Left atrial appendage closure to prevent stroke in patients with atrial fibrillation.

Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with substantial morbidity. The prevalence of AF in the United States is expected to rise to between 5.6 and 12 million in 2050.1 AF is associated with a 4- to 5-fold increased risk of ischemic stroke after adjustment for other risk factors,2 and paroxysmal, persistent, or permanent AF increases stroke risk to a similar degree. Oral anticoagulants (OACs) reduce the risk of thromboembolism, yet they are underused.3–6 Novel OACs are noninferior or superior to warfarin for the prevention of stroke and systemic embolism and are more convenient because they do not require ongoing monitoring.7–10 However, major challenges to long-term therapy with vitamin K antagonists and novel OACs include a substantial ongoing hazard of major bleeding, noncompliance, side effects, and, in the case of the novel OACs, lack of an available antidote. The left atrial appendage (LAA) is the predominant nidus for thrombus formation in AF, and transcatheter LAA closure has emerged as a potential alternative to oral anticoagulation in at-risk AF patients. AF is associated with mechanical dysfunction of atrial tissue. Loss of contractile function in the LAA can lead to local stasis and thrombus formation, which may then embolize into the systemic circulation. The observation that >90% of thrombi found in patients with nonvalvular AF and stroke are in the LAA supports this mechanistic sequence.11 In addition, low Doppler inflow velocities, spontaneous echocardiographic contrast, and the presence of thrombus in the LAA have been associated with high stroke rates in AF patients.12 These data lend support to the hypothesis that the elimination of the LAA may serve as a preventive strategy for AF-related stroke. Morphological features of the LAA may influence stroke risk. Larger LAA neck diameter …