Atrial fibrillation (AF) affects more than six million people in the United States alone. It is associated with palpitations, reduced exercise tolerance, and dyspnea. Hemodynamic impairment results from loss of synchronous atrial contraction and rapid, irregular ventricular rates. Thromboembolism and stroke are serious complications. AF has been estimated to cause nearly 40% of all strokes in patients older than 70 years. 1 Billions of health care dollars are spent each year on the care of patients with this arrhythmia and its sequelae. The incidence of AF increases with age. It induces anatomic and electrical remodeling of the atria. Myocyte degeneration, focal accumulation of endoplasmic reticulum and mitochondria, widening of portions of the intercalated discs, and replacement of myofibrils lead to patchy fibrosis, atrial dilatation, and myopathy. The atrial refractory period shortens. There is loss of the normal adaptation of refractoriness to alterations in heart rate. Both changes are proarrhythmic and contribute to arrhythmia recurrence. In spite of the clinical, pathologic, and economic importance of AF, many questions remain about its management. The complications of AF are compelling reasons to develop treatments that maintain sinus rhythm. The literature is replete with strategies for this purpose. Antiarrhythmic drugs were the mainstay of most every strategy to maintain sinus rhythm. Escalating doses of potent drugs were administered until AF was abolished or drug toxicity developed. Advocates of rhythm control argued that patients left in AF had a worse outcome compared with those treated with drugs that maintained sinus rhythm. A second treatment approach was ventricular rate control. Proponents argued that rate control was achievable in most patients, avoidance of potentially toxic antiarrhythmic drugs was desirable, and stroke risk could be reduced with anticoagulation. Eventually, low efficacy, side effects, and proarrhythmia dampened enthusiasm for the use of antiarrhythmic drugs in patients with AF and led to key randomized trials, including AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) and RACE (Rate Control Versus Electrical Cardioversion for Persistent Atrial Fibrillation), to test this basic tenet of rhythm management. 2,3 AFFIRM and RACE investigators discovered that rhythm control provided no survival advantage over ventricular rate control. Fortunately, the search for the optimal management of AF did not end here. The poor response to antiarrhythmic medications both in terms of their side effect profile and limited efficacy together with dissatisfaction over rate control as the alternate treatment option has continued to catalyze the development of nonpharmacologic approaches to treat AF. The optimal nonpharmacologic procedure would be safe, cure AF, preserve atrioventricular synchrony, restore normal atrial transport function, and reduce or eliminate the high incidence of thromboembolism. The surgical maze procedure established proof of concept that anatomically directed lines of conduction block could affect a cure. 4 Data acquired using dynamic magnetic resonance imaging, transesophageal echocardiography, and cardiac output determinations from patients more than 3 months after the maze procedure demonstrated restoration of atrioventricular synchrony (some patients required dual-chamber pacemakers), at least partial atrial transport function in most patients, and low risk of thromboembolism. Driven by these validation studies in maze patients, investigators quickly performed studies to determine how well anatomically directed catheter-based procedures measured up to the optimal nonpharmacologic approach described. Although several ablation approaches to the pulmonary veins have been championed, increasing more clinical cardiac electrophysiologists have become comfortable with circumferential pulmonary vein isolation. 5 However, most investigators in the field have been immersed in work elucidating how well each ablation approach ensures freedom from AF recurrence. Little is known regarding the impact of pulmonary vein isolation procedures on left atrial transport function and thromboembolism. In this issue of Heart Rhythm, Lemola et al 6 help fill this void of knowledge. The authors used state-of-the-art gated, multiphase, dynamic contrast-enhanced computed tomographic (CT) scans obtained from 36 consecutive patients with paroxysmal or chronic AF to determine the impact of left atrial circumferential ablation on left atrial function. The protocol used a consistent approach to left circumferential ablation; made use of data from control subjects without AF