Corrected body surface potential mapping.

In the method for body surface potential mapping described here, the influence of thorax shape on measured ECG values is corrected. The distances of the ECG electrodes from the electrical heart midpoint are determined using a special device for ECG recording. These distances are used to correct the ECG values as if they had been measured on the surface of a sphere with a radius of 10 cm with its midpoint localized at the electrical heart midpoint. The equipotential lines of the electrical heart field are represented on the virtual surface of such a sphere. It is demonstrated that the character of a dipole field is better represented if the influence of the thorax shape is reduced. The site of the virtual reference electrode is also important for the dipole character of the representation of the electrical heart field.     

Relationship of the maximum QRS vector with the left ventricular myocardial mass during the development of hypertrophy: Computer simulation and empirical data

A model of electrical activity of the heart has been used to demonstrate that, all other conditions remaining the same, the spatial vector of the heart changes, as a first approximation, proportionally to the increase in the surface area of the heart ventricles (rather than the myocardial mass) during proportional homothetic changes in the sizes of the heart and His-Purkinje system. In contrast, the electrocardiosignal (ECS) amplitude is determined, at any given moment, by the area of depolarized regions of the epicardium and endocardium, which agrees with the model of a double electrical layer on the surface of an electrically active myocardium.     

Effects of cleistanthins A and B on blood pressure and electrocardiogram in Wistar rats

We have studied the effects of cleistanthin A and cleistanthin B, phytoconstituents isolated from the leaves of Cleistanthus collinus Roxb. (Euphorbiaceae), on blood pressure, electrocardiogram, and barium chloride-induced arrhythmia in Wistar rats. The two compounds were isolated by column chromatography and their identity was confirmed spectroscopically. A healthy, male Wistar rat was used to record the invasive blood pressure and electrocardiograph. The antiarrhythmic effects of cleistanthins A and B were studied using the barium chloride model. Both cleistanthin A and cleistanthin B showed a dose-dependent hypotensive effect. Both compounds reduced the mean blood pressure significantly although the dose required for the effect was higher in the case of cleistanthin B. In the electrocardiogram, cleistanthins A and B significantly altered the electrical activity of the heart, the changes were transient and of no further consequence. Intravenous injection of 64 microg or more of cleistanthins A and B caused a sudden respiratory depression without affecting the electrocardiogram. Cleistanthins A and B did not display any antiarrhythmic effect against barium chloride-induced arrhythmia. In conclusion, both cleistanthin A and cleistanthin B exert a hypotensive effect and have no antiarrhythmic effect against barium chloride-induced arrhythmia in Wistar rats.     

Measurement of the electric field of the heart in a homogeneous volume conductor]

The paper describes a technique and some results of experimental measurements of electrical potentials generated by an isolated dog heart in homogeneous conductor, drawing equipotential maps of the field, and calculating the characteristics of the dipole equivalent generator of the heart. The form of potential distribution on a spherical surface around the heart and its ideal orthogonal vectorcardiograms are discussed.     

Physically corrected orthogonal electrocardiographic lead systems in macaques and baboons

The adequacy of various physically corrected electrocardiographic lead systems for lower primates was compared with the aid of physical models of the cardiac electrical field. Electrolytic tanks fashioned from plaster casts of the thorax of young adult male and female macaques and baboons were used. A dipole source situated at different points in the heart region simulated the electrical activity of the heart. Statistical evaluation and reciprocal comparison of the resultant parameters showed that the proposed modification of the McFee-Parungao lead system for macaques and baboons was most satisfactory, followed by the human variant of the same lead system and then by the variant for dogs. The greatest variability was displayed by parameters determined from measurements made with Frank's lead system, which was ranked last in the evaluation.     

A model of heart ventricles for electrocardiographic evaluation of the state of the myocardium

A mathematical model of heart excitation processes has been developed for describing an electrocardiogram. A verified archive of model electrocardiograms has been created with the use of the model. The model has been used to study how electrocardiograms are affected by individual variability in ventricle shape and heart position in the norm, in myocardial infarction of different localizations, and in ventricular hypertrophy. Correspondence of the specific features of real and model electrocardiograms is discussed.     

A Mathematical-Physical Model of the Genesis of the Electrocardiogram

A fundamental problem of cardiac electrophysiology is that of relating quantitatively the electrical activity within the heart to the complete timevarying potential distribution at the body surface. A new numerical method is described for the calculation of the surface potential on an irregularly shaped closed external surface due to an arbitrary source distribution in a medium containing regions of different conductivity, subject to the appropriate boundary conditions. The method is intended to provide an exact theoretical analysis of the experimental data acquired by A. M. Scher and others who have been mapping the pathways of ventricular depolarization in dogs and other animals. In anticipation of the above research program, a number of exploratory computations are reported. For example, the surface potential distribution has been calculated for a cylinder of human torso cross-section with a hemispherical dipole layer current source in approximate heart position and orientation and containing “lungs” of conductivity different from that of the surrounding medium. Under certain conditions, when lung-like inhomogeneities are introduced, a simple dipole source can generate a potential distribution having the multiple maxima and minima characteristic of higher multipole sources.     

