Refractory Ventricular Fibrillation with Underlying Coronary Artery Disease after COVID-19 Vaccine-Kounis Syndrome or Coincidence

A 63-year-old man with diabetes and asymptomatic coronary artery disease developed refractory ventricular arrhythmia at 20 hours at rest after his second COVID-19 vaccine. Despite significant stenosis in the coronary arteries, there was no evidence of acute or old myocardial infarction, heart failure, myocarditis or structural abnormalities on post-mortem to account for the substrate for the fatal arrhythmia. The refractory and incessant nature of the ventricular fibrillation and post-mortem finding of a grossly elevated unexplained IgE level (in the absence of acute myocardial infarction) suggested the possibility of Kounis Syndrome or allergic acute coronary syndrome.

Idiopathic ventricular fibrillation with fragmented QRS complex and J wave in resting electrocardiogram

Objective To describe the clinical characteristics of idiopathic ventricular fibrillation （IVF） with fragmented QRS complex （f-QRS） and J wave in resting electrocardiogram. Methods We reviewed data from 21 case subjects in our hospital who were resuscitated after cardiac arrest due to IVF and assessed the prevalence of f-QRS and J wave in resting electrocardiogram （ECG）. All the case subjects were classified among three groups based on the electrocardiographic morphology： group I, both f-QRS and J wave were observed （n = 6）, group II, only J wave was observed （n = 9）, group III, neither f-QRS nor J wave was observed （n = 6）. Population characteristics, history of syncope or sudden cardiac arrest, incidence of ventricular fibrillation （VF）, and circumstance of VF were evaluated among the three groups. Results The incidence of index events （syncope, survived cardiac arrest and VF episodes recorded in implantable cardioverter defibrillator （ICD） or pacemakers） was 13.4 ~ 5.6 per-year in group I, 10.8 ~ 3.9 per-year in group II, and 9.8 -4- 4.2 per-year in group HI. There were significant differences in incidences among the three groups, the most frequent index events were observed in group I. The hazard ratio for incidence was 3.2 （95%CI, 1.1-7.9; P = 0.01）. The history and circumstance of the index events were different among the groups. In group I, all the index events occurred during sleep in early morning. In group II, four subjects suffered VF during strenuous physical activities or agitation state, two during sleep in early morning, three in usual activity. In group III, one subject suffered VF during sleep in early morning, one in agitation state, four in usual activity. Conclusions This study suggests that the IVF patients with the combined appearance of f-QRS and J wave in the resting ECG suffer an increased risk of VF, this subgroup of IVF patients has a unique clinical feature.

Application of Positron Emission Tomography in the Detection of Myocardial Metabolism in Pig Ventricular Fibrillation and Asphyxiation Cardiac Arrest Models after Resuscitation

Objective To study the application of positron emission tomography （PET） in detection of myocardia metabolism in pig ventricular fibrillation and asphyxiation cardiac arrest models after resuscitation. Methods Thirty-two healthy miniature pigs were randomized into a ventricular fibrillation cardiac arrest （VFCA） group （n=16） and an asphyxiation cardiac arrest （ACA） group （n=16）. Cardiac arrest （CA） was induced by programmed electric stimulation or endotracheal tube clamping followed by cardiopulmonary resuscitation （CPR） and defibrillation. At four hours and 24 h after spontaneous circulation was achieved, myocardial metabolism was assessed by PET. 18F-FDG myocardial uptake in PET was analyzed and the maximum standardized uptake value （SUVmax） was measured. Results Spontaneous circulation was 200% and 62.5% in VFCA group and ACA group, respectively. PET demonstrated that the myocardial metabolism injuries was more severe and widespread after ACA than after VFCA. The SUVrnax was higher in VFCA group than in ACA group （P〈0.01）. In VFCA group, SUVmax at 24 h after spontaneous circulation increased to the level of baseline. Conclusion ACA causes more severe cardiac metabol associated with less successful resuscitation. Myocardial sm injuries than VFCA. Myocardial dysfunction is stunning does occur with VFCA but not with ACA.

Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction

Sudden cardiac death （SCD） from ventricular fibrillation （VF） during coronary artery disease （CAD） is a leading cause of total and cardiovascular mortality, and in more than half of SCD cases VF occurs as the first symptom of CAD. Several epidemiological studies have shown that sudden death of a family member is a risk factor for SCD and VF during acute myocardial infarction （MI）, independent of traditional risk factors including family history of MI, suggesting a genetic component in the susceptibility to VF. To prevent SCD and VF due to MI, we need a better understanding of the genetic and molecular mechanisms causing VF in this apparently healthy population. Even though new insights and technologies have become available, the genetic predisposition to VF during MI remains poorly understood. Findings from a variety of different genetic studies have failed to reach reproducibility, although several genetic variants, both common and rare variants, have been associated to either VF or SCD. For this review, we searched PubMed for potentially relevant articles, using the following MeSH-terms： ＂sudden cardiac death＂, ＂ventricular fibrillation＂, ＂out-of-hospital cardiac arrest＂, ＂myocardial infarction, myocardial ische- mia＂, ＂coronary artery disease＂, and ＂genetics＂. This review describes the epidemiology and evidence for genetic susceptibility to VF due to MI.

Trigger elimination of polymorphic ventricular tachycardia and ventricular fibrillation by catheter ablation:trigger and substrate modification

Ventricular fibrillation （VF） is a malignant arrhythmia, usually initiated by a ventricular premature contraction （VPC） during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPCs preceded by Purkinje potentials or from the right ventricular outflow tract （RVOT） in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. The most important issue before the ablation session is the recording of the 12-lead ECG of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pace mapping. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.

Detection of Ventricular Fibrillation Using Random Forest Classifier

Early warning and detection of ventricular fibrillation is crucial to the successful treatment of this life-threatening condition. In this paper, a ventricular fibrillation classification algorithm using a machine learning method, random forest, is proposed. A total of 17 previously defined ECG feature metrics were extracted from fixed length segments of the echocardiogram (ECG). Three annotated public domain ECG databases (Creighton University Ventricular Tachycardia database, MIT-BIH Arrhythmia Database and MIT-BIH Malignant Ventricular Arrhythmia Database) were used for evaluation of the proposed method. Window sizes 3 s, 5 s and 8 s for overlapping and non-overlapping segmentation methodologies were tested. An accuracy (Acc) of 97.17%, sensitivity (Se) of 95.17% and specificity (Sp) of 97.32% were obtained with 8 s window size for overlapping segments. The results were benchmarked against recent reported results and were found to outper-form them with lower complexity.

Factors influencing survival of patient with in-hospital ventricular fibrillation： experience of a single center

Objective To evaluate the factors influencing the outcome of patients who suffered in-hospital ventricular fibrillation （IHVF）. Methods Data of patients with IHVF in a single center were collected. Clinical characteristics of patients were compared between those survived （n=112） and those died （n=94）, and those with IHVF occurred in inpatient ward and in emergency center. Multiple logistic regression analysis was used to identify factors associated with survival. Results There were 206 events in the analysis. The most common underlying disease was coronary artery disease （CAD）, especially acute myocardial infarction （AMI）. On multiple logistic regression analysis, independent predictors for failure to survive were higher NYHA class （odds ratio 1.7, 95% CI, 1.3-2.2, P〈 0.001）, lower serum potassium concentration （ [K＋] ） （odds ratio, 2.9, 95% CI, 1.9-4.3, P--0.007） and adrenaline usage （odds ratio, 25, 95% CI 11.5-55.1, P〈 0.001）. Emergency group have better NYHA class （P = 0.012）, lower [K-] （P 〈 0.001） than in inpatient ward group. Hypokalemia （serum potassium level 〈4.5 mmol/L） was found in all patients with AMI in emergency group. In AMI sub-group, 56.9% of IHVF events occurred within the first day after AMI, and decreasing within 2 weeks. Patients with fight coronary artery as infarction related artery （IRA） oRen （8/9, 88.9~,5） had bmdycardia （R-R interval 〉 ls） before the occurrence of IHVF, while those with left anterior descending artery as IRA often showed tachycardia （R-R interval 〈 0.6s） （8/12, 66.7%）. Conclusion The most common disease causing IHVF is CAD. Keeping [K＋] above 4.5mmol/1 could prevent on-setting IHVF, especially to AMI patients. The worse heart function is associated with higher rate of IHVF and worse pmgnosis （J Geriatr Cardio12010; 7：21-24）.

