Figure 4.

Modeling fibroblast proliferation in the regions of fibrosis. (A) Effect of myocyte-fibroblast coupling (modeled as in Maleckar et al., 2009a) on spiral wave behavior in a human atrial cell monolayer model of size 4.5 × 4.5 cm. Top, control case without fibroblasts. Middle and bottom, models of low-density and high-density fibroblast proliferation (LD-Fbs and HD-Fbs) in a central circular region of the sheet. In the LD-Fbs, and HD-Fbs models, atrial myocytes (100 pF), each connecting to 4 fibroblasts (6.3 pF) within the Fb-Area, account for 12.5% and 50.0% of that area, respectively. With permission from Ashihara et al. (2012). (B) Maps of action potential duration (APD) in four human atrial models (same atrial geometry). Fibrotic lesions are modeled with (bottom row), and without (top row) myofibroblast infiltration (and coupling to myocytes), as well as with (right column), and without (left column) diffuse collagen deposition for both sets of maps. Myofibroblasts in the fibrotic regions were coupled to atrial myocytes as described in Maleckar et al. (2009a) and Maleckar et al. (2009b). Anatomical landmarks in upper-left sub-panel: right inferior, right superior, left inferior, and left superior pulmonary veins (RIPV, RSPV, LIPV, LSPV, respectively); left atrial appendage (LAA). With permission from McDowell et al. (2013).