Measurements of transmembrane potential and magnetic field at the apex of the heart

We studied the transmembrane potential and magnetic fields from electrical activity at the apex of the isolated rabbit heart experimentally using optical mapping and superconducting quantum interference device microscopy, and theoretically using monodomain and bidomain models. The cardiac apex has a complex spiral fiber architecture that plays an important role in the development and propagation of action currents during stimulation at the apex. This spiral fiber orientation contains both radial electric currents that contribute to the electrocardiogram and electrically silent circular currents that cannot be detected by the electrocardiogram but are detectable by their magnetic field, B_z. In our experiments, the transmembrane potential, V_m, was first measured optically and then B_z was measured with a superconducting quantum interference device microscope. Based on a simple model of the spiral structure of the apex, V_m was expected to exhibit circular wave front patterns and B_z to reflect the circular component of the action currents. Although the circular V_m wave fronts were detected, the B_z maps were not as simple as expected. However, we observed a pattern consistent with a tilted axis for the apex spiral fiber geometry. We were able to simulate similar patterns in both a monodomain model of a tilted stack of rings of dipole current and a bidomain model of a tilted stack of spiraled cardiac tissue that was stimulated at the apex. The fact that the spatial pattern of the magnetic data was more complex than the simple circles observed for V_m suggests that the magnetic data contain information that cannot be found electrically.     

24 h动态心电图对冠心病心律失常的临床监测价值

目的:研究24 h动态心电图对冠心病心律失常的临床监测价值。方法:对2014年7月至2015年7月在我院确诊的315例冠心病患者先后实施常规心电图及24 h动态心电图检测。对比两种检测方法对对冠心病的阳性检出结果,并调查患者对不同检测方式的评价情况。结果:24 h动态心电图的冠心病阳性检出率为81.90%,与常规心电图的76.51%相比,差异无统计学意义(P0.05)。24 h动态心电图室性二、三联律,室性早搏成对,房性早搏早发,房性早搏二、三联律,房性早搏成对,以及短阵室上速的检出率均较常规心电图明显更高,差异均有统计学意义(均P0.05)。患者对24 h动态心电图的准确性认可度高于常规心电图,差异有统计学意义(P0.05)。结论:24 h动态心电图对冠心病心律失常患者的监测价值较好,能够更加准确地呈现患者的心功能状态,值得推广。     

Effect of choice of baseline correction interval on localization of electrical heart activity]

The electric heart activity can be localised from body surface mapping data with computer algorithms. At higher heart rates the T and P waves merge. Thus, the offset can not be subtracted in the TP segment. We investigated 28 healthy volunteers with signal averaged 31-lead magnetocardiography. The offset of the baseline was determined in the TP-segment and in the PR-segment, respectively. The electrical heart activity was localised in the initial 30 ms of the QRS complex (Q), at the QRS maximum (R), and at the T wave maximum (T). The volume currents were considered by using a boundary element model with the compartments lungs and torso. The 3D positions of the dipoles, the dipole orientations, and the dipole strengths were calculated using the data preprocessed with two different offset correction intervals. The offsets of the TP and PR segments significantly differed one from another. The average deviations of the dipole localisation were within a few centimetres (Q: 20 +/- 31 mm, R: 6 +/- 13 mm, T: 14 +/- 30 mm). However, in a small number of subjects (Q: n = 5, R: n = 2, T: n = 5) we observed a deviation of more than 30 mm. These deviations were not linearly correlated to the differences in the baseline offsets. High resolution recordings continuously detect heart activity in the PR segment. The correction of the baseline in the PR segment instead of the TP segment may introduce artefacts in the source localisation and therefore should be avoided.     

Effects of gastrointestinal tissue structure on computed dipole vectors

Background  

Digestive diseases are difficult to assess without using invasive measurements. Non-invasive measurements of body surface electrical and magnetic activity resulting from underlying gastro-intestinal activity are not widely used, in large due to their difficulty in interpretation. Mathematical modelling of the underlying processes may help provide additional information. When modelling myoelectrical activity, it is common for the electrical field to be represented by equivalent dipole sources. The gastrointestinal system is comprised of alternating layers of smooth muscle (SM) cells and Interstitial Cells of Cajal (ICC). In addition the small intestine has regions of high curvature as the intestine bends back upon itself. To eventually use modelling diagnostically, we must improve our understanding of the effect that intestinal structure has on dipole vector behaviour.     

