[Ventricular fibrillation, ventricular flutter].
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Diagnosis, Differential↗
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Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation.
Ventricular fibrillation is the main mechanism of sudden cardiac death, but the source of its spontaneous initiation has not been mapped. 16 patients were investigated by electrography and radiofrequency ablation after resuscitation from recurrent idiopathic ventricular fibrillation. Triggers of ventricular fibrillation originated from various locations within the Purkinje system in 12 patients and from the ordinary myocardial muscle in four. The accuracy of mapping was confirmed by acute elimination of triggers by radiofrequency delivery, and there was no recurrence of ventricular fibrillation in 14 patients. Long-term follow-up is necessary to establish that ablation is curative and avoids use of a defibrillator.
Adolescent↗
Relationship between the extent of the hypoperfused zone of the myocardium and the occurrence of ventricular fibrillation.
Ventricular fibrillation and subsequent death frequently occur so soon after coronary artery occlusion that infarct size cannot be determined; thus the systematic study of their relationship is impossible. Recently, however, a technique has been developed that permits the assessment, in vivo, of the extent of the myocardial hypoperfused zone (HZ). Accordingly, in 55 open-chest dogs, 99mTc-labeled (8 mCi) albumin microspheres (15 microns in diameter) were injected into the left atrium 1 minute after coronary artery occlusion. The zone of hypoperfusion was analyzed in 28 dogs that had ventricular fibrillation (group A) and 27 dogs that had no ventricular fibrillation (group B). In group B, the HZ was 26.3 +/- 1.7% of the left ventricle vs 31.6 +/- 1.3% of the left ventricle in group A (p less than 0.05), showing that ventricular fibrillation occurred in dogs with larger zones of hypoperfusion.
Animals↗
A method to quantify the dynamics and complexity of re-entry in computational models of ventricular fibrillation.
Ventricular fibrillation is a deadly cardiac arrhythmia. There is evidence that electrical activity in cardiac tissue is sustained during fibrillation by re-entrant waves that rotate around filaments. In this paper we develop a method for identifying and tracking filaments in a computational model of ventricular fibrillation. This method identifies the birth, death, bifurcation and amalgamation of filaments and these events are summarized on a directed graph. The approach described in this study provides ways to quantify the complex patterns of electrical activity seen in computational models of fibrillation, to relate the behaviour of computational models to experimental data and thus to gain insights into the underlying mechanisms of this dangerous arrhythmia.
Anisotropy↗
Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation.
Ventricular fibrillation leading to sudden cardiac death can occur even in the absence of structural heart disease. One form of this so-called idiopathic ventricular fibrillation (IVF) is characterized by ST segment elevation (STE) in the electrocardiogram. Recently we found that IVF with STE is linked to mutations of SCN5A, the gene encoding the cardiac sodium channel alpha -subunit. Two types of defects were identified: loss-of-function mutations that severely truncate channel proteins and missense mutations (e.g. a double mutation, R1232W and T1620M) that cause only minor changes in channel gating. Here we show that co-expression of the R1232W+T1620M missense mutant alpha -subunits in a mammalian cell line stably transfected with human sodium channel beta(1)-subunits results in a phenotype similar to that of the truncation mutants. In the presence of beta(1)subunits the expression of both ionic currents and alpha -subunit-specific, immunoreactive protein was markedly suppressed after transfection of mutant, but not wild-type alpha -subunits when cells were incubated at physiological temperature. Expression was partially restored by incubation at reduced temperatures. Our results reconcile two classes of IVF mutations and support the notion that a reduction in the amplitude of voltage-gated sodium conductance is the primary cause of IVF.
Animals↗
Defibrillation via the elimination of spiral turbulence in a model for ventricular fibrillation.
Ventricular fibrillation, the major reason behind sudden cardiac death, is turbulent cardiac electrical activity in which rapid, irregular disturbances in the spatiotemporal electrical activation of the heart make it incapable of any concerted pumping action. Methods of controlling ventricular fibrillation include electrical defibrillation as well as injected medication. Electrical defibrillation, though widely used, involves subjecting the whole heart to massive, and often counterproductive, electrical shocks. We propose a defibrillation method that uses a very low-amplitude shock (of order mV) applied for a brief duration (of order 100 ms) and over a coarse mesh of lines on our model ventricle.
