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PubMed2004

Can local ventricular fibrillation interval predict ventricular refractory period in human hearts?

Assessment of the spatial dispersion of ventricular refractory periods has become an important part of electrophysiological study in both experimental and clinical settings, because inhomogeneity of ventricular refractoriness is associated with an increased risk of life-threatening ventricular arrhythmias. Previous animal studies in dog and sheep have demonstrated that local ventricular fibrillation (VF) intervals measured from the heart surface correlate well with the ventricular effective refractory periods measured from the same ventricular sites. We hypothesise that local VF intervals may also predict the ventricular refractory periods in human hearts, hence, can be used to assess the spatial dispersion of refractoriness and to predict the risk of ventricular arrhythmias.

Animals↗
PubMed2004

[Ionic currents and ventricular fibrillation dynamics].

Ventricular fibrillation is the principal immediate cause of sudden cardiac death. Yet, in contrast to other arrhythmias, ventricular fibrillation is considered to be inaccessible to pharmacologic therapy because of its characteristic and apparently never-ending disarray of electrical waves that seem to propagate chaotically throughout the ventricles. Its prevention has historically been focused on the suppression of ventricular ectopy, with the idea of eliminating potential triggers of fibrillation, which from a clinical standpoint has proven to be detrimental. During the last decade, the application of the theory of wave propagation in non-linear excitable media to the study of cardiac fibrillation has led to a dramatic increase in our understanding of its mechanisms. It is now clear that fibrillation is generated and maintained by rotors that gyrate at exceedingly high frequencies. From such rotors emanate spiral waves of excitation that propagate throughout the myocardium in very complex ways. Among the most important factors that determine rotor dynamics are the electrophysiological properties of the ventricular cells, established by their underlying transmembrane ionic currents. Thus, in recent years, studies have focused on the roles played by specific ionic mechanisms and their modulation by antiarrhythmic drugs in ventricular fibrillation dynamics. This review article summarizes the main findings of such studies, which pave the way for a better understanding of fibrillation, and for the development of new pharmacological approaches that aim to prevent rotor formation and maintenance rather than to suppress the triggering ectopic event.

Anti-Arrhythmia Agents↗
PubMed1975

Recurrent ventricular fibrillation and modes of death in survivors of out-of-hospital ventricular fibrillation.

We examined the causes of death in patients previously resuscitated from out-of-hospital ventricular fibrillation. In 51 months, 234 patients were sucessfully resuscitated, hospitalized and discharged home. During follow-up observation, 89 episodes of recurrent ventricular fibrillation or death (or both) occurred, 64 of which (72 per cent) were unexpected, out-of-hospital circulatory arrests. Ventricular fibrillation occurred in 77 per cent of the 44 episodes in which the electrocardiogram was observed. Ten patients survived one or more episodes of recurrent ventricular fibrillation. Median time to recurrent ciruclatory arrest was 20 weeks after the preceding episode. Prodromal symptoms were infrequent, and activity levels were generally low at the time of cardiac arrest. Recurrent ventricular fibrillation of sudden death (or both) occurred predominantly when the initial episode was not associated with acute myocardial infarction. Patients resuscitated from ventricular fibrillation are susceptible to early recurrence, probably reflecting continuing myocardial electrical instability.

Adult↗
PubMed1992

Induction of ventricular fibrillation versus monomorphic ventricular tachycardia during programmed stimulation. Role of premature beat conduction delay.

BACKGROUND: Premature stimuli can cause ventricular fibrillation (VF) during electrophysiological testing. The electrophysiological correlations associated with the onset of VF were evaluated in 40 patients who had this rhythm induced during programmed ventricular stimulation. These parameters were compared with those observed in 51 patients who had inducible sustained monomorphic ventricular tachycardia (VT) and 45 patients who had no inducible sustained ventricular tachyarrhythmias. METHODS AND RESULTS: Shortest premature coupling intervals for S2, S3, and S4 at induction of tachycardia or before achieving refractoriness, corresponding conduction latencies (defined as the time from the premature stimulus to the upstroke of the depolarization wave front recorded 35 mm away from the stimulation site), and ventricular activation times (defined as the time from the premature stimulus to the end of the depolarization wave) were compared. The mean coupling intervals were longest in the inducible VT patients: 300 +/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively. In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/- 20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194 +/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The coupling interval of the last premature extrastimulus was above 200 msec in 70% of the patients in whom VF was induced. The largest increases in latency and activation times were recorded in patients in whom VF was induced. The cumulative increase in latency, defined as increased conduction time from baseline, summed for all the premature stimuli was also the greatest at initiation of VF. In contrast, the smallest increases in these parameters were noted in the patients with no inducible VT or VF. Measurements of total activation time yielded similar results as those recorded for latencies. The most important parameters distinguishing the VT patient population from the other two groups were the low ejection fractions and the longer coupling intervals at which VT was induced, whereas in the VF group, the most important discriminating factor was cumulative activation time. Sixty-three percent of the inducible VF patients presented with abnormal hearts (myocardial infarction or cardiomyopathy), whereas 88% of the inducible VT patients had abnormal hearts. In contrast, only 25% of the patients in whom no arrhythmia was induced presented with abnormal hearts. Mean ejection fraction was 32 +/- 15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and 51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus VT). CONCLUSIONS: The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.

