Patient-specific modelling of atrial fibrosis and conduction

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Experimental evidence suggests that areas of fibrosis in the atria can cause disturbances to the electrical excitation waves, potentially leading to arrhythmogenic re-entrant waves. Current ablation treatments cauterise large damaged areas of the atria, based on statistical data. Patient specific areas of atrial fibrosis may be used to model the resultant conduction abnormalities, and guide more accurate interventions.

Patient specific atrial geometry is reconstructed from clinical MRI images. The MRI signal of the blood volume within the atria is dilated to reconstruct appropriate wall thickness. Such a dilation is specific to regions of the atrial wall (its thickness can also be obtained from MRI), resulting in a realistic reconstruction of the 3D atrial geometry. This is then combined with manually segmented pre-ablation fibrosis MRI data. Using modified Courtemanche et al. (1998) and MacCannell et al. (2007) equations to simulate the electrophysiology of the atrial myocytes and fibroblasts respectively, wave conduction through the atrial tissue was simulated. Variation of the number of fibroblasts coupled to each myocyte allows for different levels of fibrosis.

Simulations show up to 20% decrease in wave propagation velocity in areas of fibrosis (compared to healthy atrial tissue), depending on the number of fibroblasts (0–10) coupled to myocytes. This can be explained by different electrophysiological properties of the fibroblasts that are non-excitable, but have a resting potential of about − 50 mV. Electrotonic load from the fibroblasts alters the action potential properties of the coupled myocytes, slowing down the conduction.

The model developed combines patient specific atrial geometry and distribution of fibrosis with detailed electrophysiological modelling, and can be used for studying the effect of fibrosis on atrial conduction in health and disease.
Original languageEnglish
Pages (from-to)e27-e28
JournalJournal of Electrocardiology
Publication statusPublished - 2013


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