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Y Rudy

Publications and source records attributed to Y Rudy.

At least 91 records · Page 5Linked to original sources
PubMed1990

Unidirectional block and reentry of cardiac excitation: a model study.

A computer model of a ring-shaped, one-dimensional cardiac fiber was used for examination of responses of propagation to premature stimuli applied under different degrees of both cell-to-cell coupling and membrane excitability. Results demonstrated the importance of cellular uncoupling in the genesis of unidirectional block and reentry. Propagation of excitation itself created a certain degree of functional inhomogeneity that provided necessary conditions for unidirectional block and reentry. The likelihood of induction of unidirectional block was proportional to the degree of cellular uncoupling. In contrast, uniform reduction in sodium channel conductance decreased the inducibility of unidirectional block. Nonsustained and sustained reentry was induced by a properly timed single premature stimulus during the refractory period of a propagating action potential. Reduction of the size of the reentry pathway resulted in an increased degree of interaction between the wavefront and its tail, which, in turn, changed the kinetics of the slow ionic channels, bringing about shortening of action potential duration. Alternans in action potential duration were also demonstrated during circus movement and were caused by the alternating kinetic properties of the slow ionic currents. Inhomogeneity along the reentry pathway in refractory period, in membrane excitability, in fiber cross-sectional area, or in gap junction resistance also provided conditions necessary for unidirectional block. The simulations suggested that an important role was played by cellular uncoupling in the genesis and maintenance of unidirectional block and reentry.

Action Potentials↗
PubMed1990

Noninvasive recovery of epicardial potentials in a realistic heart-torso geometry. Normal sinus rhythm.

The inverse problem in electrocardiography implies the reconstruction of electrical events within the heart from information measured noninvasively on the body surface. Deduction of these electrical events is possible from measured epicardial potentials, and, thus, a noninvasive method of recovering epicardial potentials from body surface data is useful in experimental and clinical studies. In the present study, an inverse method that uses Tikhonov regularization was shown to reconstruct, with good accuracy, important events in cardiac excitation. The inverse procedure was employed on data obtained from a human-torso tank in which a beating canine heart was placed in the correct anatomical position. Comparison with the actual, measured epicardial potentials indicates that positions and shapes of potential features (maxima, minima, zero potential line, saddles, etc.) are recovered with good accuracy throughout the QRS. An error in position of up to 1 cm is typical, while amplitudes are slightly diminished. In addition, application was extended from the above setting, in which the geometry was precisely known and potentials at a large number of leads were measured accurately, to a situation that is more representative of clinical and experimental settings. Effects of inaccuracy in location of the position of the heart were examined. A stylized torso that approximates the actual geometry was designed, and its performance in the inverse computations was evaluated. A systematic method of reduction of the number of leads on the body surface was proposed, and the resulting lead configurations were evaluated in terms of the accuracy of inverse solutions. The results indicate that the inverse problem can be stabilized with respect to different types of uncertainties in measured data and offer promise in the use of the inverse procedure in clinical and experimental situations.

Animals↗
PubMed1989

Simulation of the diffusion of acetylcholine in the neuroeffector junctions of the sinus node.

Traditionally, the diffusion of acetylcholine (ACh) from a neuron to cardiac muscle in a neuroeffector junction has been modeled as radial diffusion from a nerve ending into a spherical homogeneous medium. Various microscopic structures in the heart may or may not influence the spatial distribution of ACh within neuroeffector junctions. To determine the effect of microscopic anatomy on the diffusion of ACh in neuroeffector junctions, we simulated the diffusion of ACh in a two-dimensional inhomogeneous geometry that was based on micrographs of neuroeffector junctions in the sinus node. ACh was released at sites adjacent to a neuron. Simulations showed that the times of peak concentration after release and the peak concentrations per se were distributed symmetrically above and below and to the right and left of the neuron, but not radially about the neuron. We conclude that the diffusion of ACh in the neuroeffector junctions of the sinus node cannot be predicted well by a mathematical model that assumes radial diffusion in a spherical and homogeneous medium.

Acetylcholine↗
PubMed1989

Analysis of the hypoplastic right ventricle utilizing electrocardiographic body surface potential mapping (BSPM).

The authors present electrocardiographic body surface potential maps (BSPMs) of 11 patients with hypoplastic right ventricle (HRV) of three types: type I, HRV with pulmonary atresia; type II, HRV with tricuspid atresia; and type III, HRV with tricuspid artesia and transposition of the great arteries. The BSPMs of all 11 patients demonstrated evidence for epicardial right ventricular breakthrough, indicating conduction through an intact right bundle branch and Purkinje system. Nonetheless, the BSPMs strongly suggested profound morphological, probably embryological, differences among the right ventricles of the three groups. The four patients with type I HRV had no evidence for conduction abnormality. The five patients with type II, HRV however, had very marked conduction abnormality. In four of these five, the standard ECG and VCG had initial forces suggesting left lateral wall myocardial infarction. The BSPMs showed no evidence for infarction but demonstrated very complicated slow initial activation, explaining why the initial QRS vector was to the right and posterior before extending leftward. In addition, in all five the initial positive potentials were unusually inferior and the initial negative potentials unusually superior. After the evidence for epicardial right ventricular breakthrough, the positive and negative potentials rapidly changed positions so that the positive potentials were unusually superior and the negative potentials unusually inferior, consistent with the BSPM of endocardial cushion defects. In four of these five there was marked delay of total ventricular activation time. Of the two patients with type III HRV, one had an initial QRS similar to that of type II. Neither had rapid change of inferior and superior positive and negative potentials after right ventricular breakthrough, and both had intraventricular slowing, one with partial left bundle branch block.

Adolescent↗
PubMed1989

Computational issues of importance to the inverse recovery of epicardial potentials in a realistic heart-torso geometry.

In vitro data from a realistic-geometry electrolytic tank were used to demonstrate the consequences of computational issues critical to the ill-posed inverse problem in electrocardiography. The boundary element method was used to discretize the relationship between the body surface potentials and epicardial cage potentials. Variants of Tikhonov regularization were used to stabilize the inversion of the body surface potentials in order to reconstruct the epicardial surface potentials. The computational issues investigated were (1) computation of the regularization parameter; (2) effects of inaccuracy in locating the position of the heart; and (3) incorporation of a priori information on the properties of epicardial potentials into the regularization methodology. Two methods were suggested by which a priori information could be incorporated into the regularization formulation: (1) use of an estimate of the epicardial potential distribution everywhere on the surface and (2) use of regional bounds on the excursion of the potential. Results indicate that the a posteriori technique called CRESO, developed by Colli Franzone and coworkers, most consistently derives the regularization parameter closest to the optimal parameter for this experimental situation. The sensitivity of the inverse computation in a realistic-geometry torso to inaccuracies in estimating heart position are consistent with results from the eccentric spheres model; errors of 1 cm are well tolerated, but errors of 2 cm or greater result in a loss of position and amplitude information. Finally, estimates and bounds based on accurate, known information successfully lower the relative error associated with the inverse and have the potential to significantly enhance the amplitude and feature position information obtainable from the inverse-reconstructed epicardial potential map.

Animals↗
PubMed1989

Continuous right ventricular volume assessment by catheter measurement of impedance for antitachycardia system control.

Current implantable defibrillators are unable to differentiate between hemodynamically stable and unstable arrhythmias. This may result in unnecessary high energy shocks during arrhythmias that are better managed with other interventions. This study assessed the efficacy of the impedance catheter in sensing relative volumetric changes in the right ventricle as a measure of the hemodynamic status during an arrhythmia. During electrophysiological testing, 37 arrhythmias were induced in 12 patients aged 28-74 years. Rhythms recorded were: (A) hemodynamically stable tachyarrhythmias (supraventricular tachycardia and sustained monomorphic ventricular tachycardia)--21 episodes; and (B) hemodynamically unstable ventricular arrhythmias causing syncope (hypotensive ventricular tachycardia and ventricular fibrillation)--16 episodes. During unstable arrhythmias, stroke impedance (32 +/- 17%), arterial systolic pressure (40 +/- 11%), and right ventricular pulse pressure (15 +/- 20%), expressed as percentages of corresponding sinus rhythm values, were significantly lower than in stable arrhythmias (84 +/- 26%, 72 +/- 8%, and 111 +/- 37%, respectively); P less than 0.001. There was a good correlation between stroke impedance and mean arterial pressure during arrhythmia (r = 0.84). Impedance sensing is a practical method for distinguishing between hemodynamically stable and unstable arrhythmias. Implementation of hemodynamic sensing into the algorithm of future antitachycardia systems may improve the management of arrhythmias by adding options for selective pace termination or cardioversion.

Adult↗
PubMed1989

Mathematical model of dependence of heart rate on tissue concentration of acetylcholine.

The change in sinus period elicited by vagal stimulation depends on the rate of acetylcholine (ACh) release from the nerve endings, the rate of ACh degradation in the nodal tissue, and the responsiveness of the sinus node to ACh. Vagal stimulation in anesthetized dogs prolonged sinus period. After cessation of vagal stimulation, the sinus period returned to the prestimulation period. We developed a mathematical model to analyze the dynamics of ACh degradation in the neuroeffector junction and the dependence of sinus period on the concentration of ACh. From the in vitro reaction kinetics of acetylcholinesterase, we derived an analytical expression for the rate of ACh degradation in the intact animal. Our model represents the electrical behavior of the sinus node by the electrical activity of one pacemaker cell with six membrane ionic currents. This model predicts the decline in sinus period of the intact anesthetized dog as acetylcholinesterase degrades ACh in the neuroeffector junction. The half-life of ACh after cessation of vagal stimulation was estimated to be 2.7 s. We conclude that following termination of vagal stimulation, the sinus node of the intact animal responds to ACh as if the sinus node were one oscillator.

Acetylcholine↗
PubMed1989

Muscarinic autoreceptors do not modulate kinetics of acetylcholine release in hearts.

We determined the time course of the cellular mechanism that mediates the attenuation of the chronotropic response in anesthetized dogs to decreases in the time interval (interpulse interval) between pulses of vagal stimuli. We injected propranolol, cut the cervical vagi, and repetitively stimulated the cardiac segment of the right vagus nerve with one brief burst of electrical pulses during each cardiac cycle. We recorded the initial and steady-state changes in cardiac cycle length that were induced by the phasic vagal stimulation. The decrease in the interpulse interval decreased the initial and steady-state responses. The time delay between the release of acetylcholine (ACh) from the vagal nerve endings in the heart and inhibition of the release of additional ACh was less than 4 ms. Published delays between the time of ACh release and the time of the resulting change in membrane potential, in other biological systems, are 30-12,000 ms. We conclude that the time delay was too brief for muscarinic autoreceptors to have mediated the attenuation of ACh release from postganglionic vagal nerve endings in the heart in response to decreases in interpulse interval.

Acetylcholine↗
PubMed1989

Mathematical model of the changes in heart rate elicited by vagal stimulation.

We developed a mathematical model of the underlying cellular mechanisms responsible for the changes in sinus cycle length (SCL) elicited by vagal stimulation in intact animals. The model incorporated a stimulation-mediated depletion of the releasable pool of acetylcholine (ACh) in the nerve endings, the in vitro reaction kinetics of acetylcholinesterase, and the electrical activity of a pacemaker cell with six membrane ionic currents. SCL increased linearly with the frequency of simulated vagal stimulation, as it does in animal experiments, because the concentration of ACh in the neuroeffector junction [( ACh]) saturated as the frequency of stimulation was increased and because SCL increased geometrically in response to increases in [ACh]. The dependence of SCL on the timing of vagal stimulation in the cardiac cycle resulted, in part, from the dependence of [ACh] on SCL. Simulated vagal stimulation entrained the sinus node because the rate of activation and inactivation of ACh-activated K+ channels depended only weakly on membrane potential during diastolic depolarization. SCL increased geometrically with [ACh], because 1) during diastolic depolarization, the amplitude of the ACh-activated K+ current was approximately equal to the amplitude of the sum of the other ionic currents, 2) [ACh] was low enough to saturate neither acetylcholinesterase nor the cellular system that activates the ACh-activated K+ channels, 3) the pacemaker cell membrane behaved electrotonically like a capacitor, and 4) the sum of all the ionic currents increased linearly with the amplitude of the ACh-activated K+ current.

