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Body surface potential maps (BSPM) from patients with coronary artery disease or no structural heart disease were analyzed with respect to their spatial features and QT/QTc dispersion in order to determine whether BSPM allows identification of patients with ventricular fibrillation. QRST integral maps and QT/QTc dispersion were acquired from simultaneous recordings of 62 ECG leads during sinus rhythm in patients with idiopathic ventricular fibrillation (n=13), ventricular fibrillation and coronary artery disease (n=22), coronary artery disease without ventricular fibrillation (n=21) and healthy controls (n=18). The Karhunen-Loeve transformation was applied to reduce the dimensionality of the data matrix of the QRST map to eight coefficients. Linear discriminant analysis allowed discrimination between idiopathic ventricular fibrillation patients and controls with high sensitivity (85%) and specificity (89%). However, discrimination between coronary artery disease patients with or without ventricular fibrillation was poor (68% and 67%, respectively). QTc dispersion calculated from BSPM was longer in idiopathic ventricular fibrillation patients than in controls (99+/-30 ms vs 70+/-14 ms, P=0.009) in contrast to QTc dispersion taken from 12-lead ECG (53+/-21 ms vs. 47+/-12 ms, P=n.s.). No significant difference was noted for coronary artery disease patients with or without ventricular fibrillation. In conclusion, repolarization disturbances detected by BSPM allow identification of ventricular fibrillation patients without structural heart disease. However, our results do not suggest a major impact of QT/QTc dispersion or QRST integral mapping for identification of ventricular fibrillation patients with coronary artery disease.

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In a retrospective analysis in 74 patients with coronary artery disease or no obvious heart disease, the value of "body surface potential mapping" for the identification of repolarization abnormalities was investigated compared to the standard 12-lead ECG. In patients with idiopathic ventricular fibrillation the number of extrema in the QRST integral map was significantly higher than in the control group (3.15+/-0.99 vs. 2.17+/-0.51, p<0.001) and the QT dispersion was also higher (0.10+/-0.03 vs. 0.07+/-0.01, p<0.001), whereas there was no difference between either group in the 12-lead ECG QT dispersion. In patients with coronary artery disease the number of extrema in the QRST integral map and QT dispersion were also higher compared to the control group, but there were no significant differences between patients with or without aborted sudden cardiac death.In conclusion, BSPM identifies repolarization abnormalities not detected by 12-lead ECG, thereby identifying a potential reason for cardiac arrest in patients without overt heart disease. The usefulness of this technique for risk stratification in patients with coronary artery disease remains to be elucidated.

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A computer simulation study is performed to investigate the method of current density reconstruction to localise myocardial ischaemia. A computer model of the entire human heart is used to simulate the excitation and repolarisation process in eight topographically different cases of myocardial ischaemia. The associated magnetocardiogram is calculated at 37 positions of the KRENIKON biomagnetic measurement equipment. The method of current density reconstruction is applied at the S-point (the last discernible deviation from the ST-segment at the end of the QRS-complex) of the MCG to find characteristics of the myocardial ischaemia simulated by the model. The results show that it is possible to determine the location of the ischaemia. The current density distribution may be interpreted physiologically in terms of the so-called 'injury-current'. This indicates that magnetocardiography might be a suitable method for noninvasive ischaemia diagnosis, and further investigations of the current density reconstruction method for the injury current should be performed on patients with ischaemic heart disease.

