planar and SPECT imaging, such as heart-to-mediastinum ratio, washout rate, defect score, and innervation/perfusion mismatch, predicted ventricular arrhythmias in heart failure patients. This paper introduces the current practice of ICD therapy and reviews the technical background of 1-123 MIBG planar and SPECT imaging and their clinical data in predicting ventricular arrhythmia.

Effects of Potassium Aspartate and Magnesium on Ventricular Arrhythmia in Ischemia-reperfusion Rabbit Heart

The aim of this study was to determine if the potassium aspartate and magnesium （PAM） prevent reperfusion-induced ventricular arrhythmias （RIVA） in ischemia-reperfusion （IR） rabbit heart. Thirty rabbits were randomly divided into control, ischemia and PAM groups. Arterially-perfused rabbit left ventricular preparations were made, and transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded in the whole process of all experiments. In control group rabbit ventricular wedge preparations were continuously perfused with Tyrode＇s solution, and in ischemia group and PAM groups the perfusion of Tyrode＇s solution was stopped for 30 min. Then the ischemia group was reperfused with Tyrode＇s solution and the PAM group with Tyrode＇s solution containing 2.42 mg/L PAM, respectively. ECG, QT interval, transmural repolarization dispersion （TDR） and action potentials from epicardium and endocardium were simultaneously recorded, and the RIVA of the wedge preparation was observed. Compared with control group, TDR and incidence of RIVA were significantly increased in ischemia group （P〈0.05）. The incidence of RIVA in control, ischemia and PAM group was 0/10, 9/10 and 1/10, respectively. Compared with ischemia group, TDR and incidence of RIVA were significantly reduced in PAM group （P〈0.05）. Potassium aspartate and magnesium significantly reduce TDR and prevent ventricular arrhythmia in ischemic rabbit heart.

Effects of ramipril on ventricular arrhythmia after myocardial infarction in rabbits

BACKGROUND： Ventricular arrhythmia （VA） is one of the most common complications of myocardial infarction （MI）, and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits. METHODS： Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups： sham-operated （SHAM） group （n=8）, MI group （n=8） and MI with ramipril （RAM） group （n=8）. Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and II1. After MI, rabbits in the RAM group were fed with intragastric ramipril （1 mg/kg per day ） for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation （VT/VF） episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student＇s t test and ANOVA were used for statistical analysis. RESULTS： VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks （2.6±0.8 vs. 12.±＋2.9, P〈0.05）. Twelve weeks after MI, the duration of repolarization for 90% （APD90） of three-tier ventricular myocytes in the MI group was longer than that before MI （258.2±21.1 vs. 230.1±23.2,278.0±23.8 vs. 245.8±25.4,242.6±22.7 vs. 227.0±21.7, P〈0.05）. However, the APD90 was not significantly different at 12 weeks before and after MI in the RAM group （P〉0.05）. Moreover, the transmural dispersion of repolarization （TDR） was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups （36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P〈0.05）. But the TDR was not significantly different between the RAM and SHAM groups （18.7±6.2 vs. 24.9±8.7, P〉0.05）. CONCLUSION： Ramipril may reduce the incidence of malignant ventricular arrhythmia via mprovement of transmembrance repolarization heterogeneity after MI.

Effect of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction in vivo

Acute myocardial infarction （AMI） is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-a （TNF-a） on ventricular arrhythmias induced byAMI in rats in vivo. Two hundred and forty male Wistar rats were randomized into a sham- operation group, an AMI group, and a recombinant human tumor necrosis factor receptor：Fc fusion protein（rhTNFR：Fc） group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery （LAD）, and there was no ligation but operation in the sham-operation group. The rhTNFR：Fc group was treated with rhTNFR：Fc（10 mg/kg）, a TNF-a antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-a among different groups were detected by histochemistry and real-time fluorescent quantitative PCR. Expression of TNF-a increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR：Fc group. The time- windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR：Fc group showed a lesser expression of TNF-a protein and a lower incidence of ventricular arrhythmias （P〈0.05）. There was no obvious change in the sham-operation group. The expression of TNF-a induced by AMI could contribute to the onset of ventricular arrhythmias.

