Atrial fibrillation (AF) is found in 0.4% of adults younger than age 60 years and in 2 to 4% older than age 60 years, and is associated with a high risk of thromboembolic complications. AF-paroxysmal and chronic-has many etiologies, including rheumatic and nonrheumatic heart disease and thyrotoxicosis. Knowing how strokes occur and what precipitates them e.g., differentiating between cardioembolic and cerebrovascular causes-is important when deciding on appropriate treatment. Risk factors involved in the development of thromboembolic complications associated with AF are reviewed, focusing on the contributions of thyrotoxic AF, paroxysmal AF (and its transition to chronic AF), enlargement of the left atrium, silent cerebral infarction and decreased cerebral blood flow. Data from several studies are briefly presented, highlighting major outcomes. On the basis of current information about prevention of thromboembolic complications, it seems reasonable to recommend anticoagulant treatment for patients with nonrheumatic chronic AF. (Am J Cardiol 1990;6S:24C-28C), Atrial fibrillation (AF, rapid and irregular contraction of the atrial chamber of the heart) occurs in roughly 0.4 percent of all adults; among adults over 60, the prevalence is 2 to 4 percent. Atrial fibrillation dramatically increases the risk of stoke. Among patients with AF, but without rheumatic heart disease, the rate of stroke is five times that of the general population. Patients with AF and rheumatic heart disease have 17 times the risk. Although stroke is an obvious complication, there are other thromboembolic complications which are common among patients with AF, including transient ischemic attacks and decreased cerebral blood flow. Thyrotoxicosis, a disease marked by excessive thyroid activity, also called Grave's disease, is an important cause of AF. Although studies have found a high incidence of cerebral embolism among patients with thyrotoxicosis, it appears that the toxicosis itself contributes to the increased risk. Paroxysmal atrial fibrillation does not seem to carry the same risk of cerebroembolism as chronic AF. This suggests that there may be some benefit to aggressively treating paroxysmal atrial fibrillation in order to delay the development of chronic AF. This notion has not been tested. Enlargement of the left atrium is also associated with AF; it is uncertain whether it is a cause or an effect of AF. Some studies, but not all, have been able to demonstrate an increase in the size of the left atrium over time among patients with AF. There does not, however, seem to be any relation between atrial enlargement and the risk of stroke. In a recent study, warfarin (coumadin) was found to provide a significant reduction in the incidence of thromboembolic complications. In a study of 1,007 patients with AF, 2.0 percent of the 335 patients on warfarin suffered embolic complications, compared with 5.5 percent in both the aspirin group and placebo groups. One patient in the warfarin group died of a cerebral hemorrhage. Nonetheless, in the absence of indications to the contrary, it seems reasonable to prophylactically treat AF patients with anticoagulant therapy. (Consumer Summary produced by Reliance Medical Information, Inc.)