Abstract
The onset of cardiac arrhythmias depends on the electrophysiological and structural properties of cardiac tissue. Electrophysiological remodeling of myocytes due to the presence of adipocytes constitutes a possibly important pathway in the pathogenesis of atrial fibrillation. In this paper we perform an in-silico study of the effect of such myocyte remodeling on the onset of atrial arrhythmias and study the dynamics of arrhythmia sources—spiral waves. We use the Courtemanche model for atrial myocytes and modify their electrophysiological properties based on published cellular electrophysiological measurements in myocytes co-cultered with adipocytes (a 69–87 % increase in APD90 and an increase of the RMP by 2.5–5.5 mV). In a generic 2D setup we show that adipose tissue remodeling substantially affects the spiral wave dynamics resulting in complex arrhythmia and such arrhythmia can be initiated under high frequency pacing if the size of the remodeled tissue is sufficiently large. These results are confirmed in simulations with an anatomically accurate model of the human atria.
Highlights
Atrial fibrillation (AF) forms an economic burden on modern health care (Stewart et al, 2004)
When we look at AF remodeled tissue with an AF plus adipose remodeled patch, we observe a minimal frequency between 2.0 and 2.2 Hz or a basic cycle length (BCL) that has to be smaller than 500 ms but larger than 450 ms
As an outlook toward further studies, we can say that the obstacle nature of an adipocyte creates conditions for the onset of arrhythmia, while the remodeling part makes it more persistent and increases complexity
Summary
Atrial fibrillation (AF) forms an economic burden on modern health care (Stewart et al, 2004). It affects approximately 1.5 % of the population (Lip et al, 2007) and as much as 9% of people above the age of 80 (Go et al, 2001). It was shown that it is an independent risk factor for the occurrence of AF or progression of AF severity in the absence of other risk factors like heart failure, alcohol use, or hypertension (Wang et al, 2004; Dublin et al, 2006; Tsang et al, 2008). Recent experiments have shown significant correlations between adipose infiltrations and arrhythmias (Pantanowitz, 2001; Samanta et al, 2016; Haemers et al, 2017)
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