Search PubMed⌕ Search

Biomedical subjects

J Jalife

Publications and source records attributed to J Jalife.

At least 55 records · Page 3Linked to original sources
PubMed1998

Effects of postshock atrial pacing on atrial defibrillation outcome in the isolated sheep heart.

BACKGROUND: Failed atrial defibrillation shocks are associated with organization of postshock activity and a substantial postshock electrical quiescence. We investigated the ability of a train of pacing stimuli to capture or locally entrain atrial myocardium during the quiescent period after low-energy shocks and to alter defibrillation outcome. METHODS AND RESULTS: High-resolution video imaging of near-defibrillation-threshold atrial shocks was performed in 12 Langendorff-perfused sheep hearts. A train of 10 pacing stimuli (10-ms pulse width, 200-ms cycle length) was coupled to the shock at various delays in 7 hearts. Coupling intervals of 40 to 130 ms were investigated for feasibility of capture of the first pacing stimulus. The success rate of capture was 0, 0.08+/-0.08, 0.43+/-0.13, 0.73+/-0.13, and 0.11+/-0.1 for 40-, 60-, 80-, 100-, and 120-ms coupling intervals, respectively (P<0.001). In 5 experiments, the coupling interval was fixed at 100 ms (highest success, see above), and the pacing stimulus amplitude was varied between 1.0, 2.0, and 4.0 V. Successful capture rates were 0.38+/-0.08, 0.75+/-0.08, and 0.64+/-0.08, respectively (P<0.003 for 1.0 versus 2.0 V, P=0.2 for 2.0 versus 4.0 V). Rates of successful defibrillation for the groups without and with pacing were 0.56+/-0.07 and 0.64+/-0.04, respectively (P=0.3). With capture of the first pacing stimulus, the rate of successful defibrillation rose to 0.75+/-0.05 (P<0.01); it remained unchanged without capture (0.48+/-0.07 versus 0.56+/-0.07 for no pacing). CONCLUSIONS: Pacing during the quiescent period that follows defibrillation shocks is feasible. A pacing train whose first pacing stimulus successfully captures during the quiescent period of near-defibrillation-threshold shocks appears to alter the outcome.

Animals↗
PubMed1998

Purkinje-muscle reentry as a mechanism of polymorphic ventricular arrhythmias in a 3-dimensional model of the ventricles.

Multiple electrode mapping of the ventricles during complex tachyarrhythmias has revealed focal subendocardial activation whose mechanism remains unexplained. We hypothesized that reentry involving the Purkinje-muscle junctions (PMJs) may be a mechanism for such focal excitations. We have constructed an anatomically appropriate computerized 3-dimensional model of the mammalian ventricles that includes the Purkinje conduction system and 214 PMJs distributed throughout the endocardium. Isochronal maps during normal excitation, as well as during right or left bundle branch block, resembled experimental measurements and compared well with isochronal maps of propagation in the human heart. Activity observed at both sides of a PMJ in the model showed that propagation from Purkinje fibers to muscle was slower than in the opposite direction. Under these realistic and normal conditions, the evolution of reentrant activity involving muscle and the Purkinje network was simulated. The reentry pattern was independent of the initiation site. It evolved with drifting epicardial breakthroughs and transformed on the endocardium from focal activity to figure-of-8 reentry. In addition, the ECG amplitude undulated during the evolution, and decrease in the cycle period, apparent wavelength, and propagation velocity were observed. Finally, the reentry was terminated if the Purkinje system was disconnected from the muscle before it reached a relative steady state. The simulation results suggest the following: (1) Epicardial breakthroughs and endocardial focal activity may originate at the PMJs. (2) The ECG amplitude may decrease as the reentry stabilizes and the excitation wavelength decreases. (3) The Purkinje system may have a double role in the evolution of reentry: first, it is essential to the reentry at the initial stage; second, it may lead to the establishment of intramyocardial reentry, at which time the Purkinje system becomes irrelevant.

Action Potentials↗
PubMed1998

Effects of atrial defibrillation shocks on the ventricles in isolated sheep hearts.

