Deterministic nonlinearity in ventricular fibrillation

We provide numerical evidence that the electrocardiogram data collected from pigs during induced ventricular fibrillation cannot be described by a monotonic nonlinear transformation of linearly filtered noise. To establish this we use surrogate techniques and apply two test statistics: (1) the Takens' maximum likelihood estimator of the Grassberger-Procaccia correlation dimension and (2) an improved correlation dimension estimation routine. The improved dimension estimates provide evidence that the correlation dimension of the underlying dynamics during the episode of VF in the first 30 s is slightly less than 6. This result is consistent and reproducible among subjects. (c) 2000 American Institute of Physics.     

Vulnerability to ventricular fibrillation

One of the factors that favors the development of ventricular fibrillation is an increase in the dispersion of refractoriness. Experiments will be described in which an increase in dispersion in the recovery of excitability was determined during brief episodes of enhanced sympathetic nerve activity, known to increase the risk of fibrillation. Whereas in the normal heart ventricular fibrillation can be induced by a strong electrical shock, a premature stimulus of moderate intensity only induces fibrillation in the presence of regional ischemia, which greatly increases the dispersion of refractoriness. One factor that is of importance for the transition of reentrant ventricular tachycardia to ventricular fibrillation during acute regional ischemia is the subendocardial Purkinje system. After selective destruction of the Purkinje network by lugol, reentrant tachycardias still develop in the ischemic region, but they do not degenerate into fibrillation. Finally, attempts were made to determine the minimal mass of thin ventricular myocardium required to sustain fibrillation induced by burst pacing. This was done by freezing of subendocardial and midmural layers. The rim of surviving epicardial muscle had to be larger than 20 g. Extracellular electrograms during fibrillation in both the intact and the "frozen" left ventricle were indistinguishable, but activation patterns were markedly different. In the intact ventricle epicardial activation was compatible with multiple wavelet reentry, in the "frozen" heart a single, or at most two wandering reentrant waves were seen. (c) 1998 American Institute of Physics.     

Symbolic dynamics of ventricular tachycardia and ventricular fibrillation

In this paper, the symbolic dynamics analysis was used to analyze the complexity of normal heartbeat signal (NSR), Ventricular tachycardia (VT) and ventricular fibrillation (VF) signals. By calculating the information entropy value of symbolic sequences, the complexities were quantified. Based on different information entropy values, NSR, VT and VF signals were distinguished with satisfactory results. The study showed that a sudden drop of symbolic sequence’s entropy value indicated that the patients most likely entered the episode of ventricular tachycardia and this was a crucial episode for the clinical treatment of patients. It had important clinical significance for the automatic diagnosis.     

Spiral breakup as a model of ventricular fibrillation

The phenomenon of spiral breakup in a 2D and a 3D excitable medium is described. Differences between breakup in two dimensions and in three dimensions are discussed. Spiral breakup in an anatomical model of the ventricles of the heart is also studied. The patterns of excitation in the heart are presented at different wavelengths together with their electrocardiograms. Finally it is suggested that the phenomenon of spiral breakup is a possible mechanism of the ventricular fibrillation (VF). (c) 1998 American Institute of Physics.     

Self-organization and the dynamical nature of ventricular fibrillation

This article reviews recent data supporting the conjecture that, in the structurally and electrophysiologically normal heart, cardiac fibrillation is not a totally random phenomenon. Experimental and numerical studies based on the theory of excitable media suggest that fibrillation in the mammalian ventricles is the result of self-organized three-dimensional (3-D) electrical rotors giving rise to scroll waves that move continuously (i.e., drift) throughout the heart at varying speeds. A brief review of studies on the dynamics of rotors in two-dimensional (2-D) and 3-D excitable media is presented with emphasis on the experimental demonstration of such dynamics in cardiac muscle of various species. The discussion is centered on rotor dynamics in the presence and the absence of structural heterogeneities, and in the phenomena of drifting and anchoring, which in the electrocardiogram (ECG) may manifest as life-threatening cardiac rhythm disturbances. For instance, in the rabbit heart, a single electrical rotor that drifts rapidly throughout the ventricles gives rise to complex patterns of excitation. In the ECG such patterns are indistinguishable from ventricular fibrillation. On the other hand, a rotor that anchors to a discontinuity or defect in the muscle (e.g., a scar, a large artery or a bundle of connective tissue) may result in stationary rotating activity, which in the ECG is manifested as a form of so-called "monomorphic" ventricular tachycardia. More recent data show that ventricular fibrillation occurs in mammals irrespective of size or species. While in small hearts, such as those of mice and rabbits, a single drifting or meandering rotor can result in fibrillation, in larger hearts, such as the sheep and possibly the human, fibrillation occurs in the form of a relatively small number of coexisting but short-lived rotors. Overall, the work discussed here has paved the way for a better understanding of the mechanisms of fibrillation in the normal, as well as diseased human heart. (c) 1998 American Institute of Physics.     

