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Potential mechanism by which VLDL promotes AF in MetS. In MetS, the biochemical properties of VLDL are changed. MetS-VLDL can induce cellular reactive oxygen species, atrial myocyte cytotoxicity, and excess lipid accumulation resulting in subsequent gene dysregulation corresponding to metabolic derangement. Structural and potentially electrical remodeling initiated by MetS-VLDL in concert contribute to AF vulnerability and development.