Predicting the cardiac toxicity of drugs using a novel multiscale exposure–response simulator

A common but serious side effect of many drugs is torsades de pointes, a rhythm disorder that can have fatal consequences. Torsadogenic risk has traditionally been associated with blockage of a specific potassium channel and an increased recovery period in the electrocardiogram. However, the mechanisms that trigger torsades de pointes remain incompletely understood. Here we establish a computational model to explore how drug-induced effects propagate from the single channel, via the single cell, to the whole heart level. Our mechanistic exposure–response simulator translates block-concentration characteristics for arbitrary drugs into three-dimensional excitation profiles and electrocardiogram recordings to rapidly assess torsadogenic risk. For the drug of dofetilide, we show that this risk is highly dose-dependent: at a concentration of 1x, QT prolongation is 55% but the heart maintains its regular sinus rhythm; at 5.7x, QT prolongation is 102% and the heart spontaneously transitions into torsades de points; at 30x, QT prolongation is 132% and the heart adapts a quasi-depolarized state with numerous rapidly flickering local excitations. Our simulations suggest that neither potassium channel blockage nor QT interval prolongation alone trigger torsades de pointes. The underlying mechanism predicted by our model is early afterdepolarization, which translates into pronounced U waves in the electrocardiogram, a signature that is correctly predicted by our model. Beyond the risk assessment of existing drugs, our exposure–response simulator can become a powerful tool to optimize the co-administration of drugs and, ultimately, guide the design of new drugs toward reducing life threatening drug-induced rhythm disorders in the heart.     

Noninvasive electrocardiographic imaging for cardiac electrophysiology and arrhythmia

Over 7 million people worldwide die annually from erratic heart rhythms (cardiac arrhythmias), and many more are disabled. Yet there is no imaging modality to identify patients at risk, provide accurate diagnosis and guide therapy. Standard diagnostic techniques such as the electrocardiogram (ECG) provide only low-resolution projections of cardiac electrical activity on the body surface. Here we demonstrate the successful application in humans of a new imaging modality called electrocardiographic imaging (ECGI), which noninvasively images cardiac electrical activity in the heart. In ECGI, a multielectrode vest records 224 body-surface electrocardiograms; electrical potentials, electrograms and isochrones are then reconstructed on the heart's surface using geometrical information from computed tomography (CT) and a mathematical algorithm. We provide examples of ECGI application during atrial and ventricular activation and ventricular repolarization in (i) normal heart (ii) heart with a conduction disorder (right bundle branch block) (iii) focal activation initiated by right or left ventricular pacing, and (iv) atrial flutter.     

Propagation of normal beats and re-entry in a computational model of ventricular cardiac tissue with regional differences in action potential shape and duration

There is substantial experimental evidence from studies using both intact tissue and isolated single cells to support the existence of different cell types within the ventricular wall of the heart, each possessing different electrical properties. However other studies have failed to find these differences, and instead support the idea that electrical coupling in vivo between regions with different cell types smoothes out differences in action potential shape and duration. In this study we have used a computational model of electrical activation in heterogenous 2D and 3D cardiac tissue to investigate the propagation of both normal beats and arrhythmias. We used the Luo–Rudy dynamic model for guinea pig ventricular cells, with simplified Ca²⁺ handling and transmural heterogeneity in I_Ks and I_to. With normal cell-to-cell coupling, a layer of M cells was not necessary for the formation of an upright T wave in the simulated electrocardiogram, and the amplitude and configuration of the T wave was not greatly affected by the thickness and configuration of the M cell layer. Transmural gradients in repolarisation pushed re-entrant waves with an intramural filament towards either the base or the apex of the ventricles, and caused transient break up of re-entry with a transmural filament.     

Theoretical analysis of the magnetocardiographic pattern for reentry wave propagation in a three-dimensional human heart model

We present a computational study of reentry wave propagation using electrophysiological models of human cardiac cells and the associated magnetic field map of a human heart. We examined the details of magnetic field variation and related physiological parameters for reentry waves in two-dimensional (2-D) human atrial tissue and a three-dimensional (3-D) human ventricle model. A 3-D mesh system representing the human ventricle was reconstructed from the surface geometry of a human heart. We used existing human cardiac cell models to simulate action potential (AP) propagation in atrial tissue and 3-D ventricular geometry, and a finite element method and the Galerkin approximation to discretize the 3-D domain spatially. The reentry wave was generated using an S1-S2 protocol. The calculations of the magnetic field pattern assumed a horizontally layered conductor for reentry wave propagation in the 3-D ventricle. We also compared the AP and magnetocardiograph (MCG) magnitudes during reentry wave propagation to those during normal wave propagation. The temporal changes in the reentry wave motion and magnetic field map patterns were also analyzed using two well-known MCG parameters: the current dipole direction and strength. The current vector in a reentry wave forms a rotating spiral. We delineated the magnetic field using the changes in the vector angle during a reentry wave, demonstrating that the MCG pattern can be helpful for theoretical analysis of reentry waves.     