BACKGROUND: The effects of cardioversion of atrial fibrillation on the activation sequence of the ventricles have not been previously studied. In this study we examined the events in the ventricle that follow the application of atrial defibrillatory shocks. METHODS AND RESULTS: We used video imaging technology to study the sequence of activation on the surface of the ventricles in the Langendorff-perfused sheep heart. We recorded transmembrane potentials simultaneously from over 20000 sites on the epicardium before and after biphasic shocks applied by a programmable atrial defibrillator. The first epicardial activation after the shock depended on both the voltage and timing of the shock. During ventricular diastole shocks as low as 10 V produced ventricular excitation, although the time between the shock and the first epicardial activation (latency) was approximately 30 ms. As the shock voltage was increased to 120 V, latency decreased to zero and the entire epicardium was depolarized within 30 ms. For 120-V shocks delivered late in systole, the depolarization sequence produced by the shock was similar to the previous repolarization sequence. Shocks of 120 V applied 150 to 300 ms after the previous ventricular excitation induced ventricular fibrillation. Ventricular fibrillation was induced by multiple focal beats after the shock, which produced waves that propagated but broke down into reentry within regions of high repolarization gradients. CONCLUSIONS: These results demonstrate that atrial defibrillation shocks excite the ventricles even at low shock voltages. In addition, ventricular fibrillation can be induced by shocks given in the vulnerable period by producing focal patterns that break down into reentrant waves.

Animals↗
PubMed1998

Spatial and temporal organization during cardiac fibrillation.

Cardiac fibrillation (spontaneous, asynchronous contractions of cardiac muscle fibres) is the leading cause of death in the industrialized world, yet it is not clear how it occurs. It has been debated whether or not fibrillation is a random phenomenon. There is some determinism during fibrillation, perhaps resulting from rotating waves of electrical activity. Here we present a new algorithm that markedly reduces the amount of data required to depict the complex spatiotemporal patterns of fibrillation. We use a potentiometric dye and video imaging to record the dynamics of transmembrane potentials at many sites during fibrillation. Transmembrane signals at each site exhibit a strong periodic component centred near 8 Hz. This periodicity is seen as an attractor in two-dimensional-phase space and each site can be represented by its phase around the attractor. Spatial phase maps at each instant reveal the 'sources' of fibrillation in the form of topological defects, or phase singularities, at a few sites. Using our method of identifying phase singularities, we can elucidate the mechanisms for the formation and termination of these singularities, and represent an episode of fibrillation by locating singularities. Our results indicate an unprecedented amount of temporal and spatial organization during cardiac fibrillation.

Algorithms↗
PubMed1998

Spiral waves in two-dimensional models of ventricular muscle: formation of a stationary core.

Previous experimental studies have clearly demonstrated the existence of drifting and stationary electrical spiral waves in cardiac muscle and their involvement in cardiac arrhythmias. Here we present results of a study of reentrant excitation in computer simulations based on a membrane model of the ventricular cell. We have explored in detail the parameter space of the model, using tools derived from previous numerical studies in excitation-dynamics models. We have found appropriate parametric conditions for sustained stable spiral wave dynamics (1 s of activity or approximately 10 rotations) in simulations of an anisotropic (ratio in velocity 4:1) cardiac sheet of 2 cm x 2 cm. Initially, we used a model that reproduced well the characteristics of planar electrical waves exhibited by thin sheets of sheep ventricular epicardial muscle during rapid pacing at a cycle length of 300 ms. Under these conditions, the refractory period was 147 ms; the action potential duration (APD) was 120 ms; the propagation velocity along fibers was 33 cm/s; and the wavelength along fibers was 4.85 cm. Using cross-field stimulation in this model, we obtained a stable self-sustaining spiral wave rotating around an unexcited core of 1.75 mm x 7 mm at a period of 115 ms, which reproduced well the experimental results. Thus the data demonstrate that stable spiral wave activity can occur in small cardiac sheets whose wavelength during planar wave excitation in the longitudinal direction is larger than the size of the sheet. Analysis of the mechanism of this observation demonstrates that, during rotating activity, the core exerts a strong electrotonic influence that effectively abbreviates APD (and thus wavelength) in its immediate surroundings and is responsible for the stabilization and perpetuation of the activity. We conclude that appropriate adjustments in the kinetics of the activation front (i.e., threshold for activation and upstroke velocity of the initiating beat) of currently available models of the cardiac cell allow accurate reproduction of experimentally observed self-sustaining spiral wave activity. As such, the results set the stage for an understanding of functional reentry in terms of ionic mechanisms.

