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). This paper describes results of a set of computer modeling experiments and discusses visual QRS patterns. Slowed ventricular activation in the whole left ventricle resulted in the prolongation of QRS duration, leftward shift of electrical axis, and increase in the QRS amplitude mainly in the precordial leads, having thus their main impact on simulated Sokolow-Lyon index and Cornell voltage. Slowed ventricular activation in the anteroseptal region resulted in a leftward shift of the electrical axis and increased values of ECG-LVH criteria seen in limb leads or in a combination with precordial leads (Gubner criterion, Cornell voltage). Transmural slowing and midwall slowing in two layers in the anteroseptal area led also to the QRS duration prolongation. Changes in QRS complex were more pronounced in the cases of transmural slowing as compared to the left ventricular midwall slowing. Using computer modeling, we showed that slowed ventricular activation is a potent determinant of QRS complex morphology and can mimic ECG patterns that are usually interpreted as the effect of left ventricular hypertrophy, i.e., increased left ventricular mass. These results contribute to understanding the variety of ECG finding documented in patients with LVH, considering not only anatomical enlargement but also the altered electrical properties of hypertrophied myocardium.

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. In this study we simulated the effects of slowed conduction velocity in the midwall in the left ventricle and in its anteroseptal region on the QRS morphology using a computer model. MATERIAL AND METHODS: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids; the left ventricular wall is represented by five layers. The impulse propagation velocity was decreased by 50% in one and two midwall layers, respectively, in the whole left ventricle and in LV anterior region. The effects of slowed conduction velocity on the QRS complex of the 12-lead electrocardiogram are presented as 12-lead electrocardiograms and corresponding values of ECG criteria for left ventricular hypertrophy (ECG-LVH criteria): Gubner criterion, Sokolow-Lyon index (SLI) and Cornell voltage. RESULTS: All simulated situations led to increased R wave amplitude in the lead I and of S wave in the lead III, showing a leftward shift of the electrical axis and increased values of ECG-LVH criteria based on limb leads alone or in combination with precordial leads (Gubner criterion, Cornell voltage). The slowed conduction velocity in the whole LV influenced the QRS complex voltage in precordial leads, having an impact on the SLI and Cornell voltage. The changes were pronounced if two layers were involved. CONCLUSION: Using computer modeling we showed that the midwall slowing in conduction velocity modified the QRS complex morphology. The QRS complex changes were consistent with ECG-LVH criteria, i.e. QRS patterns usually interpreted as the effect of left ventricular hypertrophy (the increased left ventricular mass).

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. The ECGs were transformed to areas projected on the image surface so as to image the process of ventricular depolarization based on the orientation and magnitude of the instantaneous QRS vectors, and the estimated "myocardium at risk" based on the ST segment deviation. RESULTS: The images are presented as Mercator projections with the texture of anatomical segments of the heart and the corresponding coronary artery distribution. The changes in depolarization sequence were visible as dislocations of activated areas circumventing the affected areas, while the "myocardium at risk" estimated from the ST segment deviation pointed to the affected area. CONCLUSION: The presented method of imaging ECG allows visualizing changes in sequence of depolarization as well as the ST segment deviations in myocardial infarction and they can be visually compared with non-ECG imaging methods.

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. An intramural electrically inactive area encircled by a transmural area with slowed impulse propagation velocity was introduced in anteroseptal and inferior locations. The effects on the QRS complex and the ST segment of the 12-lead electrocardiogram are presented. RESULTS: The intramural electrically inactive area caused QRS changes typical for corresponding locations of a myocardial infarction observed in patients, which were further considerably modified by slowed impulse propagation velocity in the surrounding area. Additionally, areas of slowed impulse propagation velocity led to ST segment deviations in the "reciprocal" leads, shifting the ST segment towards the affected areas. CONCLUSION: Using computer modeling we showed that the localized alteration of impulse propagation not only modified the QRS complex, but produced also changes in the ST segment consistent with changes which are usually interpreted as the effect of "injury current".

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. However, it has been well documented that both active and passive electrical properties in LVH are altered. Using computer simulations, we have shown that an increased LVM is not the only determinant of QRS complex changes in LVH, as these changes could also be produced without changing the left ventricular mass, implying that these QRS patterns can be present in patients before their LVM exceeds the arbitrary upper normal limits. Our results link the experimental evidence on electrical remodeling with clinical interpretation of ECG changes in patients with LVH and stress the necessity of a complex interpretation of the QRS patterns considering both spatial and nonspatial determinants in terms of the spatial angle theory. We assume that hypertrophic electrical remodeling in combination with changes in left ventricular size and shape explains the variety of ECG patterns as well as the discrepancies between ECG and left ventricular mass.

