Abstract
Atrial fibrillation (AF) is the most common treatable cardiac arrhythmia. Risk factors for AF are difficult to modify, and interventions to prevent AF in clinical trials have failed to date. Inflammation is an important pathway for the development of AF, and recent studies suggest that activation of specific innate and adaptive immune responses, such as intermediate monocytes1 and highly cytotoxic CD4+CD28null cells,2,3 may play a role in AF pathogenesis. However, it remains unclear whether immune activation is a result or a cause of AF.
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