Heterogeneous Effects of Fibroblast-Myocyte Coupling in Different Regions of the Human Atria Under Conditions of Atrial Fibrillation

Figures

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  Figure 1. Myocyte action potentials from four different regions of the atria: right atria (RA), left atria (LA), pulmonary vein (PV), and crista terminalis (CT). (A) Myocyte action potentials under normal sinus rhythm (nSR). (B) Myocyte action potentials under the effect of electrical remodeling during persistent atrial fibrillation (PeAF). (C) Myocyte action potential duration (APD90) under nSR and PeAF. (D) Myocyte action potential maximum upstroke velocity (dV/dtmax) under nSR and PeAF. (E) Myocyte action potential resting membrane potential (RMP) under nSR and PeAF.

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  Figure 2. Effect of fibroblast and myocyte coupling under persistent atrial fibrillation (PeAF) electrical remodeling in RA (baseline model). First and second rows show fibroblasts resting membrane potential (RMPf) of –26 and –45 mV, respectively, for a fibroblast membrane capacitance (Cmf) of 6.3 pF (first column) and 50.4 pF (second column). The different traces are action potentials of isolated myocytes under PeAF (blue), one myocyte under PeAF coupled to 1 fibroblast (1:1) (dashed orange), one myocyte under PeAF coupled to three fibroblasts (1:3) (dotted yellow), and one myocyte under PeAF coupled to nine fibroblasts (1:9) (dotted-dashed purple).

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  Figure 3. Action potential durations of myocytes in normal sinus rhythm (nSR), under persistent atrial fibrillation electrical remodeling (PeAF) and after being coupled to fibroblasts with a resting membrane potential (RMPf) of –26 or –45 mV in RA (baseline model). In the first column the membrane capacitance of fibroblasts is 6.3 pF and in the second column 50.4 pF. One myocyte was coupled to one fibroblast (1:1) (first row), three fibroblasts (1:3) (second row), and nine fibroblasts (1:9) (third row).

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  Figure 4. Fibroblasts coupling effect on myocyte electrophysiology. (A) Myocyte maximum upstroke velocity (dV/dtmax). (B) Myocyte resting membrane potential (RMP). The levels for myocytes in normal sinus rhythm (nSR) and persistent atrial fibrillation (PeAF) conditions are given in blue and red, respectively. Discontinuous lines are myocytes in PeAF coupled to one fibroblast (1:1), 3 (1:3), or 9 (1:9).

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  Figure 5. Myocyte action potential duration (APD) of four different regions of the atria under persistent atrial fibrillation electrical remodeling (PeAF) coupled to three fibroblasts (Fib) or myofibroblasts (MyoFib) stimulated at different basic cycle lengths (BCLs). (A) Right atria (RA), (B) Left atria (LA), (C) Pulmonary vein (PV), and (D) Crista terminalis (CT).

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  Figure 6. Conduction velocity (CV) of a tissue strand in four different regions of the atria with random fibroblasts (Fib) or myofibroblast (MyoFib) distribution and different fibroblast densities. For each density 100 random configurations were simulated. CV measurements are represented in boxplots. (A) Right atria (RA). (B) Pulmonary vein (PV), (C) Left atria (LA), and (D) Crista terminalis (CT).

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  Figure 7. Instantaneous phase maps and phase singularities (in white) for different densities of myofibroblasts (non-fibrotic, 10, 20, and 40%) in the right atria (RA) and left atria (LA) under conditions of persistent AF remodeling.

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  Figure 8. Vulnerable window to reentry in atrial tissue with different densities of myofibroblasts indicated in percentage for the right atrial (RA) in blue and the left atrial (LA) in red subject to persistent atrial fibrillation remodeling.