Infection is one of the most common triggers of new-onset AF, accounting for over 20% of cases associated with a secondary precipitant.26 Pathophysiologic hypotheses for the association include electrolyte derangement, atrial stretch due to dysregulated volume status and increased myocyte automaticity in the setting of severe inflammation.31 Indeed, the degree of inflammation, as measured by serum C-reactive protein, is correlated with the risk of developing AF during infection.32 Here, CRP is linked to infection.