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Updated: Aug 10, 2026
Patient-specific Modeling of the Heart: Estimation of Ventricular Fiber Orientations
Published on: January 8, 2013
Modeling and visualization of the activation wavefront propagation to improve understanding the QRS complex changes
Jana Svehlikova1, Jan Zelinka1, Ljuba Bacharova2
1Institute of Measurement Science SAS, Bratislava, Slovakia.
Insights
Reduced heart electrical propagation velocity significantly alters the heart vector, comparable to left ventricular hypertrophy. Conduction disturbances can increase ECG signal amplitudes, with severe QRS prolongation only at 25% velocity reduction or combined with hypertrophy.
Area of Science:
- Cardiac Electrophysiology
- Computational Cardiology
- Biomedical Engineering
Background:
- Left ventricular hypertrophy (LVH) and reduced activation velocity are key pathological conditions affecting cardiac function.
- Understanding their impact on the electrical activity of the heart is crucial for diagnosing and managing cardiac diseases.
Purpose of the Study:
- To compute and visualize activation wavefront propagation in a geometrical heart model under pathological conditions.
- To compare the effects of reduced propagation velocity and left ventricular hypertrophy on cardiac electrical parameters.
- To investigate the combined influence of these pathologies.
Main Methods:
- Development of a geometrical heart model incorporating pathological changes.
- Computation and visualization of activation wavefront propagation.
- Analysis of parameters from a multiple dipole equivalent heart generator.
- Comparison of results across different heart geometries and degrees of velocity reduction.
Main Results:
- Reduced propagation velocity caused significant changes in the heart vector magnitude, comparable to or exceeding those from LVH.
- Decreased velocity led to a longer presence of the wavefront during depolarization, increasing heart vector magnitude.
- Combined LVH and reduced velocity enhanced heart vector enlargement and prolonged depolarization duration.
- Intramyocardial conduction disturbances can alter ECG amplitudes similarly to LVH.
Conclusions:
- Reduced intramyocardial conduction velocity can significantly impact ECG signals, mimicking effects of LVH.
- The influence of reduced activation velocity on cardiac electrical parameters is greater than that of increased LV mass.
- Significant QRS complex prolongation is observed only with severe (25%) velocity reduction or in combination with LVH.
Abstract:
Activation wavefront propagation was computed and visualized in a geometrical heart model for pathological cases of reduced velocity of propagation, left ventricular hypertrophy and their combination. Selected parameters of a multiple dipole equivalent heart generator were computed and compared for three heart geometries and several degrees and extents of reduction of propagation velocity. First, the influence of geometrical changes modeling the left ventricular hypertrophy at reference propagation velocity was compared with reduction of the propagation velocity in the reference heart geometry. Reduced propagation velocity yielded similar or greater changes of the magnitude of the (electrical) heart vector representing the activation wavefront than the geometrical changes. Observations of the wavefront propagation with reduced velocity revealed longer presence of a large extent of the wavefront during depolarization which resulted in increased magnitude of the heart vector. The duration of depolarization was significantly prolonged only when the propagation velocity was decreased to 25% of its normal value. Changes of the direction of the maximal heart vector were dependent on the position of the region where the propagation velocity was reduced. Then the combination of the left ventricular hypertrophy and reduced propagation velocity was studied. Such combination enhanced the enlargement of the electrical heart vector and significantly prolonged the duration of depolarization. The influence of reduced activation velocity on the observed parameters was greater than the effect of the enlargement of the left ventricular mass. The presented study showed that intramyocardial conduction disturbances might cause increase of the actual surface area of propagation wavefront leading to changes of the amplitudes of ECG signals comparable with the changes resulting from the left ventricular hypertrophy. Intramyocardial conduction disturbances, as well as the modeled 50% increase of the thickness of the left ventricular wall, did not cause prolongation of the QRS complex out of normal range. Considerable prolongation of the QRS complex duration was observed only for transmural slowing of the propagation velocity to 25% of its reference value in large ventricular areas or for combination of such slowing with the left ventricular hypertrophy.
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