A New Algorithm to Diagnose Atrial Ectopic Origin from Multi Lead ECG Systems - Insights from 3D Virtual Human Atria and Torso

Rapid atrial arrhythmias such as atrial fibrillation (AF) predispose to ventricular arrhythmias, sudden cardiac death and stroke. Identifying the origin of atrial ectopic activity from the electrocardiogram (ECG) can help to diagnose the early onset of AF in a cost-effective manner. The complex and rapid atrial electrical activity during AF makes it difficult to obtain detailed information on atrial activation using the standard 12-lead ECG alone. Compared to conventional 12-lead ECG, more detailed ECG lead configurations may provide further information about spatio-temporal dynamics of the body surface potential (BSP) during atrial excitation. We apply a recently developed 3D human atrial model to simulate electrical activity during normal sinus rhythm and ectopic pacing. The atrial model is placed into a newly developed torso model which considers the presence of the lungs, liver and spinal cord. A boundary element method is used to compute the BSP resulting from atrial excitation. Elements of the torso mesh corresponding to the locations of the placement of the electrodes in the standard 12-lead and a more detailed 64-lead ECG configuration were selected. The ectopic focal activity was simulated at various origins across all the different regions of the atria. Simulated BSP maps during normal atrial excitation (i.e. sinoatrial node excitation) were compared to those observed experimentally (obtained from the 64-lead ECG system), showing a strong agreement between the evolution in time of the simulated and experimental data in the P-wave morphology of the ECG and dipole evolution. An algorithm to obtain the location of the stimulus from a 64-lead ECG system was developed. The algorithm presented had a success rate of 93%, meaning that it correctly identified the origin of atrial focus in 75/80 simulations, and involved a general approach relevant to any multi-lead ECG system. This represents a significant improvement over previously developed algorithms.     

Electrophysiology of Heart Failure Using a Rabbit Model: From the Failing Myocyte to Ventricular Fibrillation

Heart failure is a leading cause of death, yet its underlying electrophysiological (EP) mechanisms are not well understood. In this study, we use a multiscale approach to analyze a model of heart failure and connect its results to features of the electrocardiogram (ECG). The heart failure model is derived by modifying a previously validated electrophysiology model for a healthy rabbit heart. Specifically, in accordance with the heart failure literature, we modified the cell EP by changing both membrane currents and calcium handling. At the tissue level, we modeled the increased gap junction lateralization and lower conduction velocity due to downregulation of Connexin 43. At the biventricular level, we reduced the apex-to-base and transmural gradients of action potential duration (APD). The failing cell model was first validated by reproducing the longer action potential, slower and lower calcium transient, and earlier alternans characteristic of heart failure EP. Subsequently, we compared the electrical wave propagation in one dimensional cables of healthy and failing cells. The validated cell model was then used to simulate the EP of heart failure in an anatomically accurate biventricular rabbit model. As pacing cycle length decreases, both the normal and failing heart develop T-wave alternans, but only the failing heart shows QRS alternans (although moderate) at rapid pacing. Moreover, T-wave alternans is significantly more pronounced in the failing heart. At rapid pacing, APD maps show areas of conduction block in the failing heart. Finally, accelerated pacing initiated wave reentry and breakup in the failing heart. Further, the onset of VF was not observed with an upregulation of SERCA, a potential drug therapy, using the same protocol. The changes introduced at the cell and tissue level have increased the failing heart’s susceptibility to dynamic instabilities and arrhythmias under rapid pacing. However, the observed increase in arrhythmogenic potential is not due to a steepening of the restitution curve (not present in our model), but rather to a novel blocking mechanism.     

Visualization of cardiac health using vector cardiogram

An electrocardiogram (ECG) is an electrical recording of the heart and is used in the investigation of heart disease. It displays an apparent periodicity (of about 60–100 bpm in a healthy adult), but is not exactly periodic. The symptoms of disease may show up only during certain periods of the day, and that too may occur at random in the time scale. Visual media is a most effective tool for communication, especially when the data has subtle variations. A novel visualization technique is presented to display each ECG beat. The features like PR interval, QRS width, ST interval, are extracted from the magnitude and phase plot of different lead combinations. These features are displayed on a Cartesian quadrant as different curves, with a menu driven display strategy to visualize the ECG for a chosen interval. The scheme employed can be used to identify different types of abnormalities.