An Experimental Comparative Study on the Characteristicsof Ventricular Fibrillation during Cardiac Arrest and Methoxamine Administration

The effect of a pure α-adrenergic agent, methoxamine on ventricularfibrillation (VF) amplitude and the relation between hemodynamic parameters andsurvival in a rodent cardiopulmonary resuscitation (CPR) model were studied.Our results suggested that: 1) VF amplitude decreased during untreated VF, butit increased during pericardial chest compression ; 2) methoxamine significantly increased the mean aortic pressure (MAP) and coronary perfusion pressure (CPP)but not VF amplitude, and the survival also increased due to elevation of CPP;and 3) all surviving animals with successful defibrillhtion had a higher VF ampli-tude.

Ventricular fibrillation and sudden cardiac arrest in apical hypertrophic cardiomyopathy:Two case reports

BACKGROUND Apical hypertrophic cardiomyopathy(HCM)is considered to have a benign prognosis in terms of cardiovascular mortality.This serial case report aimed to raise awareness of ventricular fibrillation(VF)and sudden cardiac death(SCD)in apical HCM.CASE SUMMARY Here we describe two rare cases of apical HCM that presented with documented VF and sudden cardiac collapse.These patients were previously not recommended for primary prevention using implantable cardioverter-defibrillator(ICD)therapy based on current guidelines.However,both received ICD therapy for the secondary prevention of SCD.CONCLUSION These cases illustrate serious complications including VF and aborted sudden cardiac arrest in apical HCM patients who are initially not candidates for primary prevention using ICD implantation based on current guidelines.

Resuscitation from Prolonged Ventricular Fibrillation by Epinephrine Combined with Sodium-Hydrogen Exchanger Isoform-1 Inhibitor Cariporide

Objective To test the resuscitative effects from prolonged ventricular fibrillation by epinephrine combined with sodium hydrogen exchanger isoform 1 inhibitor Cariporide. Methods 16 rats were received a 3 mg/kg bolus of Cariporide or the same volume of 0.9%NaCl solution (control) 15 seconds before completion 12 minutes untreated VF. Chest compression (CC) was started for a total of 8 minutes. Adjusted the depth of compressor so that the aortic diastolic pressure to 25～28 mmHg during the 2nd minute of CC. Fix the depth of the piston and this depth was used throughout the remaining 6 minutes of CC. 10 seconds before starting the 3rd minute of chest compression, injected epinephrine (30 μg/kg). Recorded the time at which restoration of spontaneous circulation (ROSC) occurred in Cariporide treated rats. Electrical defibrillation was timed in control group to match the time of spontaneous defibrillation in Cariporide treated rats. To the rats, which cant be defibrillated spontaneously, received chest compression and rescues electrical shocks. Results compared with control group, with the same CC depth, Cariporide treated rats received the higher and longer lasting coronary perfusion pressure (P< 0.05), higher resuscitative rate (P< 0.05), less post resuscitative ventricular ectopic activities (P< 0.001), better hemodynamic effects and longer survival time (P< 0.05). Conclusion Epinephrine combined with sodium hydrogen exchanger isoform 1 inhibitor Cariporide may represent a novel and remarkably effective intervention for resuscitation from prolonged VF.