Effect of Oxidative Stress on Ventricular Arrhythmia in Rabbits with Adriamycin-induced Cardiomyopathy

The purpose of the present study was to examine the effects of oxidative stress on ventricular arrhythmias in rabbits with adriamycin-induced cardiomyopathy and the relationship between oxidative stress and ventricular arrhythmia. Forty Japanese white rabbits were randomly divided into four groups （n=10 in each）： control group, metoprolol （a selective β1 receptor blocker） group, carvedilol （a nonselective β blocker/α-1 blocker） group and adriamycin group. Models of adriamycin-induced car-diomyopathy were established by intravenously injecting adriamycin hydrochloride （1 mg/kg） to rabbits via the auri-edge vein twice a week for 8 weeks in the adriamycin, metoprolol and carvedilol groups. Rabbits in the control group were given equal volume of saline through the auri-edge vein. Rabbits in the metoprolol and carvedilol groups were then intragastrically administrated metoprolol （5 mg/kg/d） and carvedilol （5 mg/kg/d） respectively for 2 months, while those in the adriamycin and control groups were treated with equal volume of saline in the same manner as in the metroprolol and carvedilol groups. Left ventricular end diastolic diameter （LVEDd） and left ventricular ejection fraction （LVEF） were measured by echocardiography. Plasma levels of N-terminal pro B-type natriuretic peptide （NT-proBNP）, malondialdehyde （MAD） and superoxide dismutase （SOD） were detected. The left ventricular wedge preparations were perfused with Tyrode＇s solution. The transmural electrocardiogram, transmural action potentials from epicardium （Epi） and endocardium （Endo）, transmural repolarization dispersion （TDR） were recorded, and the incidences of triggered activity and ventricular arrhythmias were obtained at rapid cycle lengths. The results showed that TDR and the serum MDA and NT-proBNP levels were increased, and LVEF and the serum SOD level decreased in the adriamycin group compared with the control group. The incidences of triggered activity and ventricular arrhythmia were significantly higher in the adriamycin group than those in the control group （P〈0.05）. In the carvedilol group as compared with the adriamycin group, the serum SOD level and the LVEF were substantially increased; the TDR, and the serum MDA and NT-proBNP levels were significantly decreased; the incidences of triggered activity and ventricular arrhythmia were obviously reduced （P〈0.05）. There were no significant differences in the levels of MDA and SOD, LVEF, TDR and the incidences of triggered activity and ventricular arrhythmia between the adriamycin group and the metoprolol group. It was concluded that carvedilol may inhibit triggered activity and ventricular arrhythmias in rabbit with adriamycin-induced cardiomyopathy, which is related to the decrease in oxygen free radials.

Spontaneous type 1 pattern, ventricular arrhythmias and sudden cardiac death in Brugada Syndrome： an updated systematic review and meta-analysis

Brugada syndrome （BrS） is primary electrical disorder characterized by ST segment elevation with right bundle branch block morphology in patients with apparent structurally normal hearts, It predisposes affected individuals to ventricular tachycardia/fibrillation （VT/VF） and sudden cardiac death （SCD）.A number of studies have identified risk factors that are associated with a more malignant course of disease. These include male gender, syncope, a spontaneous type 1 ECG pattern, family history of SCD, family history of Brugada syndrome,

Function of the CaMKII-ryanodine receptor signaling pathway in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia

BACKGROUND:Calcium calmodulin-dependent kinase II(CaMKII) can be more active in patients with left ventricular hypertrophy(LVH),which in turn causes phosphorylation of ryanodine receptors,resulting in inactivation and the instability of intracellular calcium homeostasis.The present study aimed to determine the effect of CaMKII-ryanodine receptor pathway signaling in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia.METHODS:Forty New Zealand rabbits were randomized into four groups(10 per group):sham group,LVH group,KN-93 group(LVH+KN-93),and ryanodine group(LVH+ryanodine).Rabbits in the LVH,KN-93,and ryanodine groups were used to establish a left ventricular hypertrophy model by the coarctation of the abdominal aorta,while those in the sham group did not undergo the coarctation.After eight weeks,action potentials(APs) were recorded simultaneously in the endocardium and epicardium,and a transmural electrocardiogram(ECG) was also recorded in the rabbit left ventricular wedge model.Drugs were administered to the animals in the KN-93 and ryanodine groups,and the frequency of triggered APs and ventricular tachycardia was recorded after the rabbits were given isoprenaline(1 μmol/L) and high-frequency stimulation.RESULTS:The frequency(animals/group) of triggered APs was 0/10 in the sham group,10/10 in the LVH group,4/10 in the KN-93 group,and 1/10 in the ryanodine group.The frequencies of ventricular tachycardia were 0/10,9/10,3/10,and 1/10,respectively.The frequencies of polymorphic ventricular tachycardia or ventricular fibrillation were 0/10,7/10,2/10,and 1/10,respectively.The frequencies of triggered ventricular arrhythmias in the KN-93 and ryanodine groups were much lower than those in the LVH group(P<0.05).CONCLUSIONS:KN-93 and ryanodine can effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH.The CaMKII-ryanodine signaling pathway can be used as a new means of treating ventricular arrhythmia.

Effect of Electroacupuncture on Reperfusion Ventricular Arrhythmia in Rat

Protective effect and mechanism of electroacupuncture （EA） on acute reperfusion ventricular arrhthmia was investigated. Ventricular arrhythmia was induced by occlusion of the proximal left anterior descend （LAD） branch of coronary artery for 5 min and followed with 15 min reperfusion . EA on acupoint ＂Neiguan＂, ＂Jianshi＂ was performed at 30 min before ligation and continued another 5 min during ischemia. Isoprenaline （20, 30 and 50 μg/kg） or atropine （1 mg/ kg） was intravenously injected at 5min before ischemia. The results showed that EA significantly decreased the incidence of ischemia/reperfusion （I/R） induced ventricular tachycardia （VT）, ventricular fibrillation （VF） and mortality as compared to I/R group. Atropine partially suppressed the EA＇s effect of antiarrhythmia; Isoprenaline increased the incidence and severity of reperfusion arrhythmia, which was inhibited by EA, but this inhibition of EA was blocked with increasing dose of isoprenaline. The results indicated that EA treatment could prevent the occurrence of reperfusion ventricular arrhythmia in rats with myocardial ischemia, and its mechanism might be related to the regulation of EA on the β-adrenoceptors and M-cholinergic receptor activation in myocardium.

The Predictive Value of Tp-ec, Q-Tc, Tp-e/Q-T and HRV in Malignant Ventricular Arrhythmia