Spatial organization,predictability, and determinism in ventricular fibrillation

The degree of spatial organization of ventricular fibrillation (VF) is a fundamental dynamical property of the arrhythmia and may determine the success of proposed therapeutic approaches. Spatial organization is closely related to the dimension of VF, and hence to its predictability and controllability. We have explored several techniques to quantify spatial organization during VF, to predict patterns of activity, and to see how spatial organization and predictability change as the arrhythmia progresses. Epicardial electrograms recorded from pig hearts using rectangular arrays of unipolar extracellular electrodes (1 mm spacing) were analyzed. The correlation length of VF, the number of Karhunen-Loeve modes required to approximate data during VF, the number, size and recurrence of wavefronts, and the mean square error of epicardial potential fields predicted 0.256 seconds into the future were all estimated. The ability of regularly-timed pacing stimuli to capture areas of fibrillating myocardium during VF was confirmed by a significant increase in local spatial organization. Results indicate that VF is neither "low-dimensional chaos" (dimension <5) nor "random" behavior (dimension= infinity ), but is a high-dimensional response with a degree of spatial coherence that changes as the arrhythmia progresses. (c) 1998 American Institute of Physics.     

Heterogeneous signal intensity in magnetic resonance images of hypertrophied left ventricular myocardium

Left ventricular hypertrophy is associated with decreased longevity and often leads to congestive heart failure. An exploratory study of magnetic resonance imaging in human left ventricular hypertrophy was performed. First, 13 patients with left ventricular hypertrophy and 7 controls of similar ages were studied using electrocardiogramgated end-diastolic images. Visual inspection suggested that low-intensity zones were frequently found within the hypertrophied myocardium. To verify this observation, the images were processed with semi-automatic edge detection and a derivative-based tissue characterization algorithm, yielding tissue heterogeneity indices (THI-A and THI-V) which objectively measured the low-intensity zones. THI-A and THI-V were both significantly greater in left ventricular hypertrophy patients than in controls (THI-A: 0.111 vs 0.038, p = 0.009). THI was also significantly correlated with duration of disease and electrocardiographic abnormalities. To validate these initial findings prospectively, the same quantitative analysis was applied to magnetic resonance images of an additional 20 left ventricular hypertrophy patients and 12 controls from two institutions, using different imaging systems and different acquisition parameters. Again, THI was significantly greater in patients than in controls. Analysis of end-systolic images yielded similar results. In four dogs with left ventricular hypertrophy induced by aortic banding, THI showed a statistically significant increase as left ventricular hypertrophy developed. Hypertrophied myocardium thus shows reproducible differences from normal tissue with magnetic resonance imaging; hence, quantitative magnetic resonance tissue characterization may be useful in assessing pathologic changes in LVH.     

Two forms of spiral-wave reentry in an ionic model of ischemic ventricular myocardium

