Abstract
The occurrence of atrial fibrillation (AF) is associated with progressive changes in the calcium handling system of atrial myocytes. Calcium cycling instability has been implicated as an underlying mechanism of electrical alternans observed in patients who experience AF. However, the extent to which calcium-induced alternation of electrical activity in the atria contributes to arrhythmogenesis is unknown. In this study, we investigated the effects of calcium-driven alternans (CDA) on arrhythmia susceptibility in a biophysically detailed, 3D computer model of the human atria representing electrical and structural remodeling secondary to chronic AF. We found that elevated propensity to CDA rendered the atria vulnerable to ectopy-induced arrhythmia. It also increased the complexity and persistence of arrhythmias induced by fast pacing, with unstable scroll waves meandering and frequently breaking up to produce multiple wavelets. Our results suggest that calcium-induced electrical instability may increase arrhythmia vulnerability and promote increasing disorganization of arrhythmias in the chronic AF-remodeled atria, thus playing an important role in the progression of the disease.
Highlights
ObjectivesThe goal of the present study was to investigate the arrhythmogenic consequences of calcium-driven APD alternans (CDA) in a realistic 3D computer model of the human atria
Cell APs for the ALTfast and ALTslow models at different pacing CLs. (c) right atrium (RA) cell APs for the ALTfast and ALTslow models at different pacing CLs. (d) left atrium (LA) and RA regions in the human atria model. (e) Stimulus locations. (f)
We examined the effect of increased propensity to CDA on arrhythmia vulnerability in 3D models of the human atria incorporating both electrical and structural remodeling associated with Atrial fibrillation (AF)
Summary
The goal of the present study was to investigate the arrhythmogenic consequences of calcium-driven APD alternans (CDA) in a realistic 3D computer model of the human atria
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