Historically,
atrial fibrillation has been observed in clinical settings of prolonged hemodynamic stress, eg,
hypertension and
valvular heart disease. However, recently, the most prominent precedents to
atrial fibrillation are
metabolic diseases that are associated with adipose tissue
inflammation (ie,
obesity and
diabetes mellitus) and systemic inflammatory disorders (ie,
rheumatoid arthritis and
psoriasis). These patients typically have little evidence of
left ventricular hypertrophy or dilatation; instead, imaging reveals abnormalities of the structure or function of the atria, particularly the left atrium, indicative of an atrial
myopathy. The left atrium is enlarged, fibrotic and noncompliant, potentially because the predisposing disorder leads to an expansion of epicardial adipose tissue, which transmits proinflammatory mediators to the underlying left atrium. The development of an atrial
myopathy not only leads to
atrial fibrillation, but also contributes to pulmonary venous
hypertension and systemic
thromboembolism. These mechanisms explain why disorders of systemic or adipose tissue
inflammation are accompanied an increased risk of
atrial fibrillation, abnormalities of left atrium geometry and an enhanced risk of
stroke. The risk of
stroke exceeds that predicted by conventional cardiovascular risk factors or
thromboembolism risk scores used to guide the use of anticoagulation, but it is strongly linked to clinical evidence and
biomarkers of systemic
inflammation.