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This may be due to nuclear or cytoplasmic disturbances manifested as cytoplasmic vacuolization and fragmentation, a large perivitelline space, spindle disturbances, or mitochondrial aggregation [36]

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EAT derived from AF patients has been shown to secrete abundant EVs, which accelerate the progression of atrial myopathy and AF due to their strong pro-inflammatory, pro-fibrotic, and arrhythmogenic properties (87)

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