The Influence of Electrical Cardioversion for Atrial Fibrillation on Left Atrial Appendage Function: A Transesophageal Echocardiography Study.
10.4070/kcj.1997.27.1.78
- Author:
Hyeon Woo KOH
;
Won Hoh KIM
;
Jae Ki KO
- Publication Type:Original Article
- Keywords:
Atrial fibrillation;
Electricial cardioversion;
Transesophageal echocardiography
- MeSH:
Atrial Appendage*;
Atrial Fibrillation*;
Echocardiography, Transesophageal*;
Electric Countershock*;
Heart Atria;
Humans;
Thromboembolism;
Thrombosis
- From:Korean Circulation Journal
1997;27(1):78-85
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: This study evaluates the change of the left atrial appendage function before and after electrical cardioversion to understand the mechanism involved in systemic thromboembolism of atrial fibrillation. BACKGROUND: Systemic thromboembolism associated with electrical cardioversion of atrial fibrillation is thought to originate from the left atrium or left atrial appendage, or both.However, the mechanism involved is poorly understood. METHOD: We studied left atrial appendage function funcction with transesophageal echocardiography in 15 patients with atrial fibrillation before and after successful electrical cardioversion. We measured left atrial appendage emptying and filling velocities and left atrial appendage areas. Also we analysed the characteristic Dopper flow pattern of LAA. RESULT: Left atrial appendage emptying velocities before cardioversion were greater in patients without(32.0+/-13.2cm/sec) than in those with(21.4+/-7.6cm/sec) spontaneous echo contrast(SEC). Furthermore emptying velocities after cardioversion were significantly reduced group with (21.4+/-7.6 vs 12.2+/-9.6, p<0.05) and the groupwithout(32.0+/-13.2 vs 18.1+/-10.2, p<0.05)SEC. CONCLUSION: After electrical cardioversion for atrial fibrillation left atrial appendage function is impaired. These observations suggest that stunned left atrial appendage after cardioversion may predispose to thrombus formation, which may play a role in the mechanism involved in the occurrence of thromboembolism after cardioversion.