It is well known that there is considerable spatial inhomogeneity in the electrical properties of heart muscle, and that the many interventions that increase this initial degree of inhomogeneity all make it easier to induce certain cardiac arrhythmias. We consider here the specific example of myocardial ischemia, which greatly increases the electrical heterogeneity of ventricular tissue, and often triggers life-threatening cardiac arrhythmias such as ventricular tachycardia and ventricular fibrillation. There is growing evidence that spiral-wave activity underlies these reentrant arrhythmias. We thus investigate whether spiral waves might be induced in a realistic model of inhomogeneous ventricular myocardium. We first modify the Luo and Rudy [Circ. Res. 68, 1501-1526 (1991)] ionic model of cardiac ventricular muscle so as to obtain maintained spiral-wave activity in a two-dimensional homogeneous sheet of ventricular muscle. Regional ischemia is simulated by raising the external potassium concentration ([K(+)](o)) from its nominal value of 5.4 mM in a subsection of the sheet, thus creating a localized inhomogeneity. Spiral-wave activity is induced using a pacing protocol in which the pacing frequency is gradually increased. When [K(+)](o) is sufficiently high in the abnormal area (e.g., 20 mM), there is complete block of propagation of the action potential into that area, resulting in a free end or wave break as the activation wave front encounters the abnormal area. As pacing continues, the free end of the activation wave front traveling in the normal area increasingly separates or detaches from the border between normal and abnormal tissue, eventually resulting in the formation of a maintained spiral wave, whose core lies entirely within an area of normal tissue lying outside of the abnormal area ("type I" spiral wave). At lower [K(+)](o) (e.g., 10.5 mM) in the abnormal area, there is no longer complete block of propagation into the abnormal area; instead, there is partial entrance block into the abnormal area, as well as exit block out of that area. In this case, a different kind of spiral wave (transient "type II" spiral wave) can be evoked, whose induction involves retrograde propagation of the action potential through the abnormal area. The number of turns made by the type II spiral wave depends on several factors, including the level of [K(+)](o) within the abnormal area and its physical size. If the pacing protocol is changed by adding two additional stimuli, a type I spiral wave is instead produced at [K(+)](o)=10.5 mM. When pacing is continued beyond this point, apparently aperiodic multiple spiral-wave activity is seen during pacing. We discuss the relevance of our results for arrythmogenesis in both the ischemic and nonischemic heart. (c) 1998 American Institute of Physics.     

Anisotropy of ultrasonic velocity and elastic properties in normal human myocardium.

Measurements of ultrasonic quasilongitudinal velocity were made in the muscle fiber plane of excised human myocardium. Multiple adjacent planes across the left ventricular wall were interrogated to assess the transmural dependence of velocity. For each measurement plane, data were obtained in 2-deg increments through the full 360 deg relative to the myofibers. An approximate 1.3% magnitude of anisotropy was observed with maximum velocity along the muscle fibers and minimum velocity perpendicular to the muscle fibers. The known transmural shift in myofiber orientation was evidenced in the anisotropy of velocity as angular shifts between plots obtained from adjacent transmural planes within the same specimen. Measured values of velocity and density were used to estimate the effective C33 and C11 elastic constants of a thin layer of normal myocardium.     

Vortex dynamics in three-dimensional continuous myocardium with fiber rotation: Filament instability and fibrillation

Wave propagation in ventricular muscle is rendered highly anisotropic by the intramural rotation of the fiber. This rotational anisotropy is especially important because it can produce a twist of electrical vortices, which measures the rate of rotation (in degree/mm) of activation wavefronts in successive planes perpendicular to a line of phase singularity, or filament. This twist can then significantly alter the dynamics of the filament. This paper explores this dynamics via numerical simulation. After a review of the literature, we present modeling tools that include: (i) a simplified ionic model with three membrane currents that approximates well the restitution properties and spiral wave behavior of more complex ionic models of cardiac action potential (Beeler-Reuter and others), and (ii) a semi-implicit algorithm for the fast solution of monodomain cable equations with rotational anisotropy. We then discuss selected results of a simulation study of vortex dynamics in a parallelepipedal slab of ventricular muscle of varying wall thickness (S) and fiber rotation rate (theta(z)). The main finding is that rotational anisotropy generates a sufficiently large twist to destabilize a single transmural filament and cause a transition to a wave turbulent state characterized by a high density of chaotically moving filaments. This instability is manifested by the propagation of localized disturbances along the filament and has no previously known analog in isotropic excitable media. These disturbances correspond to highly twisted and distorted regions of filament, or "twistons," that create vortex rings when colliding with the natural boundaries of the ventricle. Moreover, when sufficiently twisted, these rings expand and create additional filaments by further colliding with boundaries. This instability mechanism is distinct from the commonly invoked patchy failure or wave breakup that is not observed here during the initial instability. For modified Beeler-Reuter-like kinetics with stable reentry in two dimensions, decay into turbulence occurs in the left ventricle in about one second above a critical wall thickness in the range of 4-6 mm that matches experiment. However this decay is suppressed by uniformly decreasing excitability. Specific experiments to test these results, and a method to characterize the filament density during fibrillation are discussed. Results are contrasted with other mechanisms of fibrillation and future prospects are summarized. (c)1998 American Institute of Physics.     