Defibrillators, Implantable↗
Genetic basis and molecular mechanism for idiopathic ventricular fibrillation.
Ventricular fibrillation causes more than 300,000 sudden deaths each year in the USA alone. In approximately 5-12% of these cases, there are no demonstrable cardiac or non-cardiac causes to account for the episode, which is therefore classified as idiopathic ventricular fibrillation (IVF). A distinct group of IVF patients has been found to present with a characteristic electrocardiographic pattern. Because of the small size of most pedigrees and the high incidence of sudden death, however, molecular genetic studies of IVF have not yet been done. Because IVF causes cardiac rhythm disturbance, we investigated whether malfunction of ion channels could cause the disorder by studying mutations in the cardiac sodium channel gene SCN5A. We have now identified a missense mutation, a splice-donor mutation, and a frameshift mutation in the coding region of SCN5A in three IVF families. We show that sodium channels with the missense mutation recover from inactivation more rapidly than normal and that the frameshift mutation causes the sodium channel to be non-functional. Our results indicate that mutations in cardiac ion-channel genes contribute to the risk of developing IVF.
Action Potentials↗
Ventricular fibrillation.
Ventricular fibrillation is the most common mechanism of sudden unexpected cardiac death in persons with asymptomatic or symptomatic coronary artery disease. The electrophysiologic mechanisms reviewed in this article include: automaticity of pacemaker fibers, transformation of nonpacemaker into pacemaker fibers, "injury" currents and reentry. Some of the conditions facilitating ventricular fibrillation include bradycardia, long QT syndrome, electrocution, electrolyte imbalance, drugs, sympathetic stimulation and myocardial ischemia. Electrophysiologic studies during acute myocardial ischemia suggest that the earliest activity at the onset of arrhythmia may originate at the sites of the surviving Purkinje fibers or at the epicardial rim. Reentrant arrhythmias arising in ischemic myocardium are attributed to nonhomogeneous distribution of local hyperkalemia and acidosis.
Anti-Arrhythmia Agents↗
Using an artificial neural network to detect activations during ventricular fibrillation.
Ventricular fibrillation is a cardiac arrhythmia that can result in sudden death. Understanding and treatment of this disorder would be improved if patterns of electrical activation could be accurately identified and studied during fibrillation. A feedforward artificial neural network using backpropagation was trained with the Rule-Based Method and the Current Source Density Method to identify cardiac tissue activation during fibrillation. Another feedforward artificial neural network that used backpropagation was trained with data preprocessed by those methods and the Transmembrane Current Method. Staged training, a new method that uses different sets of training examples in different stages, was used to improve the ability of the artificial neural networks to detect activation. Both artificial neural networks were able to correctly classify more than 92% of new test examples. The performance of both artificial neural networks improved when staged training was used. Thus, artificial neural networks may beuseful for identifying activation during ventricular fibrillation.
Diagnosis, Computer-Assisted↗
Effects of cardiac work on the threshold for ventricular fibrillation.
Ventricular fibrillation threshold (VFT) was measured in anesthetized dogs, while cardiac work was altered by changing arterial pressure (pressure work) or by opening an aorta to left atrial shunt (flow work). When VFT during pressure work was compared with that during flow work, at a constant heart rate, it was found that there was a negative correlation (a lower threshold for fibrillation) between VFT and flow work but not pressure work. VFT also had negative correlations with the rate of contraction and relaxation indexes; maximal +/- dp/dt and negative dp/dt were the most significant variables. On the other hand, coronary flow, oxygen consumption, end diastolic pressure, and tension time index were not correlated with VFTs. Thus, VFT depended on mechanical factors not necessarily correlated to alterations in myocardial perfusion.
Animals↗
Metabolic factors and ventricular fibrillation.
