Case report
Akita University’s Ethics Committee does not need to approve anonymized observational research. The patient provided informed consent for publication of his data.
A 64-year-old man was transferred to our hospital after being diagnosed with ATAAD. His vital signs were stable under administration of nicardipine and the echocardiography findings were unremarkable. We performed emergency total arch repair with frozen elephant trunk. Cardiopulmonary bypass (CPB) was established with bicaval drainage and left subclavian artery perfusion. We always perform antegrade infusion for cardioplegia from the ascending aorta and retrograde infusion from the coronary sinus, inserting the cannula from the right atrial appendage. We always use a self-inflating retrograde cannula (RC014T® 14Fr, Edwards Lifesciences Corp, One Edwards Way, Irvine, USA). The cannula insertion for retrograde cardioplegia was smooth. Upon infusion, the injection pressure rose to about 70 mm Hg, but it was momentarily; hence, we continued the infusion after the pressure dropped to approximately 30 mmHg, and cardiac arrest was induced. At CPB weaning, transesophageal echocardiography (TEE) showed a multivesicular space on the back of the left atrium that had no significant fistula with the left atrium (