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. We demonstrated that typical LBBB patterns were caused both by block or delay in the onset of the LV activation, as well as by impaired conduction in the myocardium itself while maintaining the location and onset of the LV activation. The most important difference was the absence of initial anteriorly oriented electrical forces in cases of the simulated complete LBBB and of incomplete LBBB if the onset of LV activation was delayed (≥ 6 milliseconds). Under the conditions defined in this model that did not consider myocardial infarction, the presence of initial anteriorly oriented electrical forces was indicative of preserved conduction in the left bundle and of impaired conduction in LV working myocardium. CONCLUSION: The elucidation of the participation of working myocardium impairment in the intraventricular conduction delay in the LV could be of vital significance for the clinical management of patients with LBBB patterns, for example, indicated for resynchronization therapy.

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. Both CV slowing and APD prolongation prolonged the QT interval; however, the secondary and primary repolarization changes differed in additional electrocardiogram (ECG) characteristics creating specific vectorcardiographic/ECG patterns. The secondary repolarization changes were characterized by prolonged QT interval, accompanied by pronounced QRS changes, including increased maximum spatial QRS vector magnitude, prolonged QRS duration, QRS morphology consistent with intraventricular conduction delay, lower values of the T/QRS duration ratio, increased maximum spatial T vector magnitude, narrow and prolonged discordant T vector loops, and discordant tall T waves creating a pattern of ST strain in the precordial ECG leads. QT prolongation in primary repolarization changes was accompanied with inconsiderable changes of QRS amplitude and duration, higher values of the T/QRS duration ratio, widened rounded T loops, and notched or bifid T waves in left precordial leads of the 12-lead ECG. These simulation data are consistent with the accumulated evidence suggesting that LVH induces changes in CV and APD. Our results emphasize the need for simultaneous consideration of morphologic QRS and T wave patterns together with QT prolongation in clinical evaluation of LVH.

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. In this study, we used a computer model to evaluate the effect of changes in anatomy and conduction velocity of the left ventricle on QRS complex characteristics. MATERIAL AND METHODS: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change dimensions of the ventricles, as well as the conduction velocity in the individual layers of myocardium. Three types of anatomic changes were simulated: concentric hypertrophy, eccentric hypertrophy, and dilatation. The conduction velocity was slowed in the inner layer of the left ventricle representing the Purkinje fiber mesh and in the layers representing the working myocardium. The outcomes of the model are presented as the time course of the spatial QRS vector magnitude, the vectorcardiographic QRS loops (VCGs) in horizontal, left sagittal, and frontal planes, as well as derived 12-lead ECGs. The following indicators of the 12-lead ECG were evaluated: the left axis deviation, the intrinsicoid deflection in V6, Cornell voltage, Cornell voltage-duration product, and Sokolow-Lyon index. RESULTS: The increase in LVM did not affect the QRS voltage proportionally, and the LVM and type of hypertrophy were not the only determinants of the QRS patterns. The conduction velocity slowing resulted in a spectrum of QRS patterns including increased QRS voltage and duration, left axis deviation, prolonged intrinsicoid deflection, VCG patterns of left bundle branch block, as well as pseudo-normal VCG/ECG patterns. The anatomic changes and conduction velocity slowing affected differently Sokolow-Lyon index and Cornell criteria. CONCLUSION: We showed that the LVM is not the only determinant of the QRS complex changes in LVH, but it is rather a combination of anatomic and electric remodeling that creates the whole spectrum of the QRS complex changes seen in LVH patients. The slowed conduction velocity in the model heart produced QRS patterns consistent with changes described in LVH, even if the LVM was not changed.

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 (1.2 mm spatial resolution), was used to produce models of circumscribed hypertrophies by increasing the wall thickness to 150% in various regions of the free left ventricular wall, the septum and the apex. Gradients of simulated transmembrane action potentials were utilized to compute resultant heart vectors at any instant of ventricular activation and recovery, as well as time courses of their characteristics and planar projections of vectorgraphic loops. Involvement of the septum and/or the anterior wall decreased the maximum QRS vector magnitude, an opposite effect resulted from involvement of the lateral and posterior wall segments. Directional vector changes predicted the diagnostic value of S waves in precordial leads. Asymmetric hypertrophy did not produce abnormal Q waves. The maximum T vector increased in hypertrophy of any part of the free wall along with an increase of the spatial angle between maximum QRS and T vectors. The results of this study may be useful for refinement of electrocardiographic and vectorcardiographic diagnostic criteria of asymmetric left ventricular hypertrophy.

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.