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. Author manuscript; available in PMC: 2017 Oct 27.
Published in final edited form as: Trends Cardiovasc Med. 2014 Dec 31;25(6):475–484. doi: 10.1016/j.tcm.2014.12.015

Figure 1.

Figure 1

Working model for AF-induced remodeling and the substrate for AF perpetuation. Sustained high frequency excitation of the atria results in a complex series of pathophysiological events involving a large number of significant players. These include oxidative stress, calcium overload, atrial dilatation, inflammation and myofibroblast activation (Figure 1), all of which are likely to be involved in AF-induced atrial extracellular matrix (ECM) and electrical remodeling through transcriptionally mediated changes in both cardiac myocytes and fibroblasts.