Atrial fibrillation (AF) is the most common sustained arrhythmia. It may cause significant symptoms and impair both functional status and quality of life. Without therapeutic intervention, affected patients are at increased risk for mortality (1.5- to 1.9-fold in the Framingham Heart Study) and morbidity (thromboembolic events and limiting symptoms).
In AF, the loss of the regular and organized contraction of the left atrium as well as the subsequent increase in ventricular rate, lead to both immediate and long-term adverse consequences: deterioration in hemodynamics secondary to increased heart rate and loss of atrioventricular (AV) synchrony, an increased risk for stroke and other embolic events from left atrial thrombi, and progressive dysfunction of the left atrium and left ventricle [1,2]. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm" and "Tachycardia-mediated cardiomyopathy".)
For each patient with AF, the two principal goals of therapy are symptom control and the prevention of thromboembolism. (See "Antithrombotic therapy to prevent embolization in atrial fibrillation" and "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm", section on 'Adverse hemodynamics in AF'.)
Rate- and rhythm-control strategies improve symptoms, but neither has been conclusively shown to improve survival compared to the other. (See 'Definitions' below.)
For each patient with AF, a decision should be made as to which approach will be used for long-term management. The following points should be kept in mind irrespective of strategy: