Biomedical subjects

Felipe Aguel

Publications and source records attributed to Felipe Aguel.

7 recordsLinked to original sources

PubMed2006

Spiral wave attachment to millimeter-sized obstacles.

BACKGROUND: Functional reentry in the heart takes the form of spiral waves. Drifting spiral waves can become pinned to anatomic obstacles and thus attain stability and persistence. Lidocaine is an antiarrhythmic agent commonly used to treat ventricular tachycardia clinically. We examined the ability of small obstacles to anchor spiral waves and the effect of lidocaine on their attachment. METHODS AND RESULTS: Spiral waves were electrically induced in confluent monolayers of cultured, neonatal rat cardiomyocytes. Small, circular anatomic obstacles (0.6 to 2.6 mm in diameter) were situated in the center of the monolayers to provide an anchoring site. Eighty reentry episodes consisting of at least 4 revolutions were studied. In 36 episodes, the spiral wave attached to the obstacle and became stationary and sustained, with a shorter reentry cycle length and higher rate. Spiral waves could attach to obstacles as small as 0.6 mm, with a likelihood for attachment that increased with obstacle size. After attachment, both conduction velocity of the wave-front tip and wavelength near the obstacle adapted from their pre-reentry values and increased linearly with obstacle size. In contrast, reentry cycle length did not correlate significantly with obstacle size. Addition of lidocaine 90 mumol/L depressed conduction velocity, increased reentry cycle length, and caused attached spiral waves to become quasi- attached to the obstacle or terminate. CONCLUSIONS: Anchored spiral waves exhibit properties of both unattached spiral waves and anatomic reentry. Their behavior may be representative of functional reentry dynamics in cardiac tissue, particularly in the setting of monomorphic tachyarrhythmias.

Animals↗

PubMed2004

Multiarm spirals in a two-dimensional cardiac substrate.

A variety of chemical and biological nonlinear excitable media, including heart tissue, can support stable, self-organized waves of activity in a form of rotating single-arm spirals. In particular, heart tissue can support stationary and meandering spirals of electrical excitation, which have been shown to underlie different forms of cardiac arrhythmias. In contrast to single-arm spirals, stable multiarm spirals (multiple spiral waves that rotate in the same direction around a common organizing center) have not been demonstrated and studied yet in living excitable tissues. Here, we show that persistent multiarm spirals of electrical activity can be induced in monolayer cultures of neonatal rat heart cells by a short, rapid train of electrical point stimuli applied during single-arm-spiral activity. Stable formation is accomplished only in monolayers that show a relatively broad and steep dependence of impulse wavelength and propagation velocity on rate of excitation. The resulting multiarm spirals emit waves of electrical activity at rates faster than for single-arm spirals and exhibit two distinct behaviors, namely "arm-switching" and "tip-switching." The phenomenon of rate acceleration due to an increase in the number of spiral arms possibly may underlie the acceleration of functional reentrant tachycardias paced by a clinician or an antitachycardia device.

Animals↗

PubMed2004

Effect of acute global ischemia on the upper limit of vulnerability: a simulation study.

The goal of this modeling research is to provide mechanistic insight into the effect of altered membrane kinetics associated with 5-12 min of acute global ischemia on the upper limit of cardiac vulnerability (ULV) to electric shocks. We simulate electrical activity in a finite-element bidomain model of a 4-mm-thick slice through the canine ventricles that incorporates realistic geometry and fiber architecture. Global acute ischemia is represented by changes in membrane dynamics due to hyperkalemia, acidosis, and hypoxia. Two stages of acute ischemia are simulated corresponding to 5-7 min (stage 1) and 10-12 min (stage 2) after the onset of ischemia. Monophasic shocks are delivered in normoxia and ischemia over a range of coupling intervals, and their outcomes are examined to determine the highest shock strength that resulted in induction of reentrant arrhythmia. Our results demonstrate that acute ischemia stage 1 results in ULV reduction to 0.8A from its normoxic value of 1.4A. In contrast, no arrhythmia is induced regardless of shock strength in acute ischemia stage 2. An investigation of mechanisms underlying this behavior revealed that decreased postshock refractoriness resulting mainly from 1) ischemic electrophysiological substrate and 2) decrease in the extent of areas positively-polarized by the shock is responsible for the change in ULV during stage 1. In contrast, conduction failure is the main cause for the lack of vulnerability in acute ischemia stage 2. The insight provided by this study furthers our understanding of mechanisms by which acute ischemia-induced changes at the ionic level modulate cardiac vulnerability to electric shocks.

Action Potentials↗

PubMed2004

Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia.

OBJECTIVES: The purpose of this study is to characterize the changes in vulnerability to electric shocks during phase 1A of global ischemia in the rabbit ventricles and to determine the mechanisms responsible for these changes. BACKGROUND: Mechanisms responsible for the changes in cardiac vulnerability over the course of ischemia phase 1A remain poorly understood. The lack of understanding results from the rapid ischemic change in cardiac electrophysiologic properties, which renders experimental evaluation of vulnerability difficult. METHODS: To examine dynamic changes in vulnerability to electric shocks over the course of acute global ischemia phase 1A, this study used a three-dimensional anatomically accurate bidomain model of ischemic rabbit ventricles. Monophasic shocks are applied at various coupling intervals to construct vulnerability grids in normoxia and at various stages of ischemia phase 1A. RESULTS: Our simulations demonstrate that 2 to 3 minutes after the onset of ischemia, the upper limit of vulnerability remains at its normoxic value (12.75 V/cm); however, arrhythmias are induced at shorter coupling intervals. As ischemia progresses, the upper limit of vulnerability decreases, reaching 6.4 V/cm in the advanced stage of ischemia phase 1A, and the vulnerable window shifts towards longer coupling intervals. CONCLUSIONS: Changes in the upper limit of vulnerability result from an increase in the spatial extent of the shock-end excitation wavefronts and the slower recovery from shock-induced positive polarization. Shifts in the vulnerable window stem from decreases in local repolarization times and the occurrence of postshock conduction failure caused by prolonged postrepolarization refractoriness.

Action Potentials↗

PubMed2004

Advances in ambulatory monitoring: regulatory considerations.

Conventional ambulatory electrocardiogram (ECG) (Holter) monitoring involves 2 or 3 surface leads recorded with electrode positions and signal characteristics that are different from diagnostic quality 12-lead ECGs due to the limitations imposed by technology on the ambulatory recorders. The rapid pace of technological development for medical devices, particularly electrocardiography, has now enabled the recording of diagnostic quality 12-lead ECG waveforms for extended time periods. This capability allows Holter recording to become another source for diagnostic 12-lead ECG records on a par with other modalities such as resting ECG and exercise stress testing. Additionally, other diagnostic techniques such as S-T segment analysis and Q-T interval analysis that rely on diagnostic quality waveforms can now be applied. All of these enhancements to the traditional Holter modality have altered the regulatory perspective of these devices, since the enhancements may represent a new intended use for the device.

Biomedical Engineering↗

PubMed2002

Computational techniques for solving the bidomain equations in three dimensions.

The bidomain equations are the most complete description of cardiac electrical activity. Their numerical solution is, however, computationally demanding, especially in three dimensions, because of the fine temporal and spatial sampling required. This paper methodically examines computational performance when solving the bidomain equations. Several techniques to speed up this computation are examined in this paper. The first step was to recast the equations into a parabolic part and an elliptic part. The parabolic part was solved by either the finite-element method (FEM) or the interconnected cable model model (ICCM). The elliptic equation was solved by FEM on a coarser grid than the parabolic problem and at a reduced frequency. The performance of iterative and direct linear equation system solvers was analyzed as well as the scalability and parallelizability of each method. Results indicate that the ICCM was twice as fast as the FEM for solving the parabolic problem, but when the total problem was considered, this resulted in only a 20% decrease in computation time. The elliptic problem could be solved on a coarser grid at one-quarter of the frequency at which the parabolic problem was solved and still maintain reasonable accuracy. Direct methods were faster than iterative methods by at least 50% when a good estimate of the extracellular potential was required. Parallelization over four processors was efficient only when the model comprised at least 500,000 nodes. Thus, it was possible to speed up solution of the bidomain equations by an order of magnitude with a slight decrease in accuracy.

Algorithms↗

PubMed1998

The role of cardiac tissue structure in defibrillation.

The purpose of this paper is to investigate the relationship between cardiac tissue structure, applied electric field, and the transmembrane potential induced in the process of defibrillation. It outlines a general understanding of the structural mechanisms that contribute to the outcome of a defibrillation shock. Electric shocks defibrillate by changing the transmembrane potential throughout the myocardium. In this process first and foremost the shock current must access the bulk of myocardial mass. The exogenous current traverses the myocardium along convoluted intracellular and extracellular pathways channeled by the tissue structure. Since individual fibers follow curved pathways in the heart, and the fiber direction rotates across the ventricular wall, the applied current perpetually engages in redistribution between the intra- and extracellular domains. This redistribution results in changes in transmembrane potential (membrane polarization): regions of membrane hyper- and depolarization of extent larger than a single cell are induced in the myocardium by the defibrillation shock. Tissue inhomogeneities also contribute to local membrane polarization in the myocardium which is superimposed over the large-scale polarization associated with the fibrous organization of the myocardium. The paper presents simulation results that illustrate various mechanisms by which cardiac tissue structure assists the changes in transmembrane potential throughout the myocardium. (c) 1998 American Institute of Physics.

Journal Article↗