Atrial fibrillation (AF) is the most common cardiac arrhythmia, which has reached the dimension of a 21st-century cardiovascular disease epidemic.1 While rate control in AF is a commonly used strategy, rhythm control with antiarrhythmic drugs or external electrical cardioversion (ECV) is frequently performed before more invasive catheter-based treatment options.

Primary AF and its commonly associated arrhythmia atrial flutter (AFL) often present with left ventricular (LV) dysfunction, valve regurgitation, and/or pulmonary hypertension related to tachycardia-induced cardiac dysfunction. This diagnosis is often made after LV function and valve regurgitation improve or normalize post-ECV, during follow-up. Atrial fibrillation also frequently develops as a manifestation of underlying structural heart disease; however, the rapid heart rate associated with AF makes assessment of underlying structural heart disease difficult by both transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE). In patients with cardiac or suspected valvular dysfunction, postcardioversion TTE is often performed to evaluate the effect of attaining sinus rhythm on cardiac function and to assess for the presence and severity of underlying structural heart disease. However, this leads to time delay, besides requiring another TTE as well as patient follow-up. Moreover, some patients may get lost to follow-up, leading to missed opportunities in reevaluating cardiac and valve function post-ECV.

The presence of spontaneous echo contrast (SEC) associated with marked atrial enlargement, atrial and LV dysfunction, dilated appendage, stenotic mitral valve lesions, and short duration of anticoagulation therapy—common since the advent of direct oral anticoagulants (DOACs)—increase the risk of atrial thrombus formation. There is increased atrial stunning post-ECV associated with an increase in SEC in the left atrium (LA) and the left atrial (LA) appendage (LAA) along with sludge formation in the LAA post-ECV,2, 3, 4 which may occasionally cause thrombus formation immediately post-ECV.5 Left atrial stunning may also cause electromechanical (EM) dissociation from lack of atrial contractile function and reduced cardiac output.

Transesophageal echocardiography is routinely used pre-ECV to shorten anticoagulation duration and facilitate early cardioversion by excluding LA and LAA thrombus.6 Transesophageal echocardiography is also used when there is uncertainty about compliance with anticoagulation or in high-risk patients, such as patients with cardiac amyloidosis, hypertrophic cardiomyopathy, mitral stenosis, and advanced LV dysfunction. According to American Heart Association–American College of Cardiology guidelines, patients with new-onset AF or AFL of 48 hours duration or longer are at risk of developing LA thrombus and should undergo TEE before ECV.

Besides excluding LAA thrombus, TEE is an ideal technique to evaluate LV and right ventricular (RV) function and valvular heart disease and can be very useful immediately post-ECV during normal sinus rhythm (NSR) when such assessment would be clinically useful. Its utility in the assessment of atrial stunning by LAA Doppler velocities and LA EM coupling during ECV has been examined in earlier small research studies.2, 3, 4 However, the safety and usefulness of keeping the TEE probe in situ during ECV to investigate immediate functional changes of ventricles and cardiac valves in routine clinical practice has not been addressed before. The purpose of this study was to determine whether using TEE before and immediately after ECV with the probe in situ during the procedure is safe and whether it provides clinically useful information with potential diagnostic and therapeutic influence on the clinical management of patients after restoration of NSR. Our primary aim in this retrospective study was to examine the effect of ECV on cardiac function in patients with baseline LV dysfunction (without prior TTE or known cardiac history), presence of clinically significant mitral or tricuspid regurgitation (MR or TR), presence of adverse appendage anatomy or presence of increased SEC or reduced appendage velocities, unknown or insufficient duration of anticoagulation therapy, or underlying regurgitant or stenotic structural heart disease on pre-ECV TEE that could be more comprehensively evaluated in the presence of NSR.