Cardiac Complexes, Premature↗
PubMed1994

Lidocaine converts inducible ventricular fibrillation into sustained ventricular tachycardia in conscious dogs with recent myocardial infarction.

The aim of the present study was to investigate the effect of lidocaine (L) on ventricular tachyarrhythmias with special reference to ventricular fibrillation (VF). Myocardial infarction (MI) was created in 39 dogs by doubly ligating the left anterior descending (LAD) coronary artery. All animals surviving the infarction (n = 33) were subjected to programmed ventricular stimulation 7.6 +/- 3.2 days later. Local electrical activity was recorded from the subepicardium of the left ventricular wall by means of a specially designed composite electrode. L (2 and 4 mg/kg i.v.) facilitated the induction of sustained monomorphic ventricular tachycardia (sVT) in 8 dogs with nonsustained polymorphic ventricular tachycardia (nsVT) in the control. In 13 dogs developing sVT during control stimulation, L slowed the rate of tachycardia in 8 animals (first-dose effect), while it abolished arrhythmia induction in 5 animals (second-dose effect). It was interesting that L (2 mg/kg) abolished reproduction of control VF in 12 animals by converting it into sVT. L significantly depressed conduction and prolonged ventricular refractoriness in the infarction zone. The results suggest that L facilitates induction of sVT in conscious dogs with recent MI, thereby decreasing susceptibility of infarcted myocardium to aggressive polymorphic nsVT or VF. The capability of L to exacerbate slow conduction in the infarction zone seems not to favor the development of VF during this stage of MI.

Animals↗
PubMed1987

Decline in ventricular fibrillation threshold after successive premature extrastimuli: a possible explantation for the induction of ventricular fibrillation during programmed stimulation with multiple extrastimuli.

To examine the relation between the ventricular fibrillation threshold and the number of premature extrastimuli delivered to the right ventricle during programmed ventricular stimulation, a clinical stimulation protocol was performed in nine normal, anaesthetised, closed chest dogs. In addition, the ventricular fibrillation threshold was measured in each dog after a train of eight paced (S1) beats (VFT-S2), after a single premature extrastimulus (VFT-S3), and after two extrastimuli (VFT-S4). The VFT-V3 was 32% lower than the VFT-S2 (16(7) mA vs 24(9) mA, p less than 0.001). The VFT-S4, or the current required by the S4 extrastimulus to induce ventricular fibrillation, was 25% lower than the VFT-S3 (12(8) mA vs 16(7) mA, p less than 0.05). The cumulative reduction in the ventricular fibrillation threshold measured by the S1S2S3S4 stimulation protocol was approximately 50%. Although in most dogs the VFT-S4 was still considerably higher than twice threshold current intensity, the results of the study suggest that a possible mechanism for the induction of non-clinical ventricular fibrillation in the clinical electrophysiology laboratory may be the progressive lowering of the ventricular fibrillation threshold caused by the addition of multiple extrastimuli. This may be particularly relevant in patients with an already reduced fibrillation threshold.

Action Potentials↗
PubMed1995

Regional capture of fibrillating ventricular myocardium. Evidence of an excitable gap.

