Abstract
We present a case of congestive heart failure with reduced ejection fraction complicated by atrial tachycardia and an oral anticoagulation-resistant left atrial appendage (LAA) thrombus. The LAA thrombus prevented sinus rhythm restoration, and the ventricular rate control was also difficult. Cardiac resynchronization therapy (CRT)-defibrillator implantation followed by atrioventricular nodal ablation was performed, and the patient’s congestive heart failure improved. Furthermore, the resolution of the LAA thrombus was achieved three months after the implantation. The atrial tachycardia was eliminated by catheter ablation thereafter. This case highlights the importance of improving congestive heart failure for the resolution of LAA thrombus and the potential usefulness of CRT with atrioventricular nodal ablation for this strategy.
Learning objective
Treatment strategies for patients with decompensated congestive heart failure are difficult, especially when complicated by atrial tachyarrhythmia and left atrial thrombus. Cardiac resynchronization therapy with atrioventricular nodal ablation may be a possible solution not only for the improvement of heart failure but also for the resolution of left atrial thrombus.
Introduction
Atrial fibrillation (AF) ablation for patients with heart failure with reduced ejection fraction is an established management strategy for congestive heart failure (CHF) [ ]. However, catheter ablation for AF or atrial tachycardia (AT) is contraindicated when complicated by left atrial thrombus. Resolution of left atrial thrombus can usually be achieved by initiating or intensifying anticoagulation therapy. If anticoagulation therapy fails to resolve the thrombus, there is no established therapy to overcome the situation.
Here, we propose cardiac resynchronization therapy (CRT) with atrioventricular nodal ablation (AVNA) as an alternative strategy for this situation. This strategy can establish prompt ventricular rate control regardless of the persistence of atrial tachyarrhythmia. Furthermore, these strategies may also contribute to the resolution of left atrial appendage (LAA) thrombus.
Case report
A 75-year-old man with CHF and AT with rapid ventricular response was referred to our hospital. He had a history of mitral valvuloplasty and maze surgery via vertical atriotomy for mitral regurgitation 11 years before, followed by mitral valve replacement via transseptal approach 4 years previously. On admission, he was administered 2.5 mg/day of bisoprolol fumarate, 0.0625 mg/day of digoxin, 40 mg/day of furosemide, and 5.5 mg/day of warfarin for the management of CHF and anticoagulation. His left ventricular ejection fraction (LVEF) decreased to 20 % ( Video 1 ), and his electrocardiogram showed AT with 2:1 atrioventricular conduction and complete left bundle branch block (CLBBB, Fig. 1 A). His N-terminal-pro-B-type natriuretic peptide (NT-proBNP) concentration was elevated to 4094 pg/mL, and prominent pulmonary congestion and pleural effusion were observed on chest X-ray ( Fig. 1 B).
As his LVEF was maintained at 44 % in sinus rhythm two years previously, despite the presence of CLBBB, we suspected that the AT was the main cause of his CHF. He had undergone extracardiac cardioversion for the AT two months prior to the referral. Before the cardioversion, the absence of LAA thrombus was confirmed on contrast-enhanced computed tomography (CECT). At that time, his prothrombin time-international normalized ratio (PT-INR) was 2.23 on 6 mg/day of warfarin. Because the AT had recurred on referral, we decided to perform catheter ablation for the AT. However, despite a PT-INR of 2.75, pre-ablation CECT and transesophageal echocardiography (TEE) showed LAA thrombus and severely decreased LAA blood flow velocity ( Fig. 1 C–E, Video 2 ).
We postponed the ablation and started the medical therapy for CHF. However, 1:1 atrioventricular conduction occurred after starting dobutamine infusion, possibly due to the positive dromotropic effect. The AT returned to 2:1 conduction after the withdrawal of dobutamine; however, further ventricular rate control by using antiarrhythmic drugs could pose a risk of worsening CHF. Cardioversion was also difficult due to the LAA thrombus. We suspected that the worsening CHF was the cause of the LAA thrombus formation and considered that improvement in CHF might resolve the thrombus. Therefore, we performed cardiac resynchronization therapy-defibrillator (CRT-D) implantation and AVNA. Following the improvement in his CHF, he was discharged on day 17. Atrial anti-tachycardia pacing was not activated to avoid inadvertent sinus rhythm conversion.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