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The boundary element method was applied in order to investigate the localization accuracy for focal sources measured from MCG data. Various homogeneous volume conductor models were composed: the individually shaped torso, a scaled standard torso, an unscaled standard torso, a scaled cuboid and a scaled ellipsoid. We implemented these models in single-dipole inverse solution techniques. High resolution multichannel data were analysed from two patients showing ventricular extrasystoles and two patients suffering from Wolff-Parkinson-White syndrome. Moreover, we report the localization of shallow- and deep-lying catheters (depth 9 cm and depth 17.5 cm below the measurement grid). Using an individually shaped homogeneous torso yields a localization error of less than 3 cm even for the deepest sources (mean error 2.4 cm). Probability-based dipole localization shows that the remaining error could only partly be explained by data noise statistics. Therefore it seems to be due to either inner inhomogeneities or the inadequacy of the single current dipole or a combination of the two. Thus clinically useful localization accuracy in the millimetre range requires more sophisticated volume conductor and source models. The evaluation of measurement data and simulation study shows that a scaled cuboid model can provide nearly the same localization accuracy as the individually shaped torso model. Single dipole reconstruction with this model is computationally faster than that with the individually shaped model of the human body and is fast enough for use in clinical applications.

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The purpose of this study was to detect ventricular late fields recorded by a biomagnetic multichannel system in patients with ventricular late potential and to determine the site of these ventricular late fields non-invasively in three dimensions. Biomagnetic signals of sinus beats during a 5-min acquisition period simultaneously recorded by a 37-channel system Krenikon were averaged in all channels. Ventricular late fields were determined in each channel according to the algorithm of Simson for ECG data. For the localization process, baseline correction from the averaged non-filtered signals was performed at the end of the QRS complex under visual control. The single current dipole model within the homogeneous half-space was applied. Eight patients post myocardial infarction with ventricular late potentials (four with recurrent sustained ventricular tachycardia) and four healthy individuals were examined. In the normal subjects, no ventricular late fields were detected. However, ventricular late fields were found in all patients, and were localized in six patients within the border zone of myocardial infarction. In the four patients with ventricular tachycardia, a spatial coincidence of the site of origin of ventricular late fields and the site of origin of ventricular tachycardia determined by catheter mapping was found in two. It is concluded that magnetocardiography is able to detect ventricular late fields and can be used to determine their site of origin.

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A computer model of the entire human heart has been developed for simulation of the excitation and repolarization process. Spatial distribution of refractory periods and conduction velocities in the different cardiac tissues, the anisotropy of conduction in the ventricles, and the cycle length dependence of refractory periods and conduction velocities are taken into account. The algorithm calculating the activation process is based on a modified version of Huygen's principle for constructing wavefronts. This study presents simulations concerning the gap phenomenon of the conduction system and the initiation of tachycardias in a heart with Wolff-Parkinson-White syndrome. Results are compared for different basic cycle lengths and for normal and prolonged refractory periods in the His-Purkinje system. The gap phenomenon was found to be present only when using the prolonged refractory periods in the His-Purkinje-system at a cycle length of 700 ms. Induction of tachycardia by a single extrastimulus in the high right atrium in a heart with a bidirectionally conducting accessory pathway is possible by properly timed extrastimuli. The coupling interval of the stimulus for initiating a reentrant tachycardia depends on the cycle length, the conduction velocities and the set of refractory periods used. The same parameters determine whether or not a gap phenomenon in atrioventricular conduction occurs. The model may be useful for investigating similar questions concerning the reentry phenomena of tachycardia.

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A computer model is presented for simulation of the spread of activation and repolarization in ventricular myocardium. The program calculating the activation sequence is based on an algorithm similar to Huygen's principle of constructing wavefronts. Physiological parameters of the heart, such as areas of early activation on the endocardium, conduction velocity, anisotropy of propagation, duration of action potentials and refractory periods are taken into account. The time-course of ECG and MCG is calculated using the equations of the bidomain model. Simulation of pathologic cases of activation is performed through variation of the physiological heart parameters. The simulations presented here show good agreement of ECG and MCG with measurements in the normal case, the case of bundle branch block and abnormal repolarization. A special feature of the model is the possibility of simulating reentry rhythms following a premature stimulus in ventricular myocardium. Two kinds of reentry are simulated: reentry around an anatomical obstacle and the leading-circle model. The widespread capability for investigating not only ECG but also MCG and various kinds of pathologic activation patterns including reentry rhythms indicates that the model may be useful in studying numerous problems in cardiologic research.

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