Abstract
Left ventricular hypertrophy (LVH) is characterised by an increase in the mass and volume of the left ventricle, typically manifested as ventricular wall thickening and/or dilation. Due to its potential to cause severe, life-threatening complications, ongoing research continues to explore its underlying mechanisms. This study aimed to determine how wall thickening and dilation specifically impact ECG waveforms, isolating these anatomical alterations without considering potential electrophysiological changes associated with LVH - a scenario achievable only through computational modelling. To accomplish this, eccentric and concentric cardiac models - with growth levels from 10% to 100% mass increase - were generated using a kinematic growth, finite element model derived from a healthy control model. Activation sequences were simulated for each model using a pseudo-bidomain reaction-eikonal approach, and 12-lead ECGs were recorded from the hypertrophy models and compared to the control. Results indicated that activation patterns in eccentric hypertrophy models resembled the healthy model, while concentric hypertrophy models displayed substantial deviations. Both types of hypertrophy types led to prolonged QRS durations by up to 21 ms - a 40% increase from baseline - even in the absence of electrical remodelling. Eccentric hypertrophy increased amplitudes in precordial leads, minimally affecting limb leads, while concentric hypertrophy impacted all 12 leads with varied amplitude changes. Leads aVL, V1 and V5/V6 emerged as the most sensitive to anatomical changes. These findings could enhance the accuracy of LVH diagnosis using ECGs, offering a cost-effective strategy to complement clinical evaluation and imaging, ultimately improving LVH detection and management. KEY POINTS: Computational simulations revealed distinct effects of anatomical changes in eccentric and concentric left ventricular hypertrophy on 12-lead ECG signals. Eccentric hypertrophy primarily affected the precordial leads, showing notable voltage amplitude increases across all precordial lead measurements. Concentric hypertrophy affected all 12 leads without a clear pattern of amplitude change, displaying both increases and decreases. Both eccentric and concentric hypertrophy resulted in a consistent prolongation of the QRS complex, showing up to 40% increase from baseline, even in the absence of electrophysiological remodelling. Leads aVL, III, V1 and V5/V6 were identified as the most sensitive to LVH, with computational results aligning well with independent clinical measurements.