Ventricular fibrillation has been studied in the isolated rabbit heart to determine the effect of factors modifying the metabolism. Sodium azide, sodium monoiodoacetate and sodium fluoride were found to cause fibrillation, the effect of sodium fluoride being neutralized by magnesium chloride. Fibrillation was also caused by lack of glucose and could be arrested by adding glucose; the effect of glucose in arresting fibrillation was facilitated by insulin. In other experiments mannose and pyruvate could arrest fibrillation due to lack of glucose, but L(-)lactate could not. The effect of temperature changes, of adrenaline and of cyanide were also studied. When all oxygen was removed from the perfusing solution fibrillation was arrested.
Arrhythmias, Cardiac↗
Predicting patterns of epicardial potentials during ventricular fibrillation.
Ventricular fibrillation (VF) is a fatal cardiac arrhythmia, characterized by uncoordinated propagation of activation wavefronts in the ventricular myocardium. Short-term predictions of epicardial potential fields during VF in pigs were attempted using linear techniques, and prediction accuracy was measured at various stages during sustained episodes. VF was induced in five pigs via premature electrical stimulation. Unipolar electrograms were recorded from an epicardial array of 506 electrodes in a 22 x 23 array with 1-mm spacing. Optimal spatial basis functions (modes) and time-varying weighting coefficients were found using the Karhunen-Loeve decomposition. Linear autoregressive (AR) models incorporating the dynamics of only a few spatial modes led to predicted patterns that were qualitatively similar to observed patterns. Predictions were made 0.256 s into the future, based on 0.768 s of past data, over an area of approximately 5 cm2 on the ventricular epicardium. The mean squared error of predictions varied from as much as 1.23 to as little as 0.14, normalized to the variance of the actual data. Inconsistency in long-term forcasts is partly due to the limitations of linear AR models. Changes in predictability, however, were consistent. Predictability varied inversely with spatial complexity, as measured by the mean squared error of a five-mode approximation. Predictability also increased significantly during the first minute of VF.
Algorithms↗
Alternans and the onset of ventricular fibrillation.
Ventricular fibrillation (VF) remains a major cause of death in the industrialized world. Alternans (a period-doubling bifurcation of cardiac electrical activity) have recently been causally linked to the progression from ventricular tachycardia (VT) to VF, a more spatiotemporally disorganized electrical activity. In this paper, we show how alternans and thus VT degenerate to chaos via multiple, specific dynamical routes, largely associated with spatial components of VF dynamics, explaining failures of many recently proposed antiarrhythmic drugs. Identification of dynamical mechanisms for the onset of VF should lead to the design of future experiments and consequently to more effective antiarrhythmic drugs.
Action Potentials↗
Spatial and temporal organization in ventricular fibrillation.
Ventricular fibrillation (VF) is the leading heart rhythm alteration that results in sudden cardiac death, yet the detailed mechanisms of the arrhythmia remain elusive. Fibrillation has been defined as "turbulent" cardiac electrical activity, which conjures up the idea of totally random and disorganized activation of the ventricles. I review theoretical concepts and recently published results based on a newly developed algorithm, "two-dimensional phase mapping," which demonstrates that VF is not random and may be analyzed quantitatively. The approach is based on video imaging of voltage-sensitive dye fluorescence to record transmembrane potential simultaneously from 20,000 sites on the epicardial surface of rabbit and sheep ventricles. During VF, activity shows a strong periodic component centered near approximately 500 beats/min. Phase maps reveal that VF depends on the organization of electrical waves around a small number of "phase singularities" that have relatively short lifespans and form as a result of interactions of wavefronts with obstacles in their paths. Overall, the evidence demonstrates that there is a high degree of temporal and spatial organization in cardiac fibrillation. The results may pave the way for a better understanding of the mechanisms of VF in normal, as well as in diseased, hearts.
Algorithms↗
Rectification of the background potassium current: a determinant of rotor dynamics in ventricular fibrillation.
