Jj. Hwang et al., LEFT ATRIAL APPENDAGE FUNCTION DETERMINED BY TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN PATIENTS WITH RHEUMATIC MITRAL-VALVE DISEASE, Cardiology, 85(2), 1994, pp. 121-128
Left atrial thrombi have been considered to be the major source of sys
temic arterial embolization in patients with rheumatic mitral valve di
sease. Almost half of the left atrial thrombi are found in the left at
rial appendage (LAA). To investigate LAA size and LAA contractile func
tion in patients with rheumatic mitral valve disease, transesophageal
echocardiographic and Doppler studies were performed in 61 patients. A
mong them, 46 patients were in atrial fibrillation (group 1), while th
e other 15 were in sinus rhythm (group 2). Thirty-six patients with no
nrheumatic atrial fibrillation were chosen as control to group 1. Anot
her 22 patients with various cardiovascular diseases and sinus rhythm
served as control to group 2. When compared to the patients with nonrh
eumatic atrial fibrillation (control group), group 1 patients tended t
o have a larger LAA maximal area (9.7 +/- 5.2 vs. 5.9 +/- 2.8 cm(2); p
< 0.001). LAA ejection fraction and LAA peak emptying velocity were a
lso lower. A significantly higher incidence of LAA spontaneous echo co
ntrast (SEC) and thrombus formation was also found in these patients.
Group 2 patients were also found to have a larger LAA maximal area whe
n compared to the control group (8.8 +/- 3.7 vs. 5.2 +/- 3.0 cm(2); p
< 0.001). LAA ejection fraction and LAA peak emptying velocity were lo
wer in this group, too. A higher incidence of LAA SEC formation was fo
und in these patients with rheumatic mitral valve disease (4/15 vs. 0/
22; p = 0.021). There was no significant difference, however, in LAA t
hrombus formation between group 2 and its control group (1/15 vs. 1/22
; p = NS). Thus, patients with rheumatic mitral valve disease tend to
have larger LAA size and poorer LAA contractile function. These promot
e the formation of LAA SEC and thrombus, especially when the patients
have atrial fibrillation. Whether the poor LAA function predisposes th
ese patients to future systemic arterial embolization still needs furt
her investigation.