bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Dominant T Wave and Its Significance
Authors: OOSTEROM ADRIAAN van 
Published: October 2003

Introduction: The shapes of the T waves as observed in different leads placed on the thorax are very similar. The dominant T wave is introduced as a means to characterize this general signal shape. Its relationship to the transmembrane potentials of cardiac myocytes is discussed. Methods and Results: The source description of a biophysical model that previously was shown to yield realistic T waveforms was analyzed in order to exploit its relation to the transmembrane potentials of the cardiac myocytes at the surface bounding the myocardium. The product of this analysis is the dominant T wave: a waveform that describes the slope of the transmembrane potential. It is shown that the dominant T wave can be estimated easily from the matrix of sampled lead potentials. The timing of its peak reveals the mean of the repolarization times of the involved transmembrane potentials. The amplitude of the peak is the maximum downward slope of the transmembrane potential. This amplitude is independent of the volume conductor effects of the tissues surrounding the heart. The estimate of the dominant T wave retains this property. Conclusion: The dominant T wave reflects the derivative of the recovery phase of a generalized transmembrane potential. Its amplitude is independent of the volume conductor properties of the tissues surrounding the heart. This is a unique feature that greatly facilitates the interpretation and application of the other signal features of the dominant T wave. (J Cardiovasc Electrophysiol, Vol. 14, pp. S180‐S187, October 2003, Suppl.)
Timing of Depolarization and Contraction in the Paced Canine Left Ventricle:
Authors: KERCKHOFFS ROY C.P. , FARIS OWEN P. , BOVENDEERD PETER H.M. , PRINZEN FRITS W. , SMITS KAREL , McVEIGH ELLIOT R. , ARTS THEO 
Published: October 2003

Introduction: For efficient pump function, contraction of the heart should be as synchronous as possible. Ventricular pacing induces asynchrony of depolarization and contraction. The degree of asynchrony depends on the position of the pacing electrode. The aim of this study was to extend an existing numerical model of electromechanics in the left ventricle (LV) to the application of ventricular pacing. With the model, the relation between pacing site and patterns of depolarization and contraction was investigated. Methods and Results: The LV was approximated by a thick‐walled ellipsoid with a realistic myofiber orientation. Propagation of the depolarization wave was described by the eikonal‐diffusion equation, in which five parameters play a role: myocardial and subendocardial velocity of wave propagation along the myofiber cm and ce; myocardial and subendocardial anisotropy am and ae; and parameter k, describing the influence of wave curvature on wave velocity. Parameters cm, ae, and k were taken from literature. Parameters am and ce were estimated by fitting the model to experimental data, obtained by pacing the canine left ventricular free wall (LVFW). The best fit was found with cm= 0.75 m/s, ce= 1.3 m/s, am= 2.5, ae= 1.5, and k= 2.1 × 10−4 m2/s. With these parameter settings, for right ventricular apex (RVA) pacing, the depolarization times were realistically simulated as also shown by the wavefronts and the time needed to activate the LVFW. The moment of depolarization was used to initiate myofiber contraction in a model of LV mechanics. For both pacing situations, mid‐wall circumferential strains and onset of myofiber shortening were obtained. Conclusion: With a relatively simple model setup, simulated depolarization timing patterns agreed with measurements for pacing at the LVFW and RVA in an LV. Myocardial cross‐fiber wave velocity is estimated to be 0.40 times the velocity along the myofiber direction (0.75 m/s). Subendocardial wave velocity is about 1.7 times faster than in the rest of the myocardium, but about 3 times slower than as found in Purkinje fibers. Furthermore, model and experiment agreed in the following respects. (1) Ventricular pacing decreased both systolic pressure and ejection fraction relative to natural sinus rhythm. (2) In early depolarized regions, early shortening was observed in the isovolumic contraction phase; in late depolarized regions, myofibers were stretched in this phase. Maps showing timing of onset of shortening were similar to previously measured maps in which wave velocity of contraction appeared similar to that of depolarization. (J Cardiovasc Electrophysiol, Vol. 14, pp. S188‐S195, October 2003, Suppl.)
Relationship Between Regional Shortening and Asynchronous Electrical Activation in a Three‐Dimensional Model of Ventricular Electromechanics
Authors: USYK TARAS P. , McCULLOCH ANDREW D. 
Published: October 2003

Introduction: Asynchronous electrical activation can cause abnormalities in perfusion and pump function. An electromechanical model was used to investigate the mechanical effects of altered cardiac activation sequence. Methods and Results: We used an anatomically detailed three‐dimensional computational model of the canine ventricular walls to investigate the relationship between regional electrical activation and the timing of fiber shortening during normal and ventricular paced beats. By including a simplified Purkinje fiber network and anisotropic impulse conduction in the model, computed electrical activation sequences were consistent with experimentally observed patterns. Asynchronous time courses of regional strains during beats stimulated from the left or right ventricular epicardium showed good agreement with published experimental measurements in dogs using magnetic resonance imaging tagging methods. When electrical depolarization in the model was coupled to the onset of local contractile tension development by a constant time delay of 8 msec, the mean delay from depolarization to the onset of systolic fiber shortening was 14 msec. However, the delay between the onset of fiber tension and initial shortening varied significantly; it was as late as 60 msec in some regions but was also as early as −50 msec (i.e., 42 msec before depolarization) in other regions, particularly the interventricular septum during free‐wall pacing. Conclusion: The large variation in delay times was attributable to several factors including local anatomic variations, the location of the site relative to the activation wavefront, and regional end‐diastolic strain. Therefore, we conclude that these factors, which are intrinsic to three‐dimensional ventricular function, make the regional sequence of fiber shortening an unreliable surrogate for regional depolarization or electromechanical activation in the intact ventricles. (J Cardiovasc Electrophysiol, Vol. 14, pp. S196‐S202, October 2003, Suppl.)
Altered T Wave Dynamics in a Contracting Cardiac Model
Authors: SMITH NICOLAS P. , BUIST MARTIN L. , PULLAN ANDREW J. 
Published: October 2003

Introduction: The implications of mechanical deformation on calculated body surface potentials are investigated using a coupled biophysically based model. Methods and Results: A cellular model of cardiac excitation‐contraction is embedded in an anatomically accurate two‐dimensional transverse cross‐section of the cardiac ventricles and human torso. Waves of activation and contraction are induced by the application of physiologically realistic boundary conditions and solving the bidomain and finite deformation equations. Body surface potentials are calculated from these activation profiles by solving Laplace's equation in the passive surrounding tissues. The effect of cardiac deformation on electrical activity, induced by contraction, is demonstrated in both single‐cell and tissue models. Action potential duration is reduced by 7 msec when the single cell model is subjected to a 10% contraction ramp applied over 400 msec. In the coupled electromechanical tissue model, the T wave of the ECG is shown to occur 18 msec earlier compared to an uncoupled excitation model. To assess the relative effects of myocardial deformation on the ECG, the activation sequence and tissue deformation are separated. The coupled and uncoupled activation sequences are mapped onto the undeforming and deforming meshes, respectively. ECGs are calculated for both mappings. Conclusion: Adding mechanical contraction to a mathematical model of the heart has been shown to shift the T wave on the ECG to the left. Although deformation of the myocardium resulting from contraction reduces the T wave amplitude, cell stretch producing altered cell membrane kinetics is the major component of this temporal shift. (J Cardiovasc Electrophysiol, Vol. 14, pp. S203‐S209, October 2003, Suppl.)
Quantitative Reconstruction of Cardiac Electromechanics in Human Myocardium:
Authors: SACHSE FRANK B. , SEEMANN GUNNAR , CHAISAOWONG KRAISORN , WEIß DANIEL 
Published: October 2003

Introduction:Myocytes from normal and failing myocardium show significant differences in electromechanical behavior. Mathematical modeling of the behavior provides insights into the underlying physiologic and pathophysiologic mechanisms. Electromechanical models of cardiomyocytes exist for various species, but models of human myocytes are lacking.Methods and Results:A mathematical model of electromechanics in normal and failing cardiac myocytes in humans was created by assembly and adaptation of parameters of an electrophysiologic model at the level of single cells and a force development model at the level of the sarcomere. The adaptation was performed using data from recent studies of ventricular myocytes and myocardium. The model was applied to quantitatively reconstruct measurement data from different experimental studies of normal and failing myocardium. Several simulations were performed to quantify the transmembrane voltageVm, intracellular concentration of calcium[Ca2+]i, the [Ca2+]i–force relationship, and force transients. Furthermore, frequency dependencies and restitution of action voltage duration to 90% recovery APD90, peak [Ca2+]i, duration to 50% force recovery FD50, and peak force were determined.Conclusion:The presented mathematical model was capable of quantitatively reconstructing data obtained from different studies of electrophysiology and force development in normal and failing myocardium of humans. In future work, the model can serve as a component for studying macroscopic mechanisms of excitation propagation, metabolism, and electromechanics in human myocardium.(J Cardiovasc Electrophysiol, Vol. 14, pp. S210‐S218, October 2003, Suppl.)
Quantitative Reconstruction of Cardiac Electromechanics in Human Myocardium:
Authors: SEEMANN GUNNAR , SACHSE FRANK B. , WEIß DANIEL L. , DÖSSEL OLAF 
Published: October 2003

Introduction: Regional heterogeneity of electrophysiologic properties within the human ventricles is based on changes in ion channel kinetics and density inside the wall. The heterogeneity not only influences the electrophysiologic properties but also cellular force development. In this study, the influence of heterogeneity was investigated using mathematical models. Methods and Results: An overview of measurements of the heterogeneity of electrophysiology and force development is presented. This knowledge is transferred to an electromechanical heart model composed of a human ionic cell model describing electrophysiologic properties and a model for the development of forces. Heterogeneity is included in the ionic model by changing ion channel kinetics and density. The characteristics and dependencies of the electromechanical model are demonstrated in a single‐cell environment and a multicell environment. In the single‐cell environment, the effects of heterogeneity on electrical activity are demonstrated. The notch in the action potential decreases from epicardium to endocardium, and action potential duration is longest in the mid‐myocardium. The developed forces are largest in the subendocardial cells and decrease continuously toward the epicardium. The multicell environment describes a transmural line of cells in the left ventricular free wall using a bidomain approach. The transmural ECG shows typical characteristics with a positive monophasic T wave. Conclusions: This work demonstrates the need to incorporate regional heterogeneity in order to model human cardiac electromechanics. The results of electrophysiologic simulations correspond to measured data. The dependencies of regional heterogeneity on force development need to be validated in experiments, because little is known about the influence of heterogeneity on electromechanical coupling. (J Cardiovasc Electrophysiol, Vol. 14, pp. S219‐S228, October 2003, Suppl.)
Spontaneous Initiation and Termination of Complex Rhythms in Cardiac Cell Culture
Authors: BUB GIL , TATENO KATSUMI , SHRIER ALVIN , GLASS LEON 
Published: October 2003

Introduction: Complex cardiac arrhythmias often start and stop spontaneously. These poorly understood behaviors frequently are associated with pathologic modification of the structural heterogeneity and functional connectivity of the myocardium. To evaluate underlying mechanisms, we modify heterogeneity by varying the confluence of embryonic chick monolayer cultures that display complex bursting behaviors. A simple mathematical model was developed that reproduces the experimental behaviors and reveals possible generic mechanisms for bursting dynamics in heterogeneous excitable systems. Methods and Results: Wave propagation was mapped in embryonic chick myocytes monolayers using calcium‐sensitive dyes. Monolayer confluence was varied by plating cultures with different cell densities and by varying times in culture. At high plating densities, waves propagate without breaks, whereas monolayers plated at low densities display spirals with frequent breaks and irregular activation fronts. Monolayers at intermediate densities display bursting rhythms in which there is paroxysmal starting and stopping of spiral waves of activity. Similar spatiotemporal patterns of activity were also observed as a function of the time in culture; irregular activity dominates the first 30 hours, followed by repetitive bursting dynamics until 54 hours, after which periodic target patterns or stable spirals prevail. In some quiescent cultures derived from older embryos, it was possible to trigger pacemaker activity following a single activation. We are able to reproduce all of these behaviors by introducing spatial heterogeneity and varying neighborhood size, equivalent to cell connectivity, in a spontaneous cellular automaton model containing a rate‐dependent fatigue term. Conclusion: We observe transitions from irregular propagating waves, to spiral waves that spontaneously start and stop, to target waves originating from localized pacemakers in cell culture and a simple theoretical model of heterogeneous excitable media. The results show how physiologic properties of spontaneous activity, heterogeneity, and fatigue can give rise to a wide range of different complex dynamic behaviors similar to clinically observed cardiac arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. S229‐S236, October 2003, Suppl.)
Effects of Lidocaine on Shock‐Induced Vulnerability
Authors: LI LI , NIKOLSKI VLADIMIR , EFIMOV IGOR R. 
Published: October 2003

