Role of left atrial appendageobliteration in stroke reductionin patients with mitral valve prosthesis

Left atrial appendage obliteration was historically ineffective for the prevention of postoperative stroke in patients with rheumatic atrial fibrillation who underwent operative mitral valvotomy. It is, however, a routine part of modern "curative" operations for nonrheumatic atrial fibrillation, such as the maze and corridor procedures. To assess the potential of left atrial appendage obliteration to prevent stroke in nonrheumatic atrial fibrillation patients, we reviewed previous reports that identified the etiology of atrial fibrillation and evaluated the presence and location of left atrial thrombus by transesophageal echocardiography, autopsy, or operation. Twenty-three separate studies were reviewed, and 446 of 3,504 (13%) rheumatic atrial fibrillation patients, and 222 of 1,288 (17%) nonrheumatic atrial fibrillation patients had a documented left atrial thrombus. Anticoagulation status was variable and not controlled for. Thrombi were localized to, or were present in the left atrial appendage and extended into the left atrial cavity in 254 of 446 (57%) of patients with rheumatic atrial fibrillation. In contrast, 201 of 222 (91%) of nonrheumatic atrial fibrillation-related left atrial thrombi were isolated to, or originated in the left atrial appendage (p < 0.0001). These data suggest that left atrial appendage obliteration is a strategy of potential value for stroke prophylaxis in nonrheumatic atrial fibrillation.

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 affected 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 aim of this study was to determine the relations between spontaneous echo contrast, left atrial appendage blood flow velocity and thromboembolism. Left atrial thrombus and spontaneous echo contrast, a putative marker of thromboembolic risk, are frequently located in the left atrial appendage. Measurement of left atrial appendage outflow Doppler velocity by transesophageal echocardiography is a recent technique for assessment of left atrial appendage function, which may be important in thrombus formation. Transthoracic and transesophageal echocardiographic studies were performed in 140 patients with atrial fibrillation (chronic in 80 patients, paroxysmal in 50 patients, first episode < 2 weeks in 10 patients). The left atrium and appendage were inspected for thrombus and spontaneous echo contrast, which was graded from 0 (none) to 4+ (severe). Outflow velocity profiles were obtained by pulsed wave Doppler at the orifice of the left atrial appendage. Left atrial spontaneous echo contrast was present in 78 patients (56%). In multivariate logistic regression analysis, spontaneous echo contrast was the only significant correlate of left atrial thrombus and was present in 14 (93%) of 15 patients. Spontaneous echo contrast and age were associated positively, and anticoagulant therapy was associated negatively, with previous thromboembolic events. Increasing grades of spontaneous echo contrast were associated with decreasing left atrial appendage blood velocity. The velocity in patients with thrombus was not significantly different from that in patients with 4+ spontaneous echo contrast. In multivariate linear regression analysis, the grade of spontaneous echo contrast was significantly and negatively associated with left atrial appendage velocity (p = -0.0001) and mitral regurgitation (p = -0.0002) and significantly and positively associated with left atrial area (p = 0.0005). The odds ratio for spontaneous echo contrast was 28:1 for low left atrial appendage blood flow velocity (< 35 cm/s) and 96:1 for low velocity and the absence of mitral regurgitation. Spontaneous echo contrast is the cardiac factor most strongly associated with left atrial appendage thrombus and embolic events. Spontaneous echo contrast formation is promoted by reduced blood flow velocity and increased left atrial size but is diminished by mitral regurgitation.