Inflammation is increasingly recognized as a possible pathway in the pathogenesis of atrial fibrillation, which is a leading cause of stroke.3 Levels of C-reactive protein are elevated in patients with atrial fibrillation and are associated with incident atrial fibrillation and with its recurrence after ablation or cardioversion. Inflammatory pathways may promote atrial fibrillation by interacting with cell signaling cascades, causing ion channel dysfunction, impairing myocyte gap junctions, promoting atrial fibrosis, and recruiting leukocytes to cardiac tissue. The relationship between inflammation and atrial fibrillation is most likely bidirectional, with atrial fibrillation causing some degree of immune activation and inflammation. The prothrombotic state seen in atrial fibrillation may reflect this inflammation, and anticoagulation with heparinoids seems to reduce biomarkers of inflammation in patients with atrial fibrillation. On the other hand, perioperative treatment with glucocorticoids reduces the incidence of atrial fibrillation after cardiac surgery, which suggests that inflammation may also have a causal role in the pathogenesis of atrial fibrillation. Once patients develop atrial fibrillation, their risk of stroke varies in proportion to known clinical risk factors, such as congestive heart failure, hypertension, age, diabetes mellitus, prior stroke, and peripheral vascular disease. However, levels of the proinflammatory cytokine interleukin 6 are also associated with stroke risk, suggesting that inflammation is an additional biomarker of stroke risk within this population. Given these data, physicians should be mindful that periods of heightened inflammation (such as acute medical illness or recent surgery) place patients at higher risk of atrial fibrillation and stroke. With further development, biomarkers of inflammation may help to stratify patients' risk of developing atrial fibrillation and stroke, allowing targeted screening, risk factor modification, and timely treatment. A better understanding of the interactions among atrial fibrillation, inflammation, and thromboembolism may lead to the development of therapeutic agents that modulate inflammatory pathways to reduce the risk of atrial fibrillation and stroke.