Left atrial appendage: structure, function, and role in thromboembolism

Abstract

The left atrial appendage (LAA) is derived from the left wall of the primary atrium, which forms during the fourth week of embryonic development. It has developmental, ultrastructural, and physiological characteristics distinct from the left atrium proper. The LAA lies within the confines of the pericardium in close relation to the free wall of the left ventricle and thus its emptying and filling may be significantly aVected by left ventricular function. The physiological properties and anatomical relations of the LAA render it ideally suited to function as a decompression chamber during left ventricular systole and during other periods when left atrial pressure is high. These properties include the position of the LAA high in the body of the left atrium; the increased distensibility of the LAA compared with the left atrium proper; the high concentration of atrial natriuretic factor (ANF) granules contained within the LAA; and the neuronal configuration of the LAA. Thrombus has a predilection to form in the LAA in patients with atrial fibrillation, mitral valve disease, and other conditions. The pathogenesis has not been fully elucidated; however, relative stasis which occurs in the appendage owing to its shape and the trabeculations within it is thought to play a major role. Obliteration or amputation of the LAA may help to reduce the risk of thromboembolism, but this may result in undesirable physiological sequelae such as reduced atrial compliance and a reduced capacity for ANF secretion in response to pressure and volume overload.

The value of left atrial strain and strain rate in predicting left atrial appendage stasis in patients with nonvalvular atrial fibrillation

“…LAA develops as a residue originating from LA at 4 weeks of embryonic development. Although the ultrastructural and physiological characteristics of LAA develop independently from LA in this process, muscle cell structures and the myocardium of both structures are similar [22]. Thus, as a component of LA, LAA functions are thought to be reflected by LA structural and functional parameters.…”

“…In healthy individuals, the highly dynamic LA and LAA structure prevents stasis. In case of its dysfunction, SEC and/ or thrombus formation may develop in association with increased stasis [22,23]. LAA develops as a residue originating from LA at 4 weeks of embryonic development.…”

Association Between Left Atrial Appendage Morphology Evaluated by Trans-Esophageal Echocardiography and Ischemic Cerebral Stroke in Patients With Atrial Fibrillation

“…3,4) As the LAA represents one of the major sources of cardiac thrombus formation responsible for stroke in patients with AF, 5,6) the imaging of the different structures and lobes is of utmost importance to diagnose the presence of thrombus, especially in patients with non-valvular AF. 7,8) Multidetector computed tomography 9) and contrast-enhanced magnetic resonance imaging 10) are able to image the LAA; however, it was concluded that magnetic resonance imaging lacks diagnostic accuracy for the detection of LAA thrombi.10) Transesophageal echocardiography (TEE) is the gold standard to detect LAA thrombus, 11) but false positive results still occur.12) In this study, we evaluated the LAA structure and functions by TEE in patients with non-valvular AF (both chronic and paroxysmal types) to study the possible association between the different LAA morphologies and functional changes with the patients' history of ischemic cerebral stroke. …”

Technological Improvements in Cardiac Thrombus Diagnosis

“…The left atrium (LA) and the LAA are important locations that are frequently associated with thrombus formation and subsequent cardioembolic events, particularly in association with dysrhythmias, such as AF [20,21]. An estimated 47% of thrombi in valvular AF and 91% of those in nonvalvular AF are located in the LAA [22].…”