The Relation Between Hypertrophied Myocardium and Ventricular Fibrillation Threshold in Spontaneously Hypertensive Rats

Objectives To investigate the relation between hypertrophied myocardium and ventricular fibrillation threshold in spontaneously hypertensive rats （SHR）. Methods 20 male SHR were randomly divided into two groups： 10 week group （n= 10） and 18 week group （n=10）. 10 week male Wistar rats were controlled group （n=10）. The systolic blood pressure （SBP）, heart mass index （HMI）, ventricular effective refractory period （VERP） and ventricular fibrillation threshold（VFT） were measured respectively.① The SBP and HMI of SHR were significantly higher than those of Wistar rats（P 〈 0.001）. The VFT of SHR were significantly lower than that of Wistar rats （P 〈 0.001）.②In SHR, the SBP and HMI of 18 week SHR were significantly higher than those of 10 week SHR （P 〈 0.001）. The VFT of 18 week SHR were significantly lower than that of 10 week SHR （P 〈 0.001）. ③There were no significant difference of VERP among 10 week SHR, 18 week SHR and Wistar rats（P 〉 0.05）. ④There was no relationship between HMI and VFT or SBP in Wistar rats. There was significant relationship between HMI and VFT or SBP in different age spontaneously hypertensive rats. ⑤HMI, age and species of animal were the major influent factors of VFT. Conclusions The VFT of hypertrophied myocardium decreased. The higher the degree of hypertrophy of myocardium and the higher the systolic blood pressure were, the lower the ventricular fibrillation threshold was.

Comparison of Plegisol and Modified ST Thomas Hospital Cardioplegic Solution in the Development of Ventricular Fibrillation after Declamping of the Aorta

Ventricular fibrillation seen just after declamping of the aorta is an undesirable condition causing myocardial injury. To return to normal rhythm, often internal shocks are applied. But defibrillation itself can also contribute to myocardial injury. So prevention of fibrillation is more important than treatment. 236 patients undergoing coronary artery by-pass surgery were included in this retrospective clinical study. 144 of those patients were operated using modified St. Thomas’ Hospital cardioplegic solution, for stopping the heart. In the other 92 patients, plegisol cardioplegic solution was used. We compared the two groups for the development of ventricular fibrilation after declamping of the aorta. In the modified St. Thomas’ Hospital group, ventricular fibrillation after declamping of the aorta was seen less frequently, this being statistically significant (22.2% vs. 52.2%, p = 0.026). This study shows that the modified St.Thomas’ Hospital cardioplegic solution is preferred for avoiding ventricular fibrillation occuring just after declamping of the aorta.

Comparison Between Diltiazem and Cedilanid-D on Ventricular Rate Control of Atrial Fibrillation and Their Effect on Atrioventricular Conduction System.

Objectives This randomized study was designed to compare the safety and efficacy of intravenous diltiazem versus intravenous cedilanid-D （deslanoside） for ventricular rate control in patients with atrial fibrillation （AF）. Analysis of the effect on conduction system of these drugs was also performed. Methods Forty three patients with AF were randomly assigned to receive intravenous therapy with 0.25mg/kg diltiazem （n = 21） or 0.4rag cedilanid-D （n = 22）. If not effective at 120 minutes （〈 20% decrease in pretreatment ventricular rate or can not convert to sinus rhythm= another dose of diltiazem or 0.2mg cedilanid-D was administered. Blood pressure and electrocardiographic recordings were performed before and after 5, 10, 20, 30, 60 minutes of drug administration. Further recordings were performed at 120 minutes in noneffective patients, and at 180 minutes in patients who received second time drug administration. To evaluate the effect on conduction system of these two drugs by measuring PA, AH and HV intervals using His bundle electrogram test another nineteen sinus rhythm patients were randomized to dihiazem （n=9） and cedilanid （n= 10） group. His bundle electrogram recordings were performed before and after 5, 10, 20 and 30 minutes of drug administration. Statistical significance was assessed with the use of t test, Fisher＇s exact test, ANOVA and LSD methodology. Results At baseline and after 5, 10, 20, 30, 60 minutes of drug administration the heart rates （mean±SD） were（133±15）, （92±20）, （87±22）, （85 ±20）, （85±21）, （85 ±23）beats/minute in diltiazem group respectively and（ 140±21 ）, （ 122±24）, （118±25）, （110±26）, （112±25）, （110±28） beats/ minute in cedilanid-D group respectively. Heart rate reduction was higher in diltiazem group than cedilanid group during 5 （41±20 vs 17±14,P 〈 0.01）; 10 （46±21 vs 22±20, P〈0.01）; 20 （48±21 vs 29±22, P〈0.01 ） ; 30（48±22 vs 27±22,P〈0.01 ）and 60 minutes （48±23 vs 29±24, P〈 0.05）. Both drugs had no effect on both systolic and diastolic blood pressure （P 〉0.05） and no major side effects were noticed. Diltiazem maintained effective ventrieular rate in 20 patients, whereas eedilanid-D maintained in 15 patients within 180 minutes （95.2%vs 68.2%,P〈 0.05）. There were no statistical significance in baseline heart rate, age and weight between the two groups. Both diltiazem and cedilanid-D can increase AH interval, but have no effect on HV and PA intervals in sinus rhythm patients. Conclusions Both dihiazem and eedilanid-D decrease ventrieular heart rate, but heart rate reduction is significantly higher in diltiazem group, thus should be considered as a drug of choice for emergency control of ventrieular rate. Under clinical monitoring this dose of diltiazem seems to be safe and applicable in AF patients with congestive heart failure. Both drugs have no effect on PA and HV intervals but increase the AH interval thereby can reduce ventricular rate.