Objective: To explore the predictive ability of Tp-ec, Q-Tc, Tp-e/Q-T and HRV on malignant arrhythmia during hospitalization. Method: 100 patients with malignant ventricular arrhythmia were included as the experimental group, another 100 patients without malignant ventricular arrhythmia were included as control group. The differences of Tp-ec, Q-Tc, Tp-e/Q-T and HRV were compared between the two groups. Multivariate logistic regression analysis was used to study variables and establish prediction model. ROC curve was used to evaluate the predictive ability and best predictive value of each index for malignant ventricular arrhythmia in hospital. Result: Compared with the control group, Tp-ec, Q-Tc, Tp-e/Q-T and HRV in the experimental group were significantly increased, (P < 0.001), HRV was decreased significantly. Multivariate logistic regression showed that the increase of Tp-ec, Q-Tc, Tp-e/Q-T and the decrease of HRV were the risk factors of malignant ventricular ventricular arrhythmia in hospital (OR = 11.169, 1.788, 1.001, 0.780), and bulid prediction model Z = -254.827 + 0.203 * Tp-ec + 0.581 * Q-Tc + 878.066 * Tp-e/Q-T-0.248 * SDNN. ROC curve showed that the area under the curve (AUC) of TP EC, Q-Tc, Tp-e/Q-T, HRV and predictive model for the diagnosis of malignant ventricular ventricular arrhythmia in hospital were 0.988, 0.905, 0.973, 0.901, 0.993, the best critical values were 100.365 ms, 447.078 ms, 0.239, 100.500, 181.792. Conclusion: The decrease of Tp-ec, Q-Tc, Tp-e/Q-T and HRV were the risk factors of malignant ventricular arrhythmia, and has predictive value for malignant ventricular arrhythmia in hospital. The prediction model combined with Tp-ec, Q-Tc, Tp-e/Q-T and HRV can improve the prediction ability of variables on malignant ventricular arrhythmia in hospital.

Effects of Dingjifumai Decoction on Electrocardiogram and sodium potassium pump of rats with ventricular arrhythmia

Objective:To investigate the effect of Dingjifumai Decoction(DJFM)on Electrocardiogram(ECG)and sodium potassium pump in rats with ventricular arrhythmia.Methods:Forty healthy male SD rats(200±20g)were randomly divided into blank group,model group,Metoprolol group and DJFM group.Ten rats in each group were fed with normal diet and free drinking water.Each group was given gavage,and the amount of gavage in each group was calculated according to body weight.In the model group,0.001%Aconitine was injected into the tail vein at 30ug/kg.In the Metoprolol group,Metoprolol suspension was given according to the standard of 5.2mg/kg per day.In the DJFM group,DJFM was given at 17.6g/kg per day.After 2 weeks of administration,the biologic experiment system BL-420F was used to monitor the II lead ECG curve,and the ECG changes were observed and recorded.Then,the left ventricle of the rat was taken,and part of the heart tissue sodium potassium pump was detected.Results:(1)The effect of DJFM on ECG of rats with ventricular arrhythmia:After intravenous injection of aconitine,the incidence of Ventricular Premature beat(VP),Ventricular Tachycardia(VT),Ventricular Fibrillation(VF)in the model group was 100%,suggesting that the model building of rats with ventricular arrhythmia was successful.(2)VP,VT,and VF time:Compared with model group,DJFM group and Metoprolol group can significantly delay the VP,VT and VF,the difference was statistically significant(P<0.05).The effect of DJFM group and Metoprolol group on delaying the appearance of VP,VT and VF was the same,there was no significant difference(P>0.05).(3)The effect of DJFM on sodium potassium pump in rat ventricular arrhythmia heart tissues:Compared with the blank group,the sodium potassium pump value in the model group was significantly decreased,and the difference was statistically significant(P<0.05).Compared with the model group,the sodium potassium pump value of the tissues in the Metoprolol group and the DJFM group increased,and the difference was statistically significant(P<0.05).There was no significant difference in sodium potassium pump between the Metoprolol group and the DJFM group(P>0.05).Conclusion:1.The rat model of ventricular arrhythmia can be successfully prepared by intravenous injection of Aconitine.2.DJFM can prolong the occurrence time of cardiac arrhythmias caused by aconitine in rats,such as VP,VT,VF,et al.The mechanism may be related to fast Na^+channel,and it may prevent and control arrhythmias by inhibiting Na^+influx and reducing the fast response cellular self-discipline.3.DJFM can protect the myocardial tissue sodium potassium pump,which can protect the myocardial cells and improve the myocardial metabolism.

