QRS complex waveform indicators of ventricular activation slowing: Simulation studies.

Diffuse or regional activation slowing in ventricular myocardium can result from different cardiac pathologies, such as left ventricular hypertrophy, ischemia or fibrosis. Altered ventricular activation sequence leads to deformations of the activation front and consequently to the changes in the QRS complex. Using a computer model we simulated the effect of slowed ventricular activation on the QRS waveform with a special interest in ECG changes which reproduce the ECG criteria of left ventricular hypertrophy (ECG-LVH).

The effect of conduction velocity slowing in left ventricular midwall on the QRS complex morphology: A simulation study.

Unlabelled: Midwall fibrosis is a frequent finding in different types of left ventricular hypertrophy. Fibrosis presents a local conduction block that can create a substrate for ventricular arrhythmias and lead to the continuous generation of reentry. Having also impact on the sequence of ventricular activation it can modify the shape of QRS complex.

Imaging QRS complex and ST segment in myocardial infarction.

Background: Acute myocardial infarction creates regions of altered electrical properties of myocardium resulting in typical QRS patterns (pathological Q waves) and ST segment deviations observed in leads related to the MI location. The aim of this study was to present a graphical method for imaging the changes in the sequence of depolarization and the ST segment deviations in myocardial infarction using the Dipolar ElectroCARdioTOpography (DECARTO) method.

Material And Methods: Simulated ECG data corresponding to intramural, electrically inactive areas encircled by transmural areas with slowed impulse propagation velocity in anteroseptal and inferior locations were used for imaging the altered sequence of depolarization and the ST vector.

QRS complex and ST segment manifestations of ventricular ischemia: the effect of regional slowing of ventricular activation.

Objective: Reduction or interruption of the blood supply to myocardium due to occlusion of coronary artery and consequent ischemia leads to changes of electrogenesis: changes in morphology and duration of action potentials and slowing of conduction velocity in the affected area. In this study we simulated the effects of localized changes in depolarization sequence on the QRS and ST segment patterns, using computer modeling.

Methods: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows changing the velocity of impulse propagation in the myocardium.

Computer simulation of ECG manifestations of left ventricular electrical remodeling.

An increased QRS voltage is considered to be specific for the electrocardiogram (ECG) diagnosis of left ventricular hypertrophy (LVH). However, the QRS-complex patterns in patients with LVH cover a broader spectrum: increased QRS voltage, prolonged QRS duration, left axis deviation, and left anterior fascicular block- and left bundle branch block-like patterns, as well as pseudo-normal QRS patterns. The classical interpretation of the QRS patterns in LVH relates these changes to increased left ventricular mass (LVM) per se, while tending to neglect the modified active and passive electrical properties of the myocardium.

Electrocardiographic patterns of left bundle-branch block caused by intraventricular conduction impairment in working myocardium: a model study.

Unlabelled: By definition, the electrocardiographic (ECG) patterns of left bundle-branch block (LBBB) represent distinctive changes in duration and shape of the QRS complex caused by intraventricular conduction delay in the left ventricle (LV) due to structural abnormalities in the His-Purkinje conduction system and/or ventricular myocardium. However, impaired conduction in the working myocardium is not taken into consideration in the practical ECG diagnosis. Because the degree of LV myocardium impairment could be of importance for clinical evaluation of patients, we studied the effects of blocked and of delayed onsets of activation in the LV to simulate complete and incomplete LBBBs and slowed conduction in the LV myocardium by applying an analytical computer model.

Secondary and primary repolarization changes in left ventricular hypertrophy: a model study.

The contributions of reduced conduction velocity (CV) and prolonged action potential duration (APD) to QT interval prolongation and T wave and T vector loop morphology in left ventricular hypertrophy (LVH) were studied using an analytical computer model. Three types of anatomic LVH were simulated: concentric and eccentric hypertrophy, and left ventricular dilatation. In each LVH type, depolarization changes were simulated by CV slowing and primary repolarization changes by APD prolongation.

Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study.

Unlabelled: The increased QRS voltage is considered to be a specific electrocardiogram (ECG) sign of left ventricular hypertrophy (LVH), and it is expected that the QRS voltage reflects the increase in left ventricular mass (LVM). However, the increased QRS voltage is only one of QRS patterns observed in patients with LVH. According to the solid angle theory, the resultant QRS voltage is influenced not only by spatial (anatomic) but also by nonspatial (electrophysiologic) determinants.

Computer model study of electrocardiologic manifestations in asymmetric left ventricular hypertrophy.

Electrocardiologic criteria of left ventricular enlargement do not take into consideration the eventuality of asymmetric hypertrophy. Since experimental techniques for production of this condition are not available, computer modeling was utilized to study its electrocardiologic manifestations. A computer model of human ventricles with analytically defined geometry, consisting of 142,000 elements (1.

Effect of different sources of ventricular repolarization heterogeneity on the resultant cardiac vectors. A model study.

The computer model of ventricular activation was used to study the effects of eventual differences in the repolarization pattern between the right and the left ventricle, as well as between the apical and the basal parts of the ventricles. All changes in model action potential durations (APDs) were performed in the range corresponding to the APD variability measured in myocytes. The vectorcar-diographical spatial T loop was very sensitive on the changes in the right to left ventricular gradient of APD, while the similar changes in the apico-basal gradient of APD influenced the T loop minimally.