Ventricular fibrillation (VF) is the leading cause of sudden cardiac death. Yet, the mechanisms of VF remain elusive. Pixel-by-pixel spectral analysis of optical signals was carried out in video imaging experiments using a potentiometric dye in the Langendorff-perfused guinea pig heart. Dominant frequencies (peak with maximal power) were distributed throughout the ventricles in clearly demarcated domains. The fastest domain (25 to 32 Hz) was always on the anterior left ventricular (LV) wall and was shown to result from persistent rotor activity. Intermittent block and breakage of wavefronts at specific locations in the periphery of such rotors were responsible for the domain organization. Patch-clamping of ventricular myocytes from the LV and the right ventricle (RV) demonstrated an LV-to-RV drop in the amplitude of the outward component of the background rectifier current (I(B)). Computer simulations suggested that rotor stability in LV resulted from relatively small rectification of I(B) (presumably I(K1)), whereas instability, termination, and wavebreaks in RV were a consequence of strong rectification. This study provides new evidence in the isolated guinea pig heart that a persistent high-frequency rotor in the LV maintains VF, and that spatially distributed gradients in I(K1) density represent a robust ionic mechanism for rotor stabilization and wavefront fragmentation.
Animals↗
Dynamics and interaction of filaments in a computational model of re-entrant ventricular fibrillation.
Ventricular fibrillation (VF) is a lethal cardiac arrhythmia. Re-entry, in which action potential wavefronts rotate around filaments, is believed to sustain VF. In this study we used a computational model of multiple wavelet fibrillation in the thin-walled right ventricle (10 mm thick) and the thicker walled left ventricle (16 mm thick) to investigate the effect of tissue thickness and initiation protocol on re-entry, and to examine whether filament dynamics and interaction in the model could explain why re-entry is both rarely observed and short-lived in experimental studies that map electrical activation on the heart surface. We found (i) that the density of filaments, the proportion of transmural filaments and the proportion of filaments visible on the model surface were all higher in the 10 mm simulation, (ii) that the initiation protocol influences the rate of filament breakdown but not the number of filaments present after 1 s, and (iii) that although many filaments are visible on the surface of the model, the majority are visible for less than one rotation. This study shows that tissue thickness, geometry and initiation protocol influence electrical activation during VF, and that the rapid motion and interaction of filaments result in transient appearance of surface re-entry.
Anisotropy↗
Bench to bedside: resuscitation from prolonged ventricular fibrillation.
Ventricular fibrillation (VF) remains the most common cardiac arrest heart rhythm. Defibrillation is the primary treatment and is very effective if delivered early within a few minutes of onset of VF. However, successful treatment of VF becomes increasingly more difficult when the duration of VF exceeds 4 minutes. Classically, successful cardiac arrest resuscitation has been thought of as simply achieving restoration of spontaneous circulation (ROSC). However, this traditional approach fails to consider the high early post-cardiac arrest mortality and morbidity and ignores the reperfusion injuries, which are manifest in the heart and brain. More recently, resuscitation from cardiac arrest has been divided into two phases; phase I, achieving ROSC, and phase II, treatment of reperfusion injury. The focus in both phases of resuscitation remains the heart and brain, as prolonged VF remains primarily a two-organ disease. These two organs are most sensitive to oxygen and substrate deprivation and account for the vast majority of early post-resuscitation mortality and morbidity. This review focuses first on the initial resuscitation (achieving ROSC) and then on the reperfusion issues affecting the heart and brain.
Animals↗
Effect of pentobarbital anesthesia on vulnerability to ventricular fibrillation.
Ventricular fibrillation threshold (VFT), frequently determined in dogs during pentobarbital sodium anesthesia, usually is replaced by a single repetitive extrasystole threshold (SRET) or a multiple repetitive extrasystole threshold (MRET) determination in conscious animals and in the human being. In the present study SRET, MRET, and VFT were determined initially in 39 pentobarbital sodium-anesthetized dogs. One week later these three thresholds were redetermined during anesthesia in 13 of the 39 dogs (control group). In the remaining 26 dogs (experimental group), thresholds were redetermined while the dogs were conscious. Significant changes in threshold values occurred only in the experimental group for VFT (P < 0.001) and MRET (P < 0.02). The square of the linear correlation coefficient showed conscious state MRET to be a good predictor of conscious state VFT (R2 = 0.90). Conscious state SRET and anesthetized state VFT showed less predictiveness for the conscious VFT (R2 = 0.72 and 0.51, respectively). These data indicate that MRET may be preferable to SRET as an index of VFT. The SRET, MRET, and VFT determined during pentobarbital anesthesia may not accurately reflect the value of these parameters in the conscious animal.
Animals↗