Lesson Eighty four Ventricular arrhythmias originating from papillary muscles in the right ventricle

Patientcharacteristics Patients in this study consisted of eight consecutive patients with frequent premature ventricular complexes(PVCs) or both PVCs and ventricular tachycardia(VT)who had been referred for catheter ablation and whose arrhythmia was mapped to one of the right ventricular(RV)papillary muscles(PAPs).The control group consisted of 10 consecutive patients who were referred for ablation of symptomatic idiopathic

Effects of antiarrhythmic peptide 10 on acute ventricular arrhythmia

Objective:To observe the effects antiarrhythmic peptide 10(AAPIO) aon acute ventricular arrhythmia and the phosphorylation state of ischemic myocardium conncxin.Methods:Acute total ischemia and partial ischemia models were established by ceasing perfusion and ligating the left anterior descending coronary artery in SD rats.The effects of AAP10(1 mg/L) on the incidence rate of ischemia-induced ventricular arrhythmia were observed.The ischemic myocardium was sampled to detect total-Cx43 and NP-Cx43 by immunofluorcsecnt staining and western blotting,the total-Cx43 expression was detected through image analysis system by semi-quantitative analysis.Results:AAP10 could significantly decrease the incidence of ischemia-induced ventricular tachycardia and ventricular fibrillation.During ischemic stage,total ischemia(TI) and AAP10 total ischemia(ATI) groups were compared with partial ischemia(Pi) and AAP10 partial ischemia(API) groups.The rates of incidence for arrhythmia in the ATI and API groups(10%and 0%) were lower than those in the TI and PI groups(60%and 45%).The difference between the two groups was statistically significant(P=0.019,P=0.020).The semi-quantitative analysis results of the ischemic myocardium showed that the total-Cx43 protein expression distribution areas for TI.ATI,PI and API groups were significantly decreased compared with the control group.On the other hand,the NP-Cx43 distribution areas of TI,ATI,PI and API groups were significantly increased compared with the control group(P>0.05).AAP10 could increase the total-Cx43 expression in the ischemic area and decrease the NP-Cx43 expression.Western blot results were consistent with the results of immunofluorescence staining.Conclusions:AAP10 can significantly decrease the rate of incidence of acute ischemia-induced ventricular tachycardia and ventricular fibrillation.Acute ischemic ventricular arrhythmias may have a relationship with the decreased phosphorylation of Cx43 induced by ischemia.AAP10 may stimulate the phosphorylation of Cx43 by increasing the totai-Cx43 expression and decreasing the NP-Cx43 expression in the ischemic area,so as to decrease ventricular arrhythmia.

C-reactive protein as a predictor of malignant ventricular arrhythmias in non-ST elevation myocardial infarction

Objective To investigate whether C-reactive protein (CRP) is a biomarker of malignant ventricular arrhythmias (MVA) occurring in non-ST elevation myocardial infarction (NSTEMI) patients with Global Registry of Acute Coronary events (GRACE) scores < 140. Methods A total of 1450 NSTEMI patients were included in this study. Hs-CRP blood levels were measured via a turbidimetric immunoassay after confirming the diagnosis of NSTEMI with GRACE scores < 140. Results Consistent with prior studies, the MVA occurrence rate in our cohort was 6.7%, and patients with MVA exhibited a reduced left ventricular ejection fraction (46.1%± 6.9% vs. 61.5%± 8.7%, P = 0.032), a higher incidence of Killip classification > 1 (34.1% vs. 24.2%, P < 0.001), an increased surgical revascularization rate (34.1% vs. 9.7%, P < 0.001), and increased mortality (16.5% vs. 5.8%, P < 0.001). Serum hs-CRP levels were higher (P = 0.003) in NSTEMI patients with MVA, and this increase appeared unrelated to other clinical parameters. The C-statistic to discriminate MVA was 0.82 (95% CI: 0.74–0.89). Using receiver operating characteristics analysis, we optimized a cutoff point of 16 mL/L, and the sensitivity and specificity were 95% and 61%, respectively;the positive predictive value was 20% and the negative predictive value was 99%. Conclusions An hs-CRP assay is a potential MVA biomarker in low-risk NSTEMI patients with GRACE scores < 140. If validated in prospective studies, hs-CRP may offer a low-cost supplementary strategy for risk stratification for NSTEMI patients.