Action Potentials↗
PubMed1998

Mechanisms of atrial fibrillation: mother rotors or multiple daughter wavelets, or both?

The mechanism of atrial fibrillation (AF) remains poorly understood. In this article, we present a new unifying hypothesis for the electrophysiologic basis of AF. We surmise that sustained AF depends on the uninterrupted periodic activity of discrete reentrant sites. The shorter reentrant circuits act as dominant frequency sources that maintain the overall activity. The rapidly succeeding wavefronts emanating from these sources propagate through both atria and interact with anatomic and/or functional obstacles, leading to the phenomenon of "vortex shedding" and to wavelet formation. As suggested by recent numerical and experimental results from our laboratory, some of such wavelets may shrink and undergo decremental conduction, others may be annihilated by collision with another wavelet or a boundary, and still others may curl to create new vortices. The end result would be the fragmentation of the periodic wavefronts into multiple independent daughter wavelets, giving rise to new wavelets, and so on in the ceaseless, globally aperiodic motion that characterizes fibrillatory conduction.

Animals↗
PubMed1997

Optical mapping of drug-induced polymorphic arrhythmias and torsade de pointes in the isolated rabbit heart.

OBJECTIVES: This study sought to 1) test the hypothesis that in the setting of bradycardia and drug-induced action potential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat changes in the origin and direction of the excitation wave front and are responsible for polymorphic arrhythmias; and 2) determine whether EADs may initiate nonstationary reentry, giving rise to the typical torsade de pointes (TDP) pattern. BACKGROUND: In the past, it has been difficult to associate EADs or reentry with the undulating electrocardiographic (ECG) patterns of TDP. METHODS: A voltage-sensitive dye was used for high resolution video imaging of electrical waves on the epicardial and endocardial surface of the Langendorff-perfused rabbit heart. ECG and monophasic action potentials from the right septal region were also recorded. Bradycardia was induced by ablation of the atrioventricular node. RESULTS: Perfusion of low potassium chloride Tyrode solution plus quinidine led to prolongation of the action potential and the QT interval. Eventually, EADs and triggered activity ensued, giving rise to intermittent episodes of polymorphic arrhythmia. In one experiment, triggered activity was followed by a long episode of vortex-like reentry with an ECG pattern characteristic of TDP. However, in most experiments, focal activity of varying origins and propagation patterns was observed. Triggered responses also showed varying degrees of local block. Similar results were obtained with E-4031. Burst pacing both at control conditions and in the presence of quinidine consistently led to vortex-like reentry whose ECG pattern resembled TDP. However, the cycle length of the arrhythmia with quinidine was longer than that for control ([mean +/- SEM] 194 +/- 12 vs. 132 +/- 8 ms, p < 0.03). CONCLUSIONS: Drug-induced polymorphic ventricular arrhythmias may result from beat to beat changes in wave propagation patterns initiated by EADs or EAD-induced nonstationary reentrant activity. In contrast, burst pacing-induced polymorphic tachycardia in the presence or absence of drugs is the result of nonstationary reentrant activity.

Action Potentials↗
PubMed1997

Video imaging of atrial defibrillation in the sheep heart.

BACKGROUND: The effects of defibrillatory shocks on the organization of atrial fibrillation (AF) have not been studied previously. In this study, we examined the events that precede, accompany, and follow the application of atrial defibrillatory shocks. METHODS AND RESULTS: We used video imaging to study the sequence of activation on the surface of the atria in the Langendorff-perfused sheep heart. We recorded transmembrane potentials simultaneously from > 20000 sites on the epicardium during AF as well as during and after biphasic shocks applied by a programmable atrial defibrillator. Defibrillatory shocks (1.2 +/- 0.6 J; n = 6) depolarized all epicardial regions of the atria, and asynchronous repolarization occurred. The shocks resulted in four types of responses: (1) immediate cessation of epicardial activity. (2) single postshock activation. (3) organized activation for 0.8 to 1.5 seconds followed by termination, and (4) organized activity followed by degeneration back into AF. Types 2 through 4 involved a quiescent period lasting 110 +/- 28 ms immediately after the shock, then an activation sequence similar to those observed during sinus rhythm. The first cycle length after the shock for types 3 and 4 (170 +/- 36 ms) was longer than during AF (144 +/- 33 ms). Repolarization time after a shock was significantly longer for successful compared with unsuccessful shocks. CONCLUSIONS: These results indicate that the shock depolarized the entire atrial epicardial surface, followed by a quiescent period, after which organized activation emanated from the sinoatrial pacemaker region.

