Abstract

The onset of cardiac arrhythmias depends on electrophysiological and structural properties of cardiac tissue. One of the most important changes leading to arrhythmias is characterised by the presence of a large number of non-excitable cells in the heart, of which the most well-known example is fibrosis. Recently, adipose tissue was put forward as another similar factor contributing to cardiac arrhythmias. Adipocytes infiltrate into cardiac tissue and produce in-excitable obstacles that interfere with myocardial conduction. However, adipose infiltrates have a different spatial texture than fibrosis. Over the course of time, adipose tissue also remodels into fibrotic tissue. In this paper we investigate the arrhythmogenic mechanisms resulting from the presence of adipose tissue in the heart using computer modelling. We use the TP06 model for human ventricular cells and study how the size and percentage of adipose infiltrates affects basic properties of wave propagation and the onset of arrhythmias under high frequency pacing in a 2D model for cardiac tissue. We show that although presence of adipose infiltrates can result in the onset of cardiac arrhythmias, its impact is less than that of fibrosis. We quantify this process and discuss how the remodelling of adipose infiltrates affects arrhythmia onset.

Highlights

  • Abnormal excitation of the heart results in cardiac arrhythmias, which is a major problem in cardiac electrophysiology

  • Infiltrations of adipose tissue within the ventricular myocardium have been associated with arrhythmogenicity in arrhythmogenic right ventricular cardiomyopathy[14] and more recently adipocyte infiltrations in the infarct border zone were associated with ventricular fibrillation[15]

  • We study how the size and density of adipose infiltrations affects the onset of cardiac arrhythmias and how it relates to arrhythmias occurring due to fibrosis

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Summary

Methods

If the placement of an additional infiltrate was longer than 2 CPU seconds, the further search was abandoned This condition was never a problem for low percentages of non-conducting tissue. For percentages around 50% this condition resulted in low probability for generation of textures, in several graphs presented in the paper the percentage of non-conducting tissue does not go beyond 50%. Fibrotic tissue percentage was slowly increased by taking a previous geometry and adding to it a few extra percent of non-conducting tissue Both fibrotic and adipose tissue were assumed to be in-excitable and electrically disconnected from the myocytes, to be passive obstacles for wave propagation[16]. When the simulation was deemed unsuccessful, this either means the minimal 25% was not reached, or no geometry was possible to generate as was described above

Results
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