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.     

Influence of cardiac tissue anisotropy on re-entrant activation in computational models of ventricular fibrillation

The aim of this study was to establish the role played by anisotropic diffusion in (i) the number of filaments and epicardial phase singularities that sustain ventricular fibrillation in the heart, (ii) the lifetimes of filaments and phase singularities, and (iii) the creation and annihilation dynamics of filaments and phase singularities. A simplified monodomain model of cardiac tissue was used, with membrane excitation described by a simplified 3-variable model. The model was configured so that a single re-entrant wave was unstable, and fragmented into multiple re-entrant waves. Re-entry was then initiated in tissue slabs with varying anisotropy ratio. The main findings of this computational study are: (i) anisotropy ratio influenced the number of filaments sustaining simulated ventricular fibrillation, with more filaments present in simulations with smaller values of transverse diffusion coefficient, (ii) each re-entrant filament was associated with around 0.9 phase singularities on the surface of the slab geometry, (iii) phase singularities were longer lived than filaments, and (iv) the creation and annihilation of filaments and phase singularities were linear functions of the number of filaments and phase singularities, and these relationships were independent of the anisotropy ratio. This study underscores the important role played by tissue anisotropy in cardiac ventricular fibrillation.     

A cellular automaton model for the ventricular myocardium considering the layer structure

A cellular automaton model for the ventricular myocardium considering the layer structure has been established. The three types of cells in this model differ principally in the repolarization characteristics. For the normal travelling waves in this model, the computer simulation results show the R, S, and T waves and they are qualitatively in agreement with the standard electrocardiograph. Phenomena such as the potential decline of point J and segment ST and the rise of the potential line after the T wave appear when the ischemia occurs in the endocardium. The spiral wave has also been simulated, and the corresponding potential has a lower amplitude, higher frequency, and wider R wave, which accords with the distinguishing feature of the clinical electrocardiograph. Mechanisms underlying the above phenomena are analyzed briefly.     

采用低维特征映射的耳语音向正常音转换

在将耳语音转换为正常音时,为了研究降维后语音特征对耳语音转换的影响,分别对耳语音和正常音谱包络进行自适应编码以提取耳语音和正常音的低维特征,然后使用BP网络建立耳语音和正常音低维谱包络特征之间的映射关系以及正常音基频和耳语音低维谱包络特征之间的关系。转换时,根据耳语音低维谱包络特征获得对应正常音的低维谱包络特征和基频,对低维谱包络特征进行解码后获得对应的正常音谱包络。实验结果表明,采用此方法转换后的语音与正常音之间的倒谱距离相比高斯混合模型方法下降了10%,转换后语音的自然度和可懂度都有所提高。     

MRI analysis of right ventricular function in normal and spontaneously hypertensive rats

Right ventricular structure and function were characterized in spontaneously hypertensive rats (SHR) using non-invasive magnetic resonance imaging (MRI) techniques. These studies therefore complement previous reports preoccupied with left ventricular changes associated with this condition. Eight SHR and eight control normotensive Wistar-Kyoto (WKY) rats were each subdivided into equal age-matched groups of 8 and 12 weeks. The right ventricle was imaged through a series of twelve contiguous 1.37–1.75 mm transverse sections at twelve equally spaced time-points that covered both systole and most of diastole thereby completely reconstructing right ventricular anatomy. This gave measurements of right ventricular myocardial mass that were consistent through all twelve time-points in all four experimental groups throughout their cardiac cycles. However, spontaneous hypertension increased this right ventricular myocardial mass, as well as the end-diastolic (EDV) and end-systolic volumes (ESV). Although stroke volume (SV) was conserved, decreases in ejection fraction (EF), a positive shift in the relationship between SV and EDV, and reduced indices of systolic ejection rates in SHR rats compared with the age-matched normal WKY controls indicated significant systolic dysfunction. Additionally, reductions in the rates of diastolic relaxation suggested the onset of diastolic dysfunction. Thus, the non-invasive nature of MRI has made it possible for the first time to demonstrate alterations in structure of the right ventricle and in quantitative indicators of its systolic and diastolic function in the SHR model of hypertension.     

