Mechanistic Inquiry into the Role of Tissue Remodeling in Fibrotic Lesions in Human Atrial Fibrillation

Kathleen S. McDowell; Fijoy Vadakkumpadan; Robert Blake; Joshua Blauer; Gernot Plank; Rob S. MacLeod; Natalia A. Trayanova

doi:10.1016/j.bpj.2013.05.025

Figure 2

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Transmembrane potential maps at three time instants in three atrial models with different arrhythmogenic outcomes: neither conduction block takes place nor reentry is established (leftmost column; exclusively diffuse collagen deposition modeled in the fibrotic lesions); conduction block occurs without the formation of a reentrant circuit (middle column; GJR and diffuse collagen deposition included in the fibrotic lesions), and both conduction block and reentry occur, initiating AF (rightmost column; GJR, diffuse collagen deposition, and myofibroblasts coupled to myocytes included in fibrotic lesions). Lines of block are marked in red. Black arrows indicate direction of propagation. Fibrotic distribution is pictured at bottom right, with anatomical labels for the LA appendage (LAA), right superior PV (RSPV), right inferior PV (RIPV), left superior PV (LSPV), and left inferior PV (LIPV).