Energy Level and Success of Internal Defibrillation for Shockable Rhythm during Cardiopulmonary Bypass in Cardiac Surgery:A Retrospective Study

Internal defibrillation is commonly indicated for shockable rhythm following cross-clamp removal in cardiac surgery.Low energy decreases the success rate of defibrillation but high energy can cause myocardial damage.This study aimed to determine the success rate of internal defibrillation for shockable arrhythmias after cardiac surgery.Retrospective data of 1,424 patients who developed shockable rhythms(ventricular fibrillation or ventricular tachycardia),and required internal defibrillation after aortic cross-clamp removal during cardiac surgery,without deep hypothermic circulatory arrest technique,from August 2015 to July 2017,were reviewed.The overall success rate of internal defibrillation in the first attempt of defibrillation was 61.5%.The success rate of the energy levels at 30,10,and 7 Jules were 66.7,64.9,and 61.5%,respectively.The success rate was higher in patients who had a better ejection fraction than those who failed after defibrillation.This was significantly associated with higher pH,higher bicarbonate,lower serum calcium,and lower total cardioplegic volume during cardiopulmonary bypass(CPB).Redo-valve surgery,valvular surgery,and combined coronary artery bypass graft with valvular surgery had a non-significantly lower success rate(p-value=0.989).Incidence of failure for defibrillate patients in redo-valvular surgery,combined coronary artery bypass graft with valve surgery,adult congenital heart defect,and valvular surgery;requiring four or five shocks was non-significantly increased.Recurrent rate of ventricular fibrillation/ventricular tachycardia was 13.5%.The success rate of internal defibrillation was not related to the dose of energy used after being weaned off CPB.

Suxiao Jiuxin Pills Prevent Ventricular Fibrillation from Inhibiting L-type Calcium Currents CaV1.2 in vivo and in vitro

Objective: To investigate whether Suxiao Jiuxin Pills(SJP), a Chinese herbal remedy, is an anti-ventricular fibrillation(VF) agent. Methods: VF was induced by isoproterenolol(ISO) intraperitoneal injection followed by electrical pacing in mice and rabbits. The effects of SJP on the L-type calcium channel current(CaV1.2), voltage-dependent sodium channel current(INa), rapid and slow delayed rectifier potassium channel current(IKr and IKs, respectively) were studied by whole-cell patch-clamp method. Computer simulation was implemented to incorporate the experimental data of SJP effects on the CaV1.2 current into the action potential(AP) and pseudo-electrocardiography(pseudo-ECG) models. Results: SJP prevented VF induction and reduced VF durations significantly in mice and rabbits. Patch-clamp experiments revealed that SJP decreased the peak amplitude of the CaV1.2 current with a half maximal concentration(IC50) value of 16.9 mg/L(SJP-30 mg/L, –32.8±6.1 pA;Verapamil, –16.2±1.8 pA;vs. control, –234.5±16.7 pA, P<0.01, respectively).The steady-state activation curve, inactivation curve, and the recovery from inactivation of the CaV1.2 current were not shifted significantly. Specifically, SJP did not altered INa, IKr, and IKs currents significantly(SJP vs.control, P>0.05). Computer simulation showed that SJP-reduced CaV1.2 current shortened the AP duration,transiting VF into sinus rhythm in pseudo-ECG. Conclusion: SJP reduced VF via inhibiting the CaV1.2 current with in vivo, in vitro, and in silico studies, which provide experimental basis for SJP anti-VF clinical application.