Introduction: Lidocaine is known to increase the defibrillation threshold (DFT) of monophasic shocks (MS) and have no effect on DFT of biphasic shocks (BS). The aim of this study was to enhance our understanding of the mechanisms of vulnerability and defibrillation through the investigation of this difference. Methods and Results: We studied the effect of 15 μM lidocaine on shock‐induced vulnerability using fluorescent imaging of Langendorff‐perfused rabbit hearts. Vulnerability was assessed as vulnerable window with shock strengths of 15 to 150 V and vulnerable period (VP) with shock delivery phase of 0% to 100% of action potential duration (% APD). With MS, lidocaine caused a significant increase in both the upper limit of vulnerability (ULV, 71 ± 17 V vs 120 ± 1.5 V, P < 0.01) and upper limit of VP (91 ± 8.0% APD vs 110 ± 4.2% APD, P < 0.01). With BS, lidocaine had no effect on ULV (40 ± 3.4 V vs 45 ± 4.5 V) and did not increase the upper limit of VP (78 ± 8.9% APD vs 96 ± 12% APD, P < 0.01). Lidocaine caused reduction of the conduction velocity during pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, P < 0.01), shock‐induced break excitation (0.82 ± 0.17 m/s vs 0.30 ± 0.07 m/s, P < 0.01), and postshock reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, P < 0.01). Lidocaine had no effect on shock‐induced virtual electrode polarization. Conclusion: Lidocaine increased MS ULV due to slowing of shock‐induced break‐excitation wavefronts, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no effect on BS ULV because no break excitation was induced by BS. Reduction of conduction velocity by lidocaine resulted in increased dispersion of repolarization and led to upper limit of VP increase for both MS and BS. (J Cardiovasc Electrophysiol, Vol. 14, pp. S237‐S248, October 2003, Suppl.)
Postshock Arrhythmogenesis in a Slice of the Canine Heart
Authors: HILLEBRENNER MATTHEW G. , EASON JAMES C. , CAMPBELL CRAIG A. , TRAYANOVA NATALIA A. 
Published: October 2003

Introduction: Recent evidence has demonstrated that defibrillation shocks terminate or reset reentrant activity in the myocardium through the generation of virtual electrode polarization (VEP). Previous research has revealed that the shock establishes phase singularities (PSs) in the tissue via the VEP mechanism. The aim of this study was to examine, as a function of shock strength and electrode configuration, the relationship between end‐shock PSs and the reentrant circuits established after failed defibrillation attempts. Methods and Results: The study uses a complex three‐dimensional finite‐element bidomain model of a slice of the canine heart characterized by realistic geometry and fiber architecture and undergoing a single scroll wave. Defibrillation shocks of increasing strength are delivered through three different electrode configurations. The results demonstrated that >98% of all PSs have a lifetime of half a reentrant cycle or less. Stronger shocks result in a faster rate of annihilation of postshock PSs. For failed shocks, the surviving PSs underlie the activity of one or more scroll waves, which remain stationary in the slice. For all electrode configurations tested, the increase in shock strength leads to a rapid initial increase in the number of postshock reentries followed by a slower decrease; similar behavior is observed with regard to end‐shock PSs. Conclusion: These results present new evidence regarding the mechanisms underlying failure of defibrillation shocks. (J Cardiovasc Electrophysiol, Vol. 14, pp. S249‐S256, October 2003, Suppl.)
Delayed Success in Termination of Three‐Dimensional Reentry:
Authors: ZEMLIN CHRISTIAN , MIRONOV SERGEY , PERTSOV ARKADY 
Published: October 2003

