LEFT ATRIAL APPENDAGE FUNCTION DETERMINED BY TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN PATIENTS WITH RHEUMATIC MITRAL-VALVE DISEASE

Citation
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
Citations number
24
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086312
Volume
85
Issue
2
Year of publication
1994
Pages
121 - 128
Database
ISI
SICI code
0008-6312(1994)85:2<121:LAAFDB>2.0.ZU;2-Y
Abstract
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.