Heart rate-adjusted PR as a prognostic marker of long-term ventricular arrhythmias and cardiac death in ICD/CRT-D recipients

Objective To evaluate the PR to RR interval ratio (PR/RR,heart rate-adjusted PR) as a prognostic marker for long-term ventricular arrhythmias and cardiac death in patients with implantable cardioverter defibrillator (ICDs) and cardiac resynchronization therapy with defibrillators (CRT-D).Methods We retrospectively analyzed data from 428 patients who had an ICD/CRT-D equipped with home monitoring.Baseline PR and RR interval data prior to ICD/CRT-D implantation were collected from standard 12-lead electrocardiograph,and the PR/RR was calculated.The primary endpoint was appropriate ICD/CRT-D treatment of ventricular arrhythmias (VAs),and the secondary endpoint was cardiac death.Results During a mean follow-up period of 38.8 ± 10.6 months,197 patients (46%) experienced VAs,and 47 patients (11%) experienced cardiac death.The overall PR interval was 160 ± 40 ms,and the RR interval was 866 ± 124 ms.Based on the receiver operating characteristic curve,a cut-off value of 18.5% for the PR/RR was identified to predict VAs.A PR/RR ≥ 18.5% was associated with an increased risk of VAs [hazard ratio (HR)= 2.243,95% confidence interval (CI)= 1.665–3.022,P < 0.001) and cardiac death (HR = 2.358,95%CI = 1.240–4.483,P = 0.009) in an unadjusted analysis.After adjustment in a multivariate Cox model,the relationship remained significant among PR/RR ≥ 18.5%,VAs (HR = 2.230,95%CI = 1.555–2.825,P < 0.001) and cardiac death (HR = 2.105,95%CI = 1.101–4.025,P = 0.024.Conclusions A PR/RR ≥ 18.5% at baseline can serve as a predictor of future VAs and cardiac death in ICD/CRT-D recipients.

Coronary Artery Bypass Surgery for Patients Presenting with Ventricular Arrhythmias: Propensity Matched Early and Late Outcome

Objectives: Patients with ischemic ventricular arrhythmia (IVA) in the form of fibrillation or tachycardia represent a surgical challenge. Evidence in the literature suggests that ventricular arrhythmia threatens survival even after cardiac surgery. We aim to review the results of our patients presenting with IVA with regard to short and long term outcome following cardiac surgery. Methods: This was a retrospective study of data entered prospectively into our cardiac surgical database between January 1999 and September 2015. A total of 9609 patients underwent Cardiac Surgery which included 54 patients after surviving IVA. The short- and long-term outcomes were compared to a propensity matched group. Actuarial survival was calculated using Kaplan Meier analysis. Results: The 54 study group patients were propensity matched on a 1:2 basis with a control group of non-IVA (n = 108). The baseline preoperative characteristics and risk factors were similar between the 2 groups and all cases underwent CABG only. Univariate analysis showed pacing postoperatively (33.3 vs 66.7%;p = 0.001) and postoperative ventricular arrhythmia (10 vs 22.2%;p = 0.039) to be significantly higher in the IVA group. Cox-multivariate analysis showed postoperative ventricular arrhythmia in either group (Hazard ratio = 1.5) to be the only significant factor to impact mortality (p 0.001). Long term survival was not significantly different between the two groups (10.4;CI: 9.08 - 11.75 vs 9.3;CI: 7.61 - 11.01 yrs, p = 0.3). Conclusion: Cardiac surgery on patients presenting with IVA can be performed safely yielding short and long term results equivalent to non-IVA cases. These patients should not be denied surgery with consideration of good long term outcome.