Epicardial wavefronts arise from widely distributed transient sources during ventricular fibrillation in the isolated swine heart

It has been proposed that VF waves emanate from stable localized sources, often called "mother rotors." However, evidence for the existence of these rotors is conflicting. Using a new panoramic optical mapping system that can image nearly the entire ventricular epicardium, we recently excluded epicardial mother rotors as the drivers of Wiggers' stage II VF in the isolated swine heart. Furthermore, we were unable to find evidence that VF requires sustained intramural sources. The present study was designed to test the following hypotheses: 1. VF is driven by a specific region, and 2. Rotors that are long-lived, though not necessarily permanent, are the primary generators of VF wavefronts. Using panoramic optical mapping, we mapped VF wavefronts from 6 isolated swine hearts. Wavefronts were tracked to characterize their activation pathways and to locate their originating sources. We found that the wavefronts that participate in epicardial reentry were not confined to a compact region; rather they activated the entire epicardial surface. New wavefronts feeding into the epicardial activation pattern were generated over the majority of the epicardium and almost all of them were associated with rotors or repetitive breakthrough patterns that lasted for less than 2 s. These findings indicate that epicardial wavefronts in this model are generated by many transitory epicardial sources distributed over the entire surface of the heart.     

Ultrastructural alterations in the ventricular myocardium of the adult Italian newt (Lissotriton italicus) following exposure to nonylphenol ethoxylate

Nonylphenols ethoxylates (NPEs) are surface active agents (surfactants) commonly used in cleaning products, in industrial processes, agricultural formulations and paints. They are found in sewage, municipal wastewaters and industrial effluents, and as contaminants in water bodies. Accumulating data suggest that exposure to NPEs can adversely affects functional properties of the neurologic, reproductive, immune, and endocrine systems. In order to examine whether NPEs exert similar damaging effects on the cardiovascular system, we used an amphibian model to examine the ultrastructural alterations of the ventricular myocardium following exposure to NPEs. Adult Lissotriton italicus in the aquatic phase were exposed to NPE10 (100 μg/L, ppb) for 96 h. Heart specimens were collected from a total of 10 individuals and processed for scanning and transmission electron microscopy. Our ultrastructural examinations demonstrated that amphibian ventricle is susceptible to the effects of NPEs. The most pronounced alterations were observed in the membrane compartments of both myocardial and endothelial cells as demonstrated by the presence of swollen mitochondria with disrupted cristae and dilated rough endoplasmic reticulum. We suggest that destabilization of the lipid milieu within membranes might represent one of the potential mechanisms by which NPEs exert their toxic effects on amphibian heart.     

Assessment of normal flow patterns in the pulmonary circulation by using 4D magnetic resonance velocity mapping

Objective

The purpose of this study was to analyze flow patterns in the pulmonary circulation of healthy volunteers by using 4D flow magnetic resonance imaging.

Materials and Methods

The study was approved by the local ethics committee and all subjects gave written informed consent. Eighteen volunteers underwent a 4D flow scan of the whole-heart. Two patients with congenital heart disease were also included to detect possible patterns of flow abnormalities (Patient 1: corrected transposition of great arteries (TGA); Patient 2: partial anomalous pulmonary venous return and atrial septal defect). To analyze flow patterns, 2D planes were placed on the main pulmonary artery (PA), left and right PA. Flow patterns were assessed manually by two independent viewers using vector fields, streamlines and particle traces, and semi-automatically by vorticity quantification.

Results

Two counter-rotating helices were found in the main PA of volunteers. Right-handed helical flow was detected in the right PA of 15 volunteers. Analysis of the helical flow by particles traces revealed that both helices contributed mainly to the flow in the right PA. In the patient with corrected TGA helical flow was not detected. Abnormal vortical flow was visualized in the main PA of patient 2, suggesting elevated mean PA pressure.

Conclusions

Helical flow is normally present in the main PA and right PA. 4D flow is an excellent tool to evaluate noninvasively complex blood flow patterns in the pulmonary circulation. Knowledge of normal and abnormal flow patterns might help to evaluate patients with congenital heart disease adding functional information undetectable with other imaging modalities.