Spatial Doppler anomaly in an excitable medium.
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Journal Article↗
Biomedical subjects
J Jalife
Publications and source records attributed to J Jalife.
Erratum: Spatial Doppler anomaly in an excitable medium
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Journal Article↗
AV nodal function during atrial fibrillation: the role of electrotonic modulation of propagation.
The irregular ventricular rhythm that accompanies atrial fibrillation (AF) has been explained in terms of concealed conduction within the AV node (AVN). However, the cellular basis of concealed conduction in AF remains poorly understood. Our hypothesis is that electrotonic modulation of AVN propagation by atrial impulses blocked repetitively within the AVN is responsible for changes in function that lead to irregular ventricular rhythms in patients with AF. We have tested this idea using two different simplified computer ionic models of the AVN. The first ("black-box") model consisted of three cells: one representing the atrium, another one representing the AVN, and a third one representing the ventricle. The black-box model was used to establish the rules of behavior and predictions to be tested in a second, more elaborate model of the AVN. The latter ("nine-cell" model) incorporated a linear array of nine cells separated into three different regions. The first region of two cells represented the atrium; the second region of five cells represented the AV node; and the third region of two cells represented the ventricle. Cells were connected by appropriate coupling resistances. During regular atrial pacing, both models reproduced very closely the frequency dependence of AV conduction and refractoriness seen in patients and experimental animals. In addition, atrial impulses blocked within the AV node led to electrotonic inhibition or facilitation of propagation of immediately succeeding impulses. During simulated AF, using the nine-cell model, random variations in the atrial (A-A) interval yielded variations in the ventricular (V-V) interval but there was no scaling, i.e., the V-V intervals were not multiples of the A-A intervals. As such, the model simulated the statistical behavior of the ventricles in patients with AF, including: (1) the ventricular rhythm was random; and (2) the coefficient of variation (standard deviation/mean) of the ventricular rhythm was relatively constant at any given mean V-V interval. Analysis of cell responses revealed that repetitive atrial input at random A-A intervals resulted in complex patterns of concealment within the AVN cells. Consequently, the effects of electrotonic modulation were also random, which resulted in a smearing of the AV conduction curve over A-A intervals that were larger than those predicted for 1:1 AV conduction. Hence, during AF, electrotonic modulation acts in concert with the frequency dependence of AVN conduction to result in complex patterns of ventricular activation. Finally, similarly to what was shown in patients, VVI pacing of the ventricle in the nine-cell model at the appropriate frequency led to blockade of nearly all anterograde (i.e., A-V) impulses. The essential feature here was that the retrograde impulse invading the AVN cells was followed by refractoriness with slow recovery of excitability, setting the stage for electrotonic inhibition of anterograde impulses. Overall, the results provide insight into the cellular mechanisms underlying AVN function and irregular ventricular response during AF.
Animals↗
Mechanisms of cardiac fibrillation.
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Animals↗
Nonstationary vortexlike reentrant activity as a mechanism of polymorphic ventricular tachycardia in the isolated rabbit heart.
BACKGROUND: Ventricular tachycardia may result from vortexlike reentrant excitation of the myocardium. Our general hypothesis is that in the structurally normal heart, these arrhythmias are the result of one or two nonstationary three-dimensional electrical scroll waves activating the heart muscle at very high frequencies. METHODS AND RESULTS: We used a combination of high-resolution video imaging, electrocardiography, and image processing in the isolated rabbit heart, together with mathematical modeling. We characterized the dynamics of changes in transmembrane potential patterns on the epicardial surface of the ventricles using optical mapping. Image processing techniques were used to identify the surface manifestation of the reentrant organizing centers, and the location of these centers was used to determine the movement of the reentrant pathway. We also used numerical simulations incorporating Fitzhugh-Nagumo kinetics and realistic heart geometry to study how stationary and nonstationary scroll waves are manifest on the epicardial surface and in the simulated ECG. We present epicardial surface manifestations (reentrant spiral waves) and ECG patterns of nonstationary reentrant activity that are consistent with those generated by scroll waves established at the right and left ventricles. We identified the organizing centers of the reentrant circuits on the epicardial surface during polymorphic tachycardia, and these centers moved during the episodes. In addition, the arrhythmias that showed the greatest movement of the reentrant centers displayed the largest changes in QRS morphology. The numerical simulations showed that stationary scroll waves give rise to monomorphic ECG signals, but nonstationary meandering scroll waves give rise to undulating ECGs characteristic of torsade de pointes. CONCLUSIONS: Polymorphic ventricular tachycardia in the healthy, isolated rabbit heart is the result of either a single or paired ("figure-of-eight") nonstationary scroll waves. The extent of the scroll wave movement corresponds to the degree of polymorphism in the ECG. These results are consistent with our numerical simulations that showed monomorphic ECG patterns of activity for stationary scroll waves but polymorphic patterns for scroll waves that were nonstationary.