Acetylcholine↗
PubMed1988

Respiration and the ECG: a study using body surface potential maps.

Body surface potential maps and an eccentric spheres model of the heart were used to investigate some of the factors that cause the surface ECG to change with respiration. Although the pattern of the surface maps shifted inferiorly with inspiration, the pattern itself did not change significantly, even with deep respiratory movements. However, the temporal ECGs at specific electrodes changed dramatically. The model simulations show that the contribution to the change in amplitude of the surface potential due to lung conductivity and ventricular volume changes is small. It is suggested that the major cause of the surface potential changes with inspiration is due to the change in heart position.

Adult↗
PubMed1988

Electrocardiographic body surface potential maps of the QRS and T of normal young men. Qualitative description and selected quantifications.

A qualitative and quantitative analysis of the Body Surface Potential Maps (BSPM) of 40 young men, ages 19-41, is presented utilizing a 180 electrode system, with 135 anterior leads and 45 posterior leads. Evidence for epicardial right ventricular breakthrough was demonstrated in 36/40 at 27.9 +/- 6.8 ms, whereas our previous studies on normal children (average age 12.5 years) have demonstrated evidence for epicardial right ventricular breakthrough at 25.0 +/- 8.9 ms. The peak-to-peak magnitude at maximal potential (at 42.3 +/- 4.8 ms) was not significantly different from that of the children (4,430 +/- 1,165 microV), and the peak-to-peak magnitude of ST-T was virtually the same as that of the children (1,182 +/- 376.2 microV). The terminal activation pattern of late QRS on the body surface map appeared in the true posterior, anterior superior, posterior right superior and/or right anterior superior positions, in order of frequency. There were other regions appearing less frequently. In contrast, this pattern in children was seen only in the anterior superior, right anterior superior, posterior right superior, and true posterior in order of frequency. In 18/40, the body surface manifestation of repolarization was seen an average of 9.4 +/- 4.8 ms before the end of the QRS. A new pseudocolor display with 31 color levels representing body surface potentials allowed excellent resolution of isopotential detail.

Adult↗
PubMed1988

The effect of variations of ventricular volume on the electrocardiogram. A comparison of two model simulations.

Two previously published models of the electrocardiogram are compared and evaluated to determine the causes and nature of the relationship between variations in ventricular volumes and surface potential. Both models included a relatively high conductivity spherical heart in a spherical torso, but in one the source was a single dipole, while in the other the source was a double-layer spherical cap. Volume conductor effects (that is the change in electrical conductivity of the torso associated with ventricular volume changes) caused a decrease in surface potential with increase in ventricular volume. Changes in position of the heart and of the strength of the activation wavefront with increases in volume may explain the increase in surface potential with ventricular volume observed in experimental studies.

Cardiac Volume↗
PubMed1988

The inverse problem in electrocardiography: solutions in terms of epicardial potentials.