Previous investigations have suggested that during ventricular fibrillation (VF) pacing stimuli are incapable of evoking propagated ventricular activations. To determine whether regional myocardial capture could be achieved during rapid pacing in VF, extracellular unipolar potentials were sampled (2 kHz) and recorded from 506 Ag-AgCl electrodes arranged in a rectangular grid (22 x 23, 1.12-mm spacing) embedded in a plaque overlying two pacing electrodes in the epicardium of the anterobasal right ventricle in pentobarbital-anesthetized pigs (25 to 30 kg, n = 6). During separate episodes of electrically induced VF, two bursts of 40 monophasic stimuli (10 mA, 2-millisecond duration) were asynchronously applied to the stimulating electrodes in either a bipolar, unipolar anodal, or unipolar cathodal mode. Evidence of regional capture was provided by (1) animating the first temporal derivative of the extracellular potentials, (2) analyzing inter-beat interval patterns, and (3) employing the Karhunen-Loeve decomposition method to quantify the repetitiveness of spatio-temporal patterns of activation. Regional capture of ventricular myocardium during VF was observed when pacing stimuli fell late in the local myocardial activation interval and when the pacing cycle length was 80% to 115% of the mean subplaque activation cycle length. When myocardial activations became phase locked to the pacing stimuli, repeatable spatiotemporal patterns of activation followed each stimulus. Poincaré sections at the plaque border revealed that during VF prior to pacing, interbeat intervals were irregular but were driven by pacing to stable fixed values at times corresponding to our qualitative declaration of regional capture. A similar correspondence was demonstrated between the time of capture, defined by direct observation of the activation patterns, and a rise in the power contained in the first two spatial modes of a Karhunen-Loeve decomposition. These data demonstrate that appropriately timed stimuli produce regional capture of fibrillating right ventricular myocardium in the pig and support the existence of an excitable gap during VF in this model.

Animals↗
PubMed2000

4-aminopyridine inhibits the occurrence of ventricular fibrillation but not ventricular tachycardia in the reperfused, P6olated rat heart.

The 4-aminopyridine (4-AP)-sensitive transient outward current (Ito) has been reported to play an important role in the ischemia- or high [Ca2+]o-induced reentrant ventricular arrhythmias. However, the role of 4-AP sensitive Ito in reperfusion arrhythmia remains unknown. Rat hearts were perfused with Tyrode solution (control), and treated with 0.5 micromol/L verapamil, 1 micromol/L glibenclamide, 10 micromol/L E-4031 or 2 mmol/L 4-AP. After a 10-min perfusion, hearts were subjected to 30-min global ischemia followed by 10-min reperfusion. The effects of the ion-channel blockers on the incidence of ventricular tachycardia (VT), torsades de pointes (Tdp) and ventricular fibrillation (VF) during the reperfusion period were investigated. Verapamil and 4-AP abolished VF and Tdp. The incidence of VT was also attenuated by verapamil, but not by 4-AP. Glibenclamide and E-4031 (a blocker of a rapidly activating component of delayed rectifier K+ current) did not affect the incidence of those tachyarrhythmias. Accordingly, (1) the underlying mechanism of VF or Tdp is different from that of VT, and (2) 4-AP sensitive Ito is required for the occurrence of reperfusion Tdp or VF in the present model.

4-Aminopyridine↗
PubMed1987

Effect of procainamide on the induction of ventricular fibrillation by sequential ventricular stimulation.

The effect of procainamide on ventricular vulnerability to fibrillation was studied in 13 anesthetized open-chest dogs. Epicardial electrograms were recorded through forty bipolar electrodes placed on the surface of exposed ventricles. Ventricular fibrillation (VF) was induced by sequential extrastimulation. The number of extrastimuli required to induce repetitive extrasystole (RE) or VF were defined as repetitive extrasystole threshold (RET) or ventricular fibrillation threshold (VFT). The epicardial electrograms at the onset of ventricular arrhythmia were divided every 100 msec after the last extrastimulation, and the ratio of recordings with activation time of more than 50 msec during each divided period was defined as "chaotic score". Intravenous injection of procainamide at the dose of 20 mg/kg failed to increase RET but successfully increased VFT from 4.4 +/- 0.9 to 7.0 +/- 1.8 in hearts with necrosis. Procainamide significantly reduced chaotic score from 36 +/- 12% to 14 +/- 7% at 5 sec after the induction of ventricular arrhythmias. We concluded that the antifibrillatory action of procainamide is based on a reduction of the number of chaotic multiple reentries, but not on the prevention of reentry per se.

Animals↗
PubMed2001

Excitable gap in canine fibrillating ventricular myocardium: effect of subacute and chronic myocardial infarction.

INTRODUCTION: The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. METHODS AND RESULTS: Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112-electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 +/- 17 msec and 37 +/- 18 msec, respectively) and chronic infarction dogs (41 +/- 14 msec and 35 +/- 14 msec, respectively) than normal dogs (32 +/- 13 msec and 30 +/- 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. CONCLUSION: During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies.

Acute Disease↗
PubMed1975

[Ventricular fibrillation in acute phase of myocardial infarct. 1. Relationship between the development of ventricular fibrillation in myocardial infarct and previous rhythm disorders].