Introduction: Defibrillation shocks slightly stronger than cardioversion threshold may defibrillate not immediately but after a transient period of postshock activity (delayed success). The effect of a defibrillation shock is that it polarizes the tissue, primarily at the surfaces; therefore, surface polarization may play an important role at near‐threshold shock intensities. Methods and Results: We numerically investigate the effect of a monophasic transmural electrical shock on a three‐dimensional (3D) reentrant wave (scroll wave). For simplicity, we assume uniform polarization of the epicardial and endocardial surfaces. We demonstrate that the effect of surface polarization alone is sufficient to induce delayed termination of self‐sustained activity (3–4 beats after the shock). In agreement with experimental observations, both successful and failed shocks cause prolongation of the action potentials on the depolarized side and shortening on the hyperpolarized side, while at the same time inducing a shift from a reentrant to a focal activation pattern. Our simulations suggest that the outcome of the shock is determined by its effect on the shape of the scroll wave's center of rotation (filament). We propose a simple rule to predict the postshock filament shape that allows us to make accurate predictions of success and failure of a termination attempt. Conclusion: Surface polarization due to an electrical shock can terminate a reentrant scroll wave. This mechanism may explain the phenomenon of delayed success in defibrillation. (J Cardiovasc Electrophysiol, Vol. 14, pp. S257‐S263, October 2003, Suppl.)
Propagation of tomato spotted wilt virus in Frankliniella occidentalis does neither result in pathological effects nor in transovarial passage of the virus
Authors: Wijkamp Ineke , Goldbach Rob , Peters Dick 
Published: October 2003

AbstractThe effect of tomato spotted wilt virus (TSWV) on Frankliniella occidentalis Pergande (Thysanoptera; Thripidae) following a 6‐hour acquisition access period on infected plants was investigated. No statistically significant differences were observed among viruliferous, non‐viruliferous and control thrips with respect to developmental time, reproduction rate and survival. Thrips larvae, exposed or non‐exposed to TSWV, developed from egg to adult in 13.1 and 13.2 days, respectively. Exposed females produced an average of 28.3 larvae whereas control thrips produced 22.3 larvae and longevity was 13.4 and 12.5 days, respectively. None of these values were significantly different. Population reproductive statistics, net reproductive rate (R0), mean generation time (T) and intrinsic rate of increase (rm) were calculated from the life fertility tables. R0 and rm were higher for viruliferous thrips as compared to non‐viruliferous and non‐exposed thrips. Virus transmission studies revealed that viruliferous thrips were able to transmit virus until death and that TSWV was not transovarially transmitted.
Evidence that mass trapping suppresses pink bollworm populations in cotton fields
Authors: Mafra‐Neto Agenor , Habib Mohamed 
Published: October 2003

AbstractMass trapping was used to control pink bollworm (PBW), Pectinophora gossypiella (Saunders) (Lepidoptera: Gelechiidae), populations in cotton fields in Brazil. Oil traps containing lures with a high dose of pheromone, installed at a density of 20 traps per ha soon after the occurrence of the first cotton fruits (or bolls), suppressed PBW populations below detection levels using Delta traps and manual examination of 100 green cotton bolls per ha. Pheromone sources of 0.2 g (approximately 150 NoMate® fibers) were effective in attracting PBW male moths to oil traps for at least three weeks. Trap captures showed that PBW males located the high concentration pheromone plumes, oriented upwind, and landed on or inside the traps. The long life of the pheromone sources and the long lasting viscosity of the oil surface ensured low trap maintenance, thus rendering mass trapping viable as an alternative technique for the control of P. gossypiella populations in commercial cotton fields. We discuss probable mechanisms promoting suppression of PBW populations in fields with mass trapping control.