Increasing evidence implicates inflammation in atrial fibrillation (AF) pathogenesis. For instance, levels of C-reactive protein (CRP), a marker of systemic inflammation, are higher in people with persistent than paroxysmal AF. Elevated CRP levels are associated with higher risk of embolism and relapse after cardioversion.6 In addition, strokes cause necrotic cell death, which triggers inflammation. This might account in part for the increased risk of AF after a stroke.21

Autonomic input is discussed in the next section

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