13th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 1998

January 24-31, 1998
Marilleva, Trento, Italy

RT-139

Atrial contractility recovery after transthoracic cardioversion (TC) of atrial fibrillation: possible role of permanent atrial pacing

Pietro Broglia, Maddalena Lettino, Stefano Perlini, Marco Ferrario, Andrea Finzi, Salvatore Romano.
Division of Cardiology, Maggiore Hospital IRCCS, Milan, Italy

Introduction

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice, with an overall prevalence increasing with age (0.5% in patients younger than 60 years and 8.8% above 80 years)¹.

The main therapeutical objectives are to restore sinus rhythm, to control the ventricular response, and to prevent thromboembolic complications. The latter is particularly relevant, since it has been shown that cerebrovascular accidents are 6-fold higher in AF patients^1-3.

Thrombus formation in the fibrillating left atrium is very likely due to blood stasis into the atrium and the appendage (according to Virchow's theory), owing to the loss of a coordinate electrical and mechanical atrial activity⁴.

Echocardiography, particularly with the transesophageal approach (TEE), is often used to exclude the presence of thrombi in the atrial cavities before elective cardioversion, even after a prolonged and effective anticoagulant therapy.

However, cardioversion itself may transiently increase the thromboembolic risk despite exclusion of a left atrial appendage thrombus before the procedure^5,6, and TEE data have documented the appearance of new and/or more pronounced spontaneous left atrial contrast during electrical cardioversion⁷. The presence of "atrial stunning" following sinus rhythm restoration (ie the absence of atrial contractile function despite evidence of a coordinate electrical activity) may further increase the thromboembolic risk after a successful cardioversion. Accordingly, anticoagulant therapy is recommended for at least 4 weeks following sinus rhythm restoration⁸.

Even though several clinical factors such as patient's age⁶, left atrial size^6,8, associated cardiovascular disease⁸, AF duration⁹, mode of cardioversion, and myocardial depressant effects of antiarrthythmic drugs¹⁰ could play a role in atrial mechanical dysfunction after cardioversion, the effects of these variables have not been adequately assessed. Electrical cardioversion has been shown to be associated with a longer duration and greater extent of left atrial mechanical dysfunction compared to pharmacological or spontaneous cardioversion¹⁰, possibly due to myocardial injury. The negative inotropic effects of some antiarrhythmic agents have been postulated to delay the recovery of atrial contractile function after cardioversion, as shown in a recent study in patients treated with sotalol¹¹. However, beyond a possible negative inotropic effect on the "stunned" atrial myocardium, sotalol clearly affects heart rate after cardioversion. To our knowledge, no study has addressed the possible role of heart rate after sinus rhythm restoration, an aspect that may be relevant to the recovery of left atrial contractile activity. The hypothesis of the present prospective study was to assess whether an higher heart rate after cardioversion may per se influence the recovery of atrial contractile activity. In the preliminary study, since the presence of a permanent atrial pacemaker (PM) offers the unique possibility of modulating heart rate without interfering with drug therapy, PM patients were paced at 80 beats/min immediately after electrical cardioversion, and the recovery of atrial contractile function was compared with a matched group of patients in spontaneous sinus rhythm.