Case Presentation
A 60-year-old Caucasian male with a past medical history of hypertension and hyperlipidemia was found to have atrial fibrillation (afib) on ECG during a routine annual exam. Metoprolol was initiated, and he was advised to hold lisinopril by his provider. Two weeks later, the patient was evaluated in our electrophysiology clinic and found to be in persistent afib (Figure 1). Salient laboratory data included serum creatinine of 1.6 mg/d, serum potassium of 6.1 mEq/L and NT proBNP of 1951 pg/mL (normal < 77). Chest X-ray revealed biatrial enlargement. A transthoracic echocardiogram (TTE) showed a structurally normal heart with an ejection fraction (EF) of 70%, biatrial enlargement, and no hemodynamically significant valvular disease. 24-hour Holter showed continuous atrial fibrillation. He was started on Apixaban 5 mg bid and referred for outpatient cardioversion with a plan to initiate antiarrhythmic drug therapy post-cardioversion. At presentation for cardioversion he had taken 3 doses of Apixaban. Transesophageal echocardiography (TEE) was performed to rule out left atrial appendage thrombus. The left atrium (LA) was severely enlarged, and the LA appendage was dilated along with an elongated large accessory lobe directed upwards (Figure 2A & 2B). Spontaneous echo contrast was identified in LA, and LA appendage and appendage body (Figure 2C) and accessory lobe velocities (Figure 2D) were mildly reduced. However, no thrombus was present ((Figure 2A & 2B), Video 1). The right atrium (RA) was severely enlarged without RA appendage thrombus. Left ventricular (LV) function was normal, and the right ventricular chamber was mild-moderately enlarged with normal systolic function. There was mild mitral regurgitation. Due to the presence of significant LA enlargement, spontaneous contrast in the dilated LA appendage, brief duration of anticoagulant therapy, unknown duration of afib, and the phenomenon of post-cardioversion LA stunning, the TEE probe was left in the esophagus during DC cardioversion to evaluate LA appendage post cardioversion. Patient converted successfully to sinus rhythm after a single 200 joule shock. Post-cardioversion ECG showed sinus rhythm (Figure 3).
Immediately after cardioversion, a further increase in spontaneous contrast was noted in the LA appendage, along with the progressive development of a thrombus in the accessory lobe of the left atrial appendage on TEE (Figures 4 A-D & video 2). Marked reduction in velocities of the main body of the LA appendage and the accessory lobe was observed (Figures 4, E & F). Injection of image-enhancing agent Lumason showed a filling defect in the LA appendage accessory lobe, followed by the uptake of contrast by the thrombus (Figure 5, A-C).
Due to the development of LA appendage thrombus on anticoagulation, the patient was hospitalized, subcutaneous Enoxaparin 100 mg twice daily was started along with Flecainide 100 mg twice daily, and Apixaban was discontinued. The patient’s hospital course was uncomplicated. Telemetry revealed sinus bradycardia with intermittent 1st-degree AV block with a heart rate range of 49-68 bpm. Lab results were significant for an elevated creatinine level of 1.43 mg/dL and a blood urea nitrogen level of 25.3 mg/dL. The patient was discharged on Enoxaparin 1 mg/kg for two weeks, followed by apixaban 5 mg once daily for four weeks. A follow-up appointment in the outpatient cardiology clinic was scheduled six weeks later. The patient was advised to continue his Flecainide until re-evaluation in the clinic.