Abstract
Premature ventricular complexes (PVCs), which are abnormal impulse propagations in cardiac tissue, can develop because of various reasons including early afterdepolarizations (EADs). We show how a cluster of EAD-generating cells (EAD clump) can lead to PVCs in a model of cardiac tissue, and also investigate the factors that assist such clumps in triggering PVCs. In particular, we study, through computer simulations, the effects of the following factors on the PVC-triggering ability of an EAD clump: (1) the repolarization reserve (RR) of the EAD cells; (2) the size of the EAD clump; (3) the coupling strength between the EAD cells in the clump; and (4) the presence of fibroblasts in the EAD clump. We find that, although a low value of RR is necessary to generate EADs and hence PVCs, a very low value of RR leads to low-amplitude EAD oscillations that decay with time and do not lead to PVCs. We demonstrate that a certain threshold size of the EAD clump, or a reduction in the coupling strength between the EAD cells, in the clump, is required to trigger PVCs. We illustrate how randomly distributed inexcitable obstacles, which we use to model collagen deposits, affect PVC-triggering by an EAD clump. We show that the gap-junctional coupling of fibroblasts with myocytes can either assist or impede the PVC-triggering ability of an EAD clump, depending on the resting membrane potential of the fibroblasts and the coupling strength between the myocyte and fibroblasts. We also find that the triggering of PVCs by an EAD clump depends sensitively on factors like the pacing cycle length and the distribution pattern of the fibroblasts.
Highlights
Life-threatening cardiac arrhythmias, like ventricular fibrillation (VF), are associated with the abnormal propagation of waves of electrical activation through cardiac tissue [1, 2]
I.e, the deposition of collagens by fibroblasts, by distributing inexcitable point obstacles randomly in our early afterdepolarizations (EADs) clump; and we show that such fibrosis pattern enhances the triggering of premature ventricular complexes (PVCs); this enhancement increases with the percentage Pf of fibrosis, reaches a maximum at Pf ’ 40%, and decreases until at Pf ’ 55% the EAD clump loses its ability to trigger PVCs
If the repolarization reserve of the myocyte is such that the EADs have a low amplitude and decaying oscillations as in type-II action potential (AP) (Fig 2(B)), the EAD clumps cannot trigger PVCs
Summary
Life-threatening cardiac arrhythmias, like ventricular fibrillation (VF), are associated with the abnormal propagation of waves of electrical activation through cardiac tissue [1, 2]. The degeneration from a normal heart beat to an irregular heart beat (like in VF) can occur, inter alia, if PLOS ONE | DOI:10.1371/journal.pone.0144979. Premature Ventricular Complexes from Cluster of Early Afterdepolarization-Capable Myocytes The degeneration from a normal heart beat to an irregular heart beat (like in VF) can occur, inter alia, if PLOS ONE | DOI:10.1371/journal.pone.0144979 December 16, 2015
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