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  • Title: QRS complex waveform indicators of ventricular activation slowing: Simulation studies.
    Author: Bacharova L, Szathmary V, Svehlikova J, Mateasik A, Tysler M.
    Journal: J Electrocardiol; 2016; 49(6):790-793. PubMed ID: 27554423.
    Abstract:
    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.
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