The objective of the inverse problem in electrocardiography is to recover noninvasively regional information about intracardiac electrical events from electrical measurements on the body surface. The choice of epicardial potentials as the solution to the inverse problem is motivated by the availability of a unique epicardial potential solution for each body surface potential distribution, by the ability to verify experimentally the inverse-recovered epicardial potentials, by the proven relationship between epicardial potentials and the details of intracardiac regional events, and by the possibility of using the inverse solution as a supplement or possible replacement to clinical epicardial potential mapping prior to surgical intervention. Although, in principle, the epicardial potential distribution can be recovered from the body surface potential distribution, the inverse problem in terms of potentials is ill-posed, and naive attempts to reconstruct the epicardial potentials result in incorrect solutions which are highly oscillatory. Large deviations from the actual solution may result from inaccuracy of the data measurement, incomplete knowledge of the potential data over the entire torso, and inaccurate description of the inhomogeneous torso volume conductor. This review begins with a mathematical and qualitative description of the inverse problem in terms of epicardial potentials. The ill-posed nature of the problem is demonstrated using a theoretical boundary value problem. Effects of inaccuracies in the body surface potential data (stability estimates) are introduced, and a sensitivity analysis of geometrical and inhomogeneity parameters is presented using an analytical eccentric spheres model. Various computational methods for relating epicardial to body surface potentials, i.e., the computation of the forward transfer matrix, are described and compared. The need for regularization of the inverse recovery of epicardial potentials, resulting from the need to invert the ill-conditioned transfer matrix, is demonstrated. Several regularization techniques are compared in terms of their performance regarding noise in the data and inaccuracies in geometry and inhomogeneities. Finally, several existing, regularized inverse procedures that compute epicardial potentials from measured body surface potential data are introduced and compared. The review concludes with a section that points toward future directions for improving the quality of the inverse-reconstructed epicardial potentials. Future directions for the use of the inverse problem to obtain epicardial potential distributions noninvasively in both experimental animals and patients in a clinical se

Animals↗
PubMed1987

A model study of the effects of the discrete cellular structure on electrical propagation in cardiac tissue.

The effects of the discrete cellular structure on propagation of electrical excitation in cardiac muscle were studied in a one-dimensional fiber model containing a periodic intercalated disk structure. Globally, the macroscopic velocity of propagation follows the behavior associated with propagation in a continuous tissue (except for high values of disk resistance). In addition, the computed spatial extracellular potential along the fiber is a smooth biphasic waveform and does not reflect the underlying discrete cellular structure of the tissue. Other results of the simulations demonstrate the discontinuous nature of propagation and the importance of the structure in arrhythmogenesis. Vmax displays a biphasic behavior as a function of increasing intercalated disk resistance. An initial "paradoxical" increase in Vmax (with a simultaneous decrease in conduction velocity) is followed by a decrease that leads to decremental propagation and conduction block. The time constant of the foot of the action potential (tau foot) increases monotonically with increasing intercalated disk resistance. An increase in the leakage current to extracellular space brings about a significant decrease in the action potential duration and a loss of the plateau. This major effect is accompanied by a relatively smaller decrease in conduction velocity. Collision of two activation wavefronts results in a significant (100%) increase in Vmax and a very small (0.6%) decrease in tau foot.

Action Potentials↗
PubMed1984

The spectrum of right bundle branch block as manifested in electrocardiographic body surface potential maps.

A wide spectrum of types of right bundle branch block (RBBB) were studied utilizing the body surface potential maps (BSPMs) of 37 children. Although the spectrum varied from very advanced RBBB to minimal partial RBBB, a common diagnostic feature was the absence of evidence for right ventricular breakthrough in the maps of all patients. Evidence for left ventricular breakthrough was usually seen, the exceptions being five patients with partial RBBB and one of 29 with advanced RBBB. The appearance of evidence for activation of the right ventricle by way of the septum was late in onset. In addition, especially in advanced RBBB, the BSPM pattern reflecting right ventricular activation was prolonged in such a manner that it appeared that utilization of right ventricular Purkinje tissue was minimal and inefficient. The BSPMs during ST-T, which were of inverse polarity, reflect repolarization that is determined by the sequence of depolarization to a greater degree than in the normal. In general, the more extensive the surgery, the more advanced the RBBB (as reflected in the BSPM), although there were exceptions. The one parameter that linked all patients with RBBB together was the absence of evidence for right ventricular epicardial breakthrough.

Adolescent↗