Influence of the distribution of fibrosis within an area of myocardial infarction on wave propagation in ventricular tissue

Figure 1. Gradient fibrosis distribution in 2D tissue and the structure of the infarcted area in the 2D circular ring model. (a) Structure of the 2D gradient fibrosis model in an ideal square tissue with a circular infarcted region. The infarcted region is separated into 5 layers; the percentage of fibrosis decreases outwards from the central region: 35%, 30%, 25%, 20% and 15%. (b) Structure of the infarcted region in a 2D, actual ventricular tissue. Inset shows the zoomed-in infarcted region from panel (b). The infarcted region is separated into 4 layers; the percentage of fibrosis decreases outwards from the central of the infarct: 35%, 25%, 15% and 5%. (c) Structure of the infarcted area in 2D circular ring tissue with different lengths (arc length), widths (width of ring strip) and locations of MI tissue (distance from the inside wall to the infarcted tissue).

Figure 2. Simulation results in 2D ideal square tissue model. (a) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 550 ms in the 2D ideal random fibrosis tissue at different times. (b) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 550 ms in the 2D ideal gradient fibrosis tissue at different times. (c) Vulnerable windows of 2D ideal random and gradient fibrosis tissue ranging from 6% to 31% fibrosis.

Figure 3. Wave propagation in the 2D actual ventricular tissue models under normal, infarcted, and MI with 20% random and gradient fibrosis conditions. (a) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 500 ms under four conditions at different times in the tissue of patient 1, including only mid-myocardial cells. (b) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 500 ms under four conditions at different times in the tissue of patient 2, including only mid-myocardial cells. (c) Structural representation and wave conduction under four conditions at different times in the tissue of patient 2, including three types of cells (endocardial cells, mid-myocardial cells and epicardial cells). (d) Vulnerable windows were calculated under four conditions in the tissue of patient 1 and patient 2 with only mid-myocardial cells as well as in the tissue of patient 2 with all three types of cells. A vulnerable window of 0 ms means that when the stimulus starts later than the lower bound of the S1-S2 interval, waves could conduct normally without the appearance of reentry waves. In the graph, the single line…

Figure 4. The role of the length of the infarcted area with a fixed width of 50% and a fixed position of 0% in excitation wave propagation in the circular ring tissue model. (a) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 520 ms in the 2D ring model of infarcted tissue without fibrosis at different times. (b) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 520 ms in the 2D ring model of infarcted tissue with 20% fibrosis at different times. (c) Change in the size of the vulnerable windows in the circular ring tissue with and without 20% fibrosis as a function of the length of the infarcted tissue. Black bars: infarcted tissue without fibrosis; Red bars: infarcted tissue with 20% random fibrosis.

Figure 5. The role of the width of the infarcted area with a fixed length of 25% and a fixed position of 0% in excitation wave propagation in the circular ring tissue. (a) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 520 ms in the 2D ring model of infarcted tissue without fibrosis at different times. (b) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 520 ms in the 2D ring model of infarcted tissue with 20% fibrosis at different times. (c) Change in the size of the vulnerable windows in the circular ring tissue with and without 20% fibrosis as a function of the width of the infarcted tissue. Black bars: infarcted tissue without fibrosis; Red bars: infarcted tissue with 20% random fibrosis.

Figure 6. The role of the position of the infarcted area with a fixed length of 25% and a fixed width of 50% in excitation wave propagation in the circular ring tissue. (a) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 520 ms in the 2D ring model of infarcted tissue without fibrosis at different times. (b) Structural representation and wave conduction tested with two stimuli with S1-S2 intervals of 520 ms in the 2D ring model of infarcted tissue with 20% fibrosis at different times. (c) Change in the size of the vulnerable windows in the circular ring tissue with and without 20% fibrosis as a function of the position of the infarcted tissue. Black bars: infarcted tissue without fibrosis; Red bars: infarcted tissue with 20% random fibrosis.

Figure 7. Wave propagation in the 2D, actual ventricular tissue and ideal circular ring tissue models. (a) Structural representation and wave propagation tested with two stimuli with S1-S2 intervals of 520 ms in the 2D actual ventricular tissue model of patient 1 and in the corresponding ideal ring strip tissue model with and without 20% fibrosis. (b) Structural representation and wave propagation tested with two stimuli with S1-S2 intervals of 520 ms in the 2D actual ventricular tissue model of patient 3 and in the corresponding ideal ring strip tissue model with and without 20% fibrosis. (c) The vulnerable windows of the actual infarcted tissues of patient 1 and patient 3 and their corresponding ring strip tissues with and without 20% fibrosis. Black bars: tissue without fibrosis; Red bars: tissue with 20% random fibrosis.

Figure 8. Modeling process and wave propagation in 3D real ventricular models. (a) Real scar modeling process in 3D real ventricular models, including segmentation, interpolation, reconstruction, smoothing and combination. (b) Ideal scar modeling process in 3D real ventricular models, including 2D graphic plotting, interpolation, reconstruction, smoothing and combination. (c) Wave propagation in 3D real ventricular models with real and ideal 20% fibrotic scar areas tested with three stimuli at 0 ms, 387 ms and 720 ms in turn at the same position (LV: left ventricle; RV: right ventricle).