Animals↗
A model study of changes in excitability of ventricular muscle cells: inhibition, facilitation, and hysteresis.
A model study was carried out to investigate the mechanism of changes in excitability at long cycle lengths (i.e., > 1,000 ms), which are responsible for various phenomena, including electrotonic inhibition, active facilitation, and hysteresis of excitability in ventricular muscle at slow frequencies of stimulation. Experimental studies suggested that with repetitive activity the inward rectifier potassium current (IK1) is not a passive component of membrane response and that the dynamics of IK1 are responsible for the changes in excitability at long cycle lengths. In the present study, we have used new experimental data as the basis to modify the equations for IK1 in the ionic model for ventricular muscle of the Luo and Rudy (LR) model. The modified equations for IK1 incorporate an additional slow gate (s-gate), which governs the transition from a high steady-state conductance at rest to a lower conductance with repetitive stimulation. In simulation studies, electronic inhibition was seen in the original and the modified LR model and was shown to depend on changes in the delayed rectifier current (IK). However, addition of the s-gate to IK1 of the LR model extended the frequency dependence of excitability to longer cycle lengths and allowed for the demonstration of active facilitation and hysteresis. These results support the hypothesis that the inward rectifier is involved in the dynamic control of membrane excitability. The overall results provide mechanistic explanations for heart rate-dependent excitation abnormalities that may be involved in the genesis of cardiac arrhythmias.
Algorithms↗
Effects of pacing on stationary reentrant activity. Theoretical and experimental study.
It is well known that electrical pacing may either terminate or change the rate and/or ECG appearance of reentrant ventricular tachycardia. However, the dynamics of interaction of reentrant waves with waves initiated by external pacing are poorly understood. Prevailing concepts are based on simplistic models in which propagation occurs in one-dimensional rings of cardiac tissue. Since reentrant activation in the ventricles occurs in two or three dimensions, such concepts might be insufficient to explain the mechanisms of pacing-induced effects. We used numerical and biological models of cardiac excitation to explore the phenomena, which may take place as a result of electrical pacing during functionally determined reentry. Computer simulations of a two-dimensional array of electrically coupled FitzHugh-Nagumo cells were used to predict the response patterns expected from thin slices of sheep ventricular epicardial muscle, in which self-sustaining reentrant activity in the form of spiral waves was consistently initiated by premature stimulation and monitored by means of video mapping techniques. The results show that depending on their timing and shape, externally induced waves may collide with the self-sustaining spiral and result in one of three possible outcomes: (1) direct annihilation of the spiral, (2) multiplication of the spiral, or (3) shift of the spiral center (ie, core). Multiplication and shift of the spiral core were attended by changes in rate and morphology of the arrhythmia as seen by "pseudo-ECGs." Furthermore, delayed termination (ie, termination of the activity one to three cycles after the stimulus) occurred after both multiplication and shift of the spiral center. Both numerical predictions and experimental results support the hypothesis that whether a pacing stimulus will terminate a reentrant arrhythmia or modify its ECG appearance depends on whether the interactions between the externally induced wave and the spiral wave result in the de novo formation of one or more "wavebreaks." The final outcome depends on the stimulus parameters (ie, position and size of the electrodes and timing of the stimulus) as well as on the position of the newly formed wavebreak(s) in relation to that of the original wave.
Acceleration↗
Electrotonic inhibition and active facilitation of excitability in ventricular muscle.
INTRODUCTION: The effects of subthreshold electrical pulses on the response to subsequent stimulation have been described previously in experimental animal studies as well as in the human heart. In addition, previous studies in cardiac Purkinje fibers have shown that diastolic excitability may decrease after activity (active inhibition) and, to a lesser extent, following subthreshold responses (electrotonic inhibition). However, such dynamic changes in excitability have not been explored in isolated ventricular muscle, and it is uncertain whether similar phenomena may play any role in the activation patterns associated with propagation abnormalities in the myocardium. METHODS AND RESULTS: Experiments were performed in isolated sheep Purkinje fibers and papillary muscles, and in enzymatically dissociated guinea pig ventricular myocytes. In all types of preparations introduction of a conditioning subthreshold pulse between two suprathreshold pulses was followed by a transient decay in excitability (electrotonic inhibition). The degree of inhibition was directly related to the amplitude and duration of the conditioning pulse and inversely related to the postconditioning interval. Yet, inhibition could be demonstrated long after (> 1 sec) the end of the conditioning pulse. Electronic inhibition was found at all diastolic intervals and did not depend on the presence of a previous action potential. In Purkinje fibers, conditioning action potentials led to active inhibition of subsequent responses. In contrast, in muscle cells, such action potentials had a facilitating effect (active facilitation). Electrotonic inhibition and active facilitation were observed in both sheep ventricular muscle and guinea pig ventricular myocytes. Accordingly, during repetitive stimulation with pulses of barely threshold intensity, we observed: (1) bistability (i.e., with the same stimulating parameters, stimulus:response patterns were either 1:1 or 1:0, depending on previous history), and (2) abrupt transitions between 1:1 and 1:0 (absence of intermediate Wenckebach-like patterns). Simulations utilizing an ionic model of cardiac myocytes support the hypothesis that electrotonic inhibition in well-polarized ventricular muscle is the result of partial activation of IK following subthreshold pulses. On the other hand, active facilitation may be the result of an activity-induced decrease in the conductance of IK1. CONCLUSION: Diastolic excitability of well-polarized ventricular myocardium may be transiently depressed following local responses and transiently enhanced following action potentials. On the other hand, diastolic excitability decreases during quiescence. Active facilitation and electrotonic inhibition may have an important role in determining the dynamics of excitation of the myocardium in the presence of propagation abnormalities.
Action Potentials↗
Immunohistochemical localization of gap junction protein channels in hamster sinoatrial node in correlation with electrophysiologic mapping of the pacemaker region.
INTRODUCTION: Gap junction proteins are thought to form the low resistance pathways that connect neighboring cells within the sinoatrial node, and to mediate pacemaker synchronization. METHODS AND RESULTS: We have carried out microelectrode mapping experiments of the hamster sinoatrial region to localize the primary pacemaker area for subsequent light, electron, and immunofluorescence microscopic studies aimed at testing the hypothesis that the major cardiac gap junction protein (connexin43) is present in such an area. The site of earliest activation is unifocal and the pattern of activation, obtained by multiple sequential microelectrode recordings of the sinoatrial region, is qualitatively similar to that previously described for other species. However, quantitatively, the impulse transmission time from the primary pacemaker area to the crista (sulcus) terminalis in the hamster sinoatrial node is about 50% briefer than that of the guinea pig and five times faster than that of the rabbit. Immunolocalization studies in the hamster sinoatrial node using anti-connexin43 antisera demonstrated specific staining at the areas of cell-to-cell apposition and suggested that the apparently high degree of electrical coupling in this tissue is the result of abundant connexin43 expression. The immunofluorescence data were supported by light microscopic studies, which demonstrated the typical morphologic characteristics of sinus nodal cells in the pacemaker area. In addition, an electron microscopic study of the sinoatrial region revealed the presence of gap junctions in the junctional complex at areas of cell-to-cell contact. CONCLUSION: Our results demonstrate that cells in the sinoatrial region of the hamster heart are electrically well coupled and strongly suggest that such coupling is mediated by gap junctional channels formed by connexin43.
Amino Acid Sequence↗
Is the "funny" current funnier than we thought?
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Amino Acid Sequence↗
Wave-front curvature as a cause of slow conduction and block in isolated cardiac muscle.
