Abstract
BackgroundAtrial fibrillation (AF) is accompanied by progressive epicardial fibrosis, dissociation of electrical activity between the epicardial layer and the endocardial bundle network, and transmural conduction (breakthroughs). However, causal relationships between these phenomena have not been demonstrated yet. Our goal was to test the hypothesis that epicardial fibrosis suffices to increase endo–epicardial dissociation (EED) and breakthroughs (BT) during AF.MethodsWe simulated the effect of fibrosis in the epicardial layer on EED and BT in a detailed, high-resolution, three-dimensional model of the human atria with realistic electrophysiology. The model results were compared with simultaneous endo–epicardial mapping in human atria. The model geometry, specifically built for this study, was based on MR images and histo-anatomical studies. Clinical data were obtained in four patients with longstanding persistent AF (persAF) and three patients without a history of AF.ResultsThe AF cycle length (AFCL), conduction velocity (CV), and EED were comparable in the mapping studies and the simulations. EED increased from 24.1 ± 3.4 to 56.58 ± 6.2% (p < 0.05), and number of BTs per cycle from 0.89 ± 0.55 to 6.74 ± 2.11% (p < 0.05), in different degrees of fibrosis in the epicardial layer. In both mapping data and simulations, EED correlated with prevalence of BTs. Fibrosis also increased the number of fibrillation waves per cycle in the model.ConclusionA realistic 3D computer model of AF in which epicardial fibrosis was increased, in the absence of other pathological changes, showed increases in EED and epicardial BT comparable to those in longstanding persAF. Thus, epicardial fibrosis can explain both phenomena.
Highlights
The progression of atrial fibrillation (AF) is mediated by ionchannel remodeling and structural alterations including fibrosis (Schotten et al, 2011)
Average AF cycle length (AFCL) ranged from 143.4 ± 2 to 148.7 ± 1.4 ms in control and severe fibrotic tissue, respectively
We developed the first computer model for AF that includes an epicardial layer and endocardial bundle network with realistic assumptions on fiber directions and can simulate three-dimensional propagation of fibrillation waves similar to patterns observed in clinical mapping studies
Summary
The progression of atrial fibrillation (AF) is mediated by ionchannel remodeling and structural alterations including fibrosis (Schotten et al, 2011). Verheule et al (2013, 2014) demonstrated that the endomysial fibrosis that accompanies the transition from persistent to permanent AF in goats occurs almost exclusively within the epicardial layer, in the outer 1 mm of the atrial wall, while endocardial bundles remain unaffected. It is not obvious and experimentally difficult to test whether this preferentially epicardial distribution of fibrosis suffices to explain the observed increase in EED and BTs or whether other mechanisms underlie these phenomena. Our goal was to test the hypothesis that epicardial fibrosis suffices to increase endo–epicardial dissociation (EED) and breakthroughs (BT) during AF
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