Introduction

The left atrial appendage (LAA) is a unique structure that lies within the pericardium, close to the free wall of the left ventricle. It has unique developmental, ultrasound, and physiological characteristics that separate it from the left atrium proper.[1] In normal cardiac physiology, the LAA plays an essential role in the regulation of intravascular volume. The LAA also plays a vital role in the pathogenesis of transient ischemic attack (TIA) and stroke in patients with atrial fibrillation (AF).[2] 

Structure and Function

The LAA is often described as a small ear-shaped outpouching of the muscular wall of the left atrium. It lies anteriorly in the atrioventricular sulcus, close to the left circumflex artery, phrenic nerve, and pulmonary veins.[3][4] It is adjacent to the free wall of the left ventricle, thus, is closely associated with left ventricular function. Although several physiological variants exist, in most individuals, the LAA is a unilobar structure lying parallel to the left superior pulmonary vein. A structural analysis of the LAA using computerized tomography (CT) in 612 individuals suggested that, on average, the appendage is 46 mm long and has a volume of approximately 9 mL.[2]

In normal cardiac physiology, the LAA is an essential modulator of intravascular volume. In response to increased myocyte stretch, the LAA releases atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) into the coronary sinus. From here, these peptides enter the general circulation and regulate blood pressure and volume via their diuretic, natriuretic, and vasodilatory effects.[5]

The LAA is also implicated in the pathogenesis of strokes and arterio-occlusive events in patients with AF.

Embryology

The LAA develops during the fourth week of embryonic development as a remnant of the embryonic left atrium (LA), which forms during the third week of gestation.[1][6] This development contrasts with the rest of the LA cavity, which develops as an outgrowth of the pulmonary veins.[7]

Nerves

The left atrial appendage does not have significant nervous innervation.

Muscles

The left atrial appendage does not perfuse any muscles.

Physiologic Variants

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.

Surgical Considerations

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]

Clinical Significance

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]