We have investigated the role of wave-front curvature on propagation by following the wave front that was diffracted through a narrow isthmus created in a two-dimensional ionic model (Luo-Rudy) of ventricular muscle and in a thin (0.5-mm) sheet of sheep ventricular epicardial muscle. The electrical activity in the experimental preparations was imaged by using a high-resolution video camera that monitored the changes in fluorescence of the potentiometric dye di-4-ANEPPS on the surface of the tissue. Isthmuses were created both parallel and perpendicular to the fiber orientation. In both numerical and biological experiments, when a planar wave front reached the isthmus, it was diffracted to an elliptical wave front whose pronounced curvature was very similar to that of a wave front initiated by point stimulation. In addition, the velocity of propagation was reduced in relation to that of the original planar wave. Furthermore, as shown by the numerical results, wave-front curvature changed as a function of the distance from the isthmus. Such changes in local curvature were accompanied by corresponding changes in velocity of propagation. In the model, the critical isthmus width was 200 microns for longitudinal propagation and 600 microns for transverse propagation of a single planar wave initiated proximal to the isthmus. In the experiments, propagation depended on the width of the isthmus for a fixed stimulation frequency. Propagation through an isthmus of fixed width was rate dependent both along and across fibers. Thus, the critical isthmus width for propagation was estimated in both directions for different frequencies of stimulation. In the longitudinal direction, for cycle lengths between 200 and 500 milliseconds, the critical width was < 1 mm; for 150 milliseconds, it was estimated to be between 1.3 and 2 mm; and for the maximum frequency of stimulation (117 +/- 15 milliseconds), it was > 2.5 mm. In the transverse direction, critical width was between 1.78 and 2.32 mm for a basic cycle length of 200 milliseconds. It increased to values between 2.46 and 3.53 mm for a basic cycle length of 150 milliseconds. The overall results demonstrate that the curvature of the wave front plays an important role in propagation in two-dimensional cardiac muscle and that changes in curvature may cause slow conduction or block.
Animals↗
A structural basis for the unequal sensitivity of the major cardiac and liver gap junctions to intracellular acidification: the carboxyl tail length.
The regulation of junctional conductance (Gi) of the major cardiac (connexin43; Cx43) and liver (connexin32; Cx32) gap junction proteins by intracellular hydrogen ion concentration (pH; pHi), as well as well as that of a truncation mutant of Cx43 (M257) with 125 amino acids deleted from the COOH terminus, was characterized in pairs of Xenopus laevis oocytes expressing homologous channels. Oocytes were injected with 40 nl mRNAs (2 micrograms/microliters) encoding the respective proteins; subsequently, cells were stripped, paired, and incubated for 20-24 h. Gj was measured in oocyte pairs using the dual electrode voltage-clamp technique, while pHi was recorded simultaneously in the unstimulated cell by means of a proton-selective microelectrode. Because initial experiments showed that the pH-sensitive microelectrode responded more appropriately to acetate than to CO2 acidification, oocytes expressing Cx32 and wild type and mutant Cx43 were exposed to a sodium acetate saline, which was balanced to various levels of pH using NaOH and HCl. pH was changed in a stepwise manner, and quasi-steady-state Gj -pHi relationships were constructed from data collected at each step after both Gj and pHi had reached their respective asymptotic values. A moderate but significant increase of Gj was observed in Cx43 pairs as pHi decreased from 7.2 to 6.8. In both Cx32 and M257 pairs, Gj increased significantly over a wider pH range (i.e., between 7.2 and 6.3). Further acidification reversibly reduced Gj to zero in all oocyte pairs. Pooled data for the individual connexins obtained during uncoupling were fitted by the Hill equation; apparent 50%-maximum (pK;pKa) values were 6.6 and 6.1 for Cx43 and Cx32, respectively, and Hill coefficients were 4.2 for Cx43 and 6.2 for Cx32. Like Cx32, M257 had a more acidic pKa (6.1) and steeper Hill coefficient (6.0) than wild type Cx43. The pKa and Hill coefficient of M257 were very similar to those of Cx32. These experiments provide the first direct comparison of the effects of acidification on Gj in oocyte pairs expressing Cx43 or Cx32. The results indicate that structural differences in the connexins are the basis for their unequal sensitivity to intracellular acidification in vivo. The data further suggest that a common pH gating mechanism may exist between amino acid residues 1 and 256 in both Cx32 and Cx43. However, the longer carboxyl tail of Cx43 relative to Cx32 or M257 provides additional means to facilitate acidification-induced gating; its presence shifts the pKa from 6.1 (Cx32 and M257) to 6.6 (Cx43) in the conductance of these channels.
Animals↗
Effects of diacetyl monoxime on the electrical properties of sheep and guinea pig ventricular muscle.
OBJECTIVE: Diacetyl monoxime (DAM), a nucleophilic agent with "phosphatase-like" activity, has been found to effectively and reversibly block cardiac muscle contraction, while the cells remain capable of generating transmembrane action potentials. The aim of this study was to characterise the effects of DAM on the electrical properties of cardiac muscle. METHODS: Sheep epicardial muscle, guinea pig papillary muscle, and guinea pig ventricular myocytes were studied using conventional microelectrode techniques as well as single electrode current and voltage clamp techniques. RESULTS: DAM (5-20 mM) decreased action potential duration at 50% and 90% repolarisation levels (APD50, APD90) and refractory period in a dose dependent manner without causing significant changes in action potential amplitude, maximum upstroke velocity, or resting membrane potential. DAM induced a slight decrease in action potential conduction velocity in both the longitudinal and transverse directions, but on average the conduction velocity recorded in the presence of the drug was not significantly different from control. The time course of the APD restitution curve was not significantly changed but the frequency dependent APD variations were reduced. The ionic bases for these changes were studied in guinea pig ventricular myocytes. As with the results obtained in tissue preparations, DAM 15 mM decreased APD50 and APD90 by 35% and 29%, respectively. Under voltage clamp conditions, DAM led to a 35% reduction of ICa. The delayed rectifier IK current and the inward rectifier background current were also partially depressed by DAM but to a lesser extent. All of these effects were reversible upon washout. CONCLUSIONS: Aside from its well known effect as an electromechanical uncoupler, DAM causes a small, reversible, and non-selective reduction of several membrane conductances. Provided such effects are taken into consideration, DAM is a valuable tool in electrophysiological studies.
Action Potentials↗
Ionic mechanisms of electronic inhibition and concealed conduction in rabbit atrioventricular nodal myocytes.
BACKGROUND: The term "concealed conduction" is used in electrocardiography when a proximal (atrial or ventricular) impulse penetrates the atrioventricular (AV) node but fails to traverse it completely. Its penetration into the node is inferred by its after effects on the propagation of succeeding impulses. Concealed AV nodal conduction is a well-established phenomenon, but its precise cellular and subcellular mechanisms are unknown. It has been suggested that concealed conduction results from a transient impairment of excitability caused by the subthreshold depolarization (ie, electrotonic inhibition) that is elicited downstream of the site of block. METHODS AND RESULTS: We studied the ionic mechanism of electrotonic inhibition and concealed conduction in single myocytes isolated from the rabbit AV node. Cells were paced using just-threshold current pulses delivered at a constant (basic) cycle length of 1 second. Appropriately timed interpolation of a conditioning pulse of depolarizing but subthreshold current led to failure of the subsequent, previously successful activation. The ability of the subthreshold response to inhibit subsequent excitation was increased when the interval between the conditioning and succeeding pulses was shortened, when the amplitude of the conditioning pulse was increased, or when the inward sodium current was blocked by superfusion with tetrodotoxin (30 microM). Voltage clamp analysis demonstrated that electrotonic inhibition results from partial inactivation of the transient calcium current (ICa.T). Similar results were obtained using a mathematical model (Hodgkin-Huxley type) of the AV nodal myocyte. Additional simulations in a linear array of AV nodal cells showed that when a premature impulse fails to traverse the AV node, the subthreshold depolarization elicited downstream of the site of block may lead to a transient reduction of excitability with consequent delay or block of the succeeding impulse. CONCLUSIONS: The overall data strongly suggest that some of the electrocardiographic manifestations of concealed AV conduction are the result of electrotonic inhibition of excitability secondary to a transient decrease in ICa.T.
Animals↗
Spiral waves of excitation underlie reentrant activity in isolated cardiac muscle.
The mechanism of reentrant ventricular tachycardia was studied in computer simulations and in thin (approximately 20 x 20 x 0.5-mm) slices of dog and sheep ventricular epicardial muscle. A two-dimensional matrix consisting of 96 x 96 electrically coupled cells modeled by the FitzHugh-Nagumo equations was used to analyze the dynamics of self-sustaining reentrant activity in the form of elliptical spiral waves induced by premature stimulation. In homogeneous anisotropic media, spirals are stationary and may last indefinitely. However, the presence of small parameter gradients may lead to drifting and eventual termination of the spiral at the boundary of the medium. On the other hand, spirals may anchor and rotate around small discontinuities within the matrix. Similar results were obtained experimentally in 10 preparations whose electrical activity was monitored by means of a potentiometric dye and high-resolution optical mapping techniques; premature stimulation triggered reproducible episodes of sustained or nonsustained reentrant tachycardia in the form of spiral waves. As a rule, the spirals were elongated, with the major hemiaxis parallel to the longitudinal axis of the cells. The period of rotation (183 +/- 68 msec [mean +/- SD]) was longer than the refractory period (131 +/- 38 msec) and appeared to be determined by the size of the spiral's core, which was measured using a newly devised "frame-stack" plot. Drifting of spiral waves was also observed experimentally. Drift velocity was 9.8% of the velocity of wave propagation. In some cases, the core became stationary by anchoring to small arteries or other heterogeneities, and the spiral rotated rhythmically for prolonged periods of time. Yet, when drift occurred, spatiotemporal variations in the excitation period were manifested as a result of a Doppler effect, with the excitation period ahead of the core being 20 +/- 6% shorter than the excitation period behind the core. As a result of these coexisting frequencies, a pseudoelectrocardiogram of the activity in the presence of a drifting spiral wave exhibited "QRS complexes" with an undulating axis, which resembled those observed in patients with torsade de pointes. The overall results show that spiral wave activity is a property of cardiac muscle and suggest that such activity may be the common mechanism of a number of monomorphic and polymorphic tachycardias.
Animals↗
Stationary and drifting spiral waves of excitation in isolated cardiac muscle.
Excitable media can support spiral waves rotating around an organizing centre. Spiral waves have been discovered in different types of autocatalytic chemical reactions and in biological systems. The so-called 're-entrant excitation' of myocardial cells, causing the most dangerous cardiac arrhythmias, including ventricular tachycardia and fibrillation, could be the result of spiral waves. Here we use a potentiometric dye in combination with CCD (charge-coupled device) imaging technology to demonstrate spiral waves in the heart muscle. The spirals were elongated and the rotation period, Ts, was about 180 ms (3-5 times faster than normal heart rate). In most episodes, the spiral was anchored to small arteries or bands of connective tissue, and gave rise to stationary rotations. In some cases, the core drifted away from its site of origin and dissipated at a tissue border. Drift was associated with a Doppler shift in the local excitation period, T, with T ahead of the core being about 20% shorter than T behind the core.
Animals↗
Analytical modeling of the hysteresis phenomenon in guinea pig ventricular myocytes.
In the present study, we have demonstrated hysteresis phenomena in the excitability of single, enzymatically dissociated guinea pig ventricular myocytes. Membrane potentials were recorded with patch pipettes in the whole-cell current clamp configuration. Repetitive stimulation with depolarizing current pulses of constant cycle length and duration but varying strength led to predictable excitation (1:1) and non-excitation (1:0) patterns depending on current strength. In addition, transition between patterns depended on the direction of current intensity change and stable hysteresis loops were obtained in stimulus:response pattern vs. current intensity plots in 14 cells. Increase of pulse duration and decrease of stimulation rate contributed to a reduction in hysteresis loop areas. Changes in amplitude and shape of the subthreshold responses during the transitions from one stable pattern to the other, suggested that activity led to an increase in membrane resistance, particularly in the voltage domain between resting potential, and threshold. Therefore, we modelled the dynamic behaviour of the single cells as a function of diastolic membrane resistance, using previously published analytical solutions. Numerical iteration of the analytical model equations closely reproduced the experimental hysteresis loops in both qualitative and quantitative ways. In particular, the effect of stimulation frequency on the model was similar to the experimental findings. The overall study suggests that the excitability pattern of guinea pig ventricular myocytes accounts for hysteresis and bistabilities when current intensity is allowed to fluctuate around threshold levels.
Action Potentials↗
Spatiotemporal irregularities of spiral wave activity in isolated ventricular muscle.
Voltage-sensitive dyes and high resolution optical mapping were used to analyze the characteristics of spiral waves of excitation in isolated ventricular myocardium. In addition, analytical techniques, which have been previously used in the study of the characteristics of spiral waves in chemical reactions, were applied to determine the voltage structure of the center of the rotating activity (ie, the core). During stable spiral wave activity local activation occurs in a periodic fashion (ie, 1:1 stimulus: response activation ratio) throughout the preparation, except at the core, which is a small elongated area where the activity is of low voltage and the activation ratio is 1:0. The voltage amplitude increases gradually from the center of the core to the periphery. In some cases, however, regular activation patterns at the periphery may coexist with irregular local activation patterns near the core. Such a spatiotemporal irregularity is attended by variations in the core size and shape and results from changes in the core position. The authors conclude that functionally determined reentrant activity in the heart may be the result of spiral waves of propagation and that local spatiotemporal irregularities in the activation pattern are the result of changes in the core position.
Animals↗