PMC:6019327 / 41521-42374 JSONTXT

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AF itself leads to electrical remodeling and fibrosis of the atria.157,158 Experimental and clinical data point to a complex pathophysiology involving diverse factors, including oxidative stress, calcium overload, atrial dilatation, microRNAs, inflammation, and myofibroblast activation.141,159,160,161,162 In a recent study of transcriptional changes associated with AF, susceptibility to the arrhythmia was associated with decreased expression of targets of several transcription factors related to inflammation, oxidation, and cellular stress responses.163 However, it is unknown to what extent and at which time points such alterations influence the remodeling process that perpetuates AF. Moreover, rapid atrial rates activate fibroblasts to increase collagen-gene activity, and AF in isolation might promote cardiac fibrosis.131,133,134"}