Optimal antiarrhythmic drug therapy for electrical storm

Electrical storm, defined as 3 or more separate episodes of ventricular tachycardia or ventricular fibrillation within 24 hours, carries significant morbidity and mortality. These unstable ventricular arrhythmias have been described with a variety of conditions including ischemic heart disease, structural heart disease, and genetic conditions. While implantable cardioverter defibrillator implantation and ablation may be indicated and required, anti- arrhythmic medication remains an important adjunctive therapy for these persons.

Comparison of Cerebral Metabolism between Pig Ventricular Fibrillation and Asphyxial Cardiac Arrest Models

Background：Morbidity and mortality after resuscitation largely depend on the recovery of brain function.Ventricular fibrillation cardiac arrest （VFCA） and asphyxial cardiac arrest （ACA） are the two most prevalent causes of sudden cardiac death.Up to now,most studies have focused on VFCA.However,results from the two models have been largely variable.So,it is necessary to characterize the features of postresuscitation cerebral metabolism of both models.Methods：Forty-four Wuzhishan miniature inbred pigs were randomly divided into three groups：18 for VFCA group,ACA group,respectively,and other 8 for sham-operated group （SHAM）.VFCA was induced by programmed electric stimulation,andACA was induced by endotracheal tube clamping.After 8 min without treatment,standard cardiopulmonary resuscitation （CPR） was initiated.Following neurological deficit scores （NDS） were evaluated at 24 h after achievement of spontaneous circulation,cerebral metabolism showed as the maximum standardized uptake value （SUVmax） was measured by 18F-fluorodeoxyglucose positron emission tomography/computed tomography.Levels of serum markers of brain injury,neuron specific enolase （NSE）,and S100β were quantified with an enzyme-linked immunosorbent assay.Results：Compared with VFCA group,fewer ACA animals achieved restoration of spontaneous circulation （61.1% vs.94.4%,P 〈 0.01） and survived 24-h after resuscitation （38.9% vs.77.8%,P 〈 0.01） with worse neurological outcome （NDS：244.3 ± 15.3 vs.168.8 ± 9.71,P 〈 0.01）.The CPR duration of ACA group was longer than that of VFCA group （8.1 ± 1.2 min vs.4.5 ± 1.1 min,P 〈 0.01）.Cerebral energy metabolism showed as SUVmax in ACA was lower than in VFCA （P 〈 0.05 or P 〈 0.01）.Higher serum biomarkers of brain damage （NSE,S100β） were found inACA than VFCA after resuscitation （P 〈 0.01）.Conclusions：Compared with VFCA,ACA causes more severe cerebral metabolism injuries with less successful resuscitation and worse neurological outcome.

Efficacy of amiodarone and lidocaine for preventing ventricular fibrillation after aortic cross-clamp release in open heart surgery:a meta-analysis of randomized controlled trials

Objective： The relative preventative efficacy of amiodarone and lidocaine for ventricular fibrillation（VF） after release of an aortic cross-clamp（ACC） during open heart surgery has not been determined. This meta-analysis was designed to systematically evaluate the influence of amiodarone, lidocaine, or placebo on the incidence of VF after ACC. Methods： Prospective randomized controlled trials（RCTs） that compared the VF-preventative effects of amiodarone with lidocaine, or amiodarone or lidocaine with placebo were included. Pub Med, EMBASE, and the Cochrane Library were searched for relevant RCTs. Fixed or randomized effect models were applied according to the heterogeneity of the data from the selected studies. Results： We included eight RCTs in the analysis. Pooled results suggested that the preventative effects of amiodarone and lidocaine were comparable（relative risk（RR）=1.12, 95% confidence interval（CI）： 0.70 to 1.80, P=0.63）, but both were superior to the placebo（amiodarone, RR=0.71, 95% CI： 0.51 to 1.00, P=0.05; lidocaine, RR=0.63, 95% CI： 0.46 to 0.88, P=0.006）. The percentage of patients requiring electric defibrillation counter shocks（DCSs） did not differ significantly among patients administered amiodarone（RR=0.21, 95% CI： 0.04 to 1.19, P=0.08）, lidocaine（RR=2.44, 95% CI： 0.13 to 44.02, P=0.55）, or the placebo（RR=0.56, 95% CI： 0.25 to 1.25, P=0.16）. Conclusions： Amiodarone and lidocaine are comparably effective in preventing VF after ACC, but the percentage of patients who subsequently require DCSs does not differ among those administered amiodarone, lidocaine, or placebo.

Tumor necrosis factor-α： a new mechanism of ischemic ventricular fibrillation？

Ventricular fibrillation （VF） in myocardial ischemia is called ＂ischemic VF＂. As a severe morbid state and a leading cause of sudden cardiac attack, ischemic VF induces approximately 3 million deaths in the United States each year. Ischemic VF is caused by ＂triggers＂ such as ventricular premature beat or ventricular tachycardia in the presence of a suitable ＂substrate＂. The triggers frequently occur at the border zone and the substrate is required for the maintenance of ischemic VE The critical factors for the initiation and maintenance of ischemic VF are obscure. Tumor necrosis factor-α （TNF-α）, an inflammatory cytokine expressed in myocardial ischemia, plays an important role in the pathophysiological process of acute myocardial infarction （AMI）. TNF-α also causes arrhythmia by action potential prolongation and abnormal Ca^2＋ handling, which also contribute to ischemic VE But the relationship between TNF-α and ischemic VF is unknown. In this article, we suggest that TNF-α may be a novel substrate of ischemic VE This may be a new mechanism for ischemic VF.

Ibutilide decreases defibrillation threshold by the reduction of activation pattern complexity during ventricular fibrillation in canine hearts

Background Ibutilide has been commonly used for pharmacologic cardioversion of atrial fibrillation and flutter in clinical settings. The objective of this study was to investigate the effects of ibutilide on the defibrillation threshold （DFT）, restitution properties, dispersion of refractoriness and activation patterns during ventricular fibrillation （VF）. Methods Ibutilide was administrated intravenously in six open-chest beagles. Before and after the drug administration, 20-second episodes of VF were electrically induced and recorded with a 10×10 unipolar electrode plaque sutured on the lateral epicardium of the left ventricle. DFT and VF activation patterns, including type of epicardial activation maps, VF cycle length （VF-CL）, conduction velocity, wavelength （WL） and reentry incidence, were measured. Restitution properties and dispersion of refractoriness were estimated from activation recovery intervals （ARI） during pacing. Results Compared to baseline, ibutilide markedly decreased the DFT by 31% （（491±14） V vs. （337±59） V, P 〈0.01）. The drug significantly reduced the maximal slope of the restitution curve （1.34±0.08 vs. 0.76±0.06, P 〈0.01） and its epicardial dispersion （0.36±0.09 vs. 0.21±0.06, coefficient of variation, P=0.03）. The dispersion of refractoriness was enhanced at the pacing cycle length of 300 ms to 160 ms by ibutilide. The drug significantly increased the VF-CL （（96±19） ms vs. （112±20） ms, P 〈0.01） and the WL （（41±9） mm vs. （52±14） mm, P=0.02） during VF, and reduced the reentry incidence by 25% （0.08±0.02 vs. 0.06±0.02, P 〈0.01）. In the epicardial activation maps, ibutilide significantly reduced the percentage of more complex activation maps during VF. Conclusions Intravenous ibutilide significantly decreased the DFT. It might be due to reduction of activation pattern complexity during VF.