The left atrial appendage does not perfuse any muscles.

There are several well-described LAA morphologies. The LAA classification system has its basis on the shape, the relationship of the LAA to the left superior pulmonary vein, length from the ostium to apex, number of lobes, angle of the fist bend formed by the primary lobe and the distance from the first bend to the LAA orifice. Based on these features, Wang et. described four classical structural morphologies accounting for the majority of anatomical variants seen.[2]

The “chicken wing” morphology describes an LAA with an obvious bend in the proximal or middle part of the dominant lobe. The “windsock” morphology describes an LAA in which one dominant lobe of sufficient length is the primary structure. A “cauliflower” LAA’s main characteristic is an LAA that has limited overall length with complex internal features. Finally, the “cactus” LAA has a dominant central lobe with secondary lobes extending from the central lobe in both superior and inferior directions.

The windsock is the most common morphology, representing 46.7% of 612 individuals scanned.[2] There is little data that explores the impact of demographic characteristics such as race or gender on the structural variations of the LAA.

In open cardiac procedures, such as coronary artery bypass grafts (CABG), the LAA is often isolated or ligated. This process is especially important in patients with a history of AF, as isolation and catheter ablation correlates with a decrease in AF recurrence and a reduction in stroke risk.[8] There are also several complications associated with the implantation of LAA exclusion devices for patients with AF. These include hematoma demonstrate associations with vascular access, air embolism related to device-delivery sheaths, and pericardial effusion associated with the transseptal puncture approach for device implantation.[9]

The LAA is implicated in the pathogenesis of several conditions, including AF and hypertension.

It is well established that the LAA is the primary site of thrombi formation in patients with nonvalvular AF.[2] Researchers postulate that the LAA is the source of thromboembolism in up to 90% of these patients.[10] Therefore, anticoagulation therapy and/or LAA occlusion systems are often used prophylactically to reduce stroke risk in these patients. Until recently, there has been little published data on the impact that LAA isolation has on the release of ANP. Several animal models demonstrated an immediate reduction in the immediate levels of ANP secretion following an atrial appendectomy.[5] However, these studies did not explore the long-term effects on ANP levels associated with the isolation of the LAA.

The 2018 LAA HOMEOSTASIS study was one of the first studies which examined the impact of epicardial and endocardial LAA occlusion techniques on neurohormonal modulation in humans. This study, consisting of 77 patients, found that after epicardial LAA closure, ANP and BNP levels decrease significantly immediately post-procedure, began to rise at 24 hours, and normalized at three months. In patients undergoing endocardial LAA device implantations, the ANP/BNP levels significantly increased post-procedure and normalized by three months. Of note, epicardial LAA devices were associated with a down-regulation of the adrenergic system and RAAS, resulting in a significant decrease in systolic blood pressure. No such effect was noted in endocardial device implantations.[11] Further studies are required to determine what effect, if any, these changes in neurohormonal regulation may have on outcomes or patient management.

 LAA morphology has demonstrated a correlation with the risk of stroke in patients with atrial fibrillation. A multicenter study found that in patients with AF, the cauliflower morphology was associated with the highest risk of stroke, while those with the chicken wing morphology had the lowest risk of stroke.[3] This consideration may be a valuable consideration when developing a more sophisticated risk assessment for the chronic management of individuals with AF.

There have also been reports of tears in the LAA associated with the blunt chest wall trauma from motor vehicle accidents. Despite being a rare complication, these injuries correlate with high morbidity and mortality. Approximately 10% of blunt trauma to the chest involves the LAA, and mortality estimates range between 50% to 80%.[12] There are multiple causes for cardiac rupture, ranging from simple blows to severe directional forces. The heart is particularly vulnerable as it hangs freely in the mediastinum, suspended by the great vessels between the sternum and thoracic vertebrae.[13] All chambers of the heart are susceptible to injury, but the LAA is particularly vulnerable to its relative thinness. The presence of an intact pericardium is a protective factor in these injuries—restricting the effects of tamponade, thereby preventing fatal exsanguination and allowing for patients to survive the journey to the hospital.[12]