The author analyses the results of experimental studies in dogs and cats, that included a continuous recording of ECG, electrogram and monophase cardiac potentials during 1 hour following coronary artery ligation. The ligation caused bradycardia, but no correlation was found between the degree of bradycardia and the development of extrasystole and ventricular fibrillation. Extrasystole developed in 100% of the experiments in which the coronary artery ligation resulted in ventricular fibrillation, and in 66% and 87% of those without this complication, conducted in dogs and cats respectively. The rate of extrasystole proved important for the prognosis of fibrillation. The number of extrasystoli noted during the mean time of the development of fibrillation was 5 times higher in the experiments with ventricular fibrillation than in those without fibrillation. In the experiments with fibrillation the extrasystoli tended to occur earlier within the cardiac cycle. Of the total number of extrasystoli, grouped extrasystoli comprised 89% in the experiments with ventricular fibrillation, and 21%--in those without fibrillation. Ventricular tachystystole was noted in 50% of the experiments with fibrillation and in 17% of those without this complication. In the experiments complicated by fibrillation the period of ventricular tachysystole was characterized by a gradual shortening of the cardiac cycles.

Acute Disease↗
PubMed1997

Idiopathic ventricular fibrillation.

Idiopathic ventricular fibrillation is defined as cardiac arrest in the absence of structural heart disease and other identifiable causes of ventricular fibrillation. It occurs in 1% to 9% of survivors of out-of-hospital cardiac arrest. The mean age of these patients is 35 to 40 years, and 70% to 75% are male. The pathogenesis is unknown; psychosocial factors may play a role. Baseline clinical characteristics have not been found to identify the 20% to 30% of patients who will have recurrent cardiac arrest. At present, implantation of an automatic defibrillator is the treatment of choice. Two registries have been established to enhance our knowledge of this unusual catastrophic entity.

Adult↗
PubMed2006

Outcomes of in-hospital ventricular fibrillation in children.

BACKGROUND: Ventricular fibrillation and ventricular tachycardia are less common causes of cardiac arrest in children than in adults. These tachyarrhythmias can also begin during cardiopulmonary resuscitation (CPR), presumably as reperfusion arrhythmias. We determined whether the outcome is better for initial than for subsequent ventricular fibrillation or tachycardia. METHODS: All cardiac arrests in persons under 18 years of age were identified from a large, multicenter, in-hospital cardiac-arrest registry. The results from children with initial ventricular fibrillation or tachycardia, children in whom ventricular fibrillation or tachycardia developed during CPR, and children with no ventricular fibrillation or tachycardia were compared by chi-square and multivariable logistic-regression analysis. RESULTS: Of 1005 index patients with in-hospital cardiac arrest, 272 (27 percent) had documented ventricular fibrillation or tachycardia during the arrest. In 104 patients (10 percent), ventricular fibrillation or tachycardia was the initial pulseless rhythm; in 149 patients (15 percent), it developed during the arrest. The time of initiation of ventricular fibrillation or tachycardia was not documented in 19 patients. Thirty-five percent of patients with initial ventricular fibrillation or tachycardia survived to hospital discharge, as compared with 11 percent of patients with subsequent ventricular fibrillation or tachycardia (odds ratio, 2.6; 95 percent confidence interval, 1.2 to 5.8). Twenty-seven percent of patients with no ventricular fibrillation or tachycardia survived to hospital discharge, as compared with 11 percent of patients with subsequent ventricular fibrillation or tachycardia (odds ratio, 3.8; 95 percent confidence interval, 1.8 to 7.6). CONCLUSIONS: In pediatric patients with in-hospital cardiac arrests, survival outcomes were highest among patients in whom ventricular fibrillation or tachycardia was present initially than among those in whom it developed subsequently. The outcomes for patients with subsequent ventricular fibrillation or tachycardia were substantially worse than those for patients with asystole or pulseless electrical activity.

Adolescent↗
PubMedDate not supplied

Ultrastructural-functional basis for spontaneous termination of ventricular fibrillation in mammals.

Ventricular fibrillation in humans is generally sustained (SVF), but it can be also transient (TVF), reverting spontaneously to sinus rhythm. In previous studies we have shown that: a) TVF appears in all young mammals and varies according to age and species; b) it requires synchronization of myocardial cell activity; c) infusion of certain drugs may change the type of ventricular fibrillation from sustained into transient. We hypothesize that the synchronization required for TVF depends on the electrical conductivity of intercellular structures. These intercellular couplings differ among species and decrease with age. Comparison between the inter- and intra-specific variations of intercellular connective structure described in the literature with the type of ventricular fibrillation found in our previous studies on various animals of different ages showed a clear relationship between these histological variations and the changes in the type of ventricular fibrillation. In this study we examined intercellular connective structures ultrastructurally in 3 groups of cats: a. control, untreated cats exhibiting sustained ventricular fibrillation; b. untreated cats exhibiting transient ventricular fibrillation; c. treated cats exhibiting sustained ventricular fibrillation before infusion of a defibrillating drug and transient ventricular fibrillation thereafter. It was found that the intercellular connective structure in cats exhibiting sustained ventricular fibrillation differs significantly from that in cats exhibiting transient fibrillation. In hearts exhibiting sustained ventricular fibrillation, many intercellular connective structures are widened and the degree of widening is pronounced, forming a continuous line, while in hearts exhibiting transient ventricular fibrillation the widened junctions are rare and isolated and the widening is relatively small. These preliminary results strongly support our above-mentioned hypothesis, providing an explanation for the origin of transient ventricular fibrillation and a tool for the development of new defibrillating drugs.

Animals↗
PubMed2000

[Mechanism of induction and termination of ventricular fibrillation--significance of dispersion of ventricular repolarization].

It has been known for many years that ventricular fibrillation may be induced and terminated by electrical field stimuli. Recent experimental studies have shown that both fibrillation and defibrillation have a common electrophysiologic mechanism that is based on the interaction between the electrical field stimulus and ventricular repolarization. Ventricular fibrillation will be induced if the field stimulus is applied with the area of vulnerability, this area of vulnerability is defined two dimensionally by the shock coupling interval and shock strength, and is modified by the configuration of the shock. A field shock that is applied within the area of vulnerability causes heterogeneity of ventricular repolarization immediately after the shock (postshock dispersion), thereby enabling the development of circuit movements and reentry, and resulting in ventricular fibrillation. High energy shocks, however, that are applied above the area of vulnerability (i.e., above the upper limit of vulnerability) will not induce ventricular fibrillation due to homogeneous prolongation of repolarization and a resulting small postshock dispersion. In analogy, ventricular fibrillation will continue after unsuccessful low-energy defibrillation shocks due to high postshock dispersion, whereas a high-energy shock will synchronize ventricular repolarization, thereby causing small postshock dispersion and termination of ventricular fibrillation. This paper describes the relation between fibrillation, defibrillation and ventricular repolarization based on experimental findings. A possible clinical application of these findings is that the upper limit of vulnerability may be used as a surrogate for the defibrillation threshold. Thus, defibrillation threshold testing may not be necessary during future implantations of automatic cardioverter defibrillators.

Defibrillators, Implantable↗
PubMed2003

[Analysis of ventricular fibrillation signals for the evaluation of defibrillation success in the treatment of ventricular fibrillation].

OBJECTIVE: Precise detection of ventricular fibrillation (VF), reliable prediction of defibrillation success and adjustment of the discharge waveform to the patient's transthoracic impedance may contribute to a reduction of electricity-associated myocardial injury caused by unnecessary counter shocks. Specifically, asystole thresholds distinguish between VF and asystole, and thus prevent unnecessary defibrillation attempts. We reviewed various studies and manufacturer characteristics regarding the parameters and algorithms for analyzing arrhythmia ECG signals. METHODS: Asystole threshold values of several defibrillator manufacturers were collected and a literature review was performed including the following parameters: amplitude, frequency, bispectral analysis, amplitude spectrum area, wavelets, nonlinear dynamics, N(alpha)histograms, and combinations of various parameters. RESULTS: The manufacturer dependent asystole thresholds vary substantially. We show ways to optimize an ECG-based analysis for the next technological generation of defibrillators. During advanced cardiac life support (ACLS) the probability of defibrillation success should be estimated. Optimal defibrillation waveform, depending on transthoracic resistance, should be individually determined. In case of prolonged VF with a low ECG amplitude defibrillation should not be attempted unless coronary perfusion has been improved by further measures of ACLS. The combined evaluation of VF amplitude and frequency is effective in predicting defibrillation success. Estimation of further parameters is potentially useful for guiding optimal timing of defibrillation. At present, the implementation of most parameters in out-of-hospital cardiopulmonary resuscitation (CPR) is limited by the lack of technical feasibility of online computing. CONCLUSION: Analysis of VF ECG signals should allow adequate VF detection as well as prediction of defibrillation success. Suitable asystole thresholds for analysis of ECG signals have to be determined, and the adverse effects of CPR associated artefacts on data analysis have to be reduced. Analysis of VF ECG signals is a precondition of individually optimized defibrillation and may contribute substantially to an increased quality of CPR.

Algorithms↗