Right atrial thrombi and depressed right atrial appendage function after cardioversion of atrial fibrillation

Background: It has been, shown that cardioversion of atrial fibrillation ma y result in, left atrial chamber and appendage dysfunction and cause new th rombi in the left atrium. The aim of this prospective study was to investig ate right atrial appendage function and assess the incidence of new right a trial thrombi after electrical cardioversion. Methods: Transthoracic echoca rdiography was performed in 25 patients 4 h before and at 24 h and 7 days a fter electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical card ioversion, n = 9), as assessed by peak A wave velocities derived from the t ranstricuspid and transmitral velocity profiles. In addition, transesophage al echocardiography was performed 4 h before and 24 h after cardioversion t o evaluate postcardioversion thrombus formation in the right and Left atria l chambers and to assess right and left atrial appendage function. The degr ee of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. Results: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 /- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0. 15 vs 0.4 +/-: 0. 15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the Left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardio version. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m /sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective va lues for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0 .16 m/sec (P = 0. 009). No thrombi were found in either the right or Left a trium before cardioversion. In two patients, new thrombi in the right atriu m were detected 24 h after internal atrial defibrillation. Thrombi were loc ated at the superior rim of the fossa ovalis in both patients with patent f oramen ovale. Another patient had developed a thrombus in the left atrial a ppendage. Conclusions: Electrical cardioversion may not only cause left atr ial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thr ombi in the body of the right atrium.