Analysis of Variance↗
PubMed1997

Spatio-temporal patterns of atrial fibrillation: role of the subendocardial structure.

Despite many years of research and speculation, the precise mechanisms underlying atrial fibrillation remain elusive. Prevalent understanding relies on assumptions, which are based on two-dimensional numerical simulations and on the idea that atrial fibrillation is the result of total disorganization of electrical activity, with multiple wavelets wandering randomly throughout the atria. However, recent studies both clinical and basic, have suggested that focal mechanisms, either re-entrant or automatic, may explain fibrillatory activity in some cases. Here we review the major hypotheses that have prevailed at one time or another to explain this complex arrhythmia and discuss some recent experimental results that strongly suggest that, whatever the electrophysiological basis of atrial fibrillation may be, it must involve complex patterns of propagation through the intricate multidimensional anatomical structure of the atria.

Animals↗
PubMed1996

Incomplete reentry and epicardial breakthrough patterns during atrial fibrillation in the sheep heart.

BACKGROUND: The mechanisms underlying atrial fibrillation and its initiation are not fully understood. Our hypothesis is that atrial fibrillation results from complex activation involving the subendocardial muscle network. METHODS AND RESULTS: We have used video imaging to study the sequence of activation on the surface of the right atrium of the Langendorff-perfused sheep heart during pacing, atrial fibrillation, and its initiation. We recorded transmembrane potentials simultaneously from over 20,000 sites. We observed two types of patterns of wave propagation during the initiation of atrial fibrillation. The first type resulted from heterogeneties of refractoriness and transmural propagation near the stimulating electrode. The second type involved heterogeneity in conduction away from the pacing site. During atrial fibrillation, the average period of activation was 138 +/- 25 ms (n = 6), and complete reentrant pathways were never observed. Propagation patterns were characterized by a combination of incomplete reentry, breakthrough patterns, and wave collisions. Incomplete reentry occurred when waves propagated around thin lines of block and then terminated. Breakthrough patterns were frequent and occurred every 215 ms on average. The location of these breakthrough sites and the lines of block during incomplete reentry were not randomly distributed but appeared to be related to preferential propagation in the underlying subendocardial muscle structures. A computer model of atrial free wall connected to a pectinate muscle suggested that subendocardial muscles lead to epicardial breakthrough patterns that act to destabilize reentry. CONCLUSIONS: These results suggest that the complex three-dimensional structure of the atria plays a major role in the activation sequences during atrial fibrillation and its initiation.

Action Potentials↗
PubMed1996

Vortex shedding as a precursor of turbulent electrical activity in cardiac muscle.

In cardiac tissue, during partial blockade of the membrane sodium channels, or at high frequencies of excitation, inexcitable obstacles with sharp edges may destabilize the propagation of electrical excitation waves, causing the formation of self-sustained vortices and turbulent cardiac electrical activity. The formation of such vortices, which visually resembles vortex shedding in hydrodynamic turbulent flows, was observed in sheep epicardial tissue using voltage-sensitive dyes in combination with video-imaging techniques. Vortex shedding is a potential mechanism leading to the spontaneous initiation of uncontrolled high-frequency excitation of the heart.

Animals↗
PubMed1996

Drifting vortices of electrical waves underlie ventricular fibrillation in the rabbit heart.

Ventricular fibrillation is the most important cause of cardiac electrical instability leading to sudden death. Fibrillation is believed to be associated with complex three-dimensional (3-D) spatio-temporal patterns of electrical excitation of the myocardium. However, to this date, such patterns have not been directly observed or characterized, and little is known about their dynamics. In this paper, we present results that strongly support the hypothesis that at least some cases of ventricular fibrillation in the structurally normal heart may be the result of a single 3-D electrical scroll wave that moves rapidly throughout the ventricles, giving rise to complex patterns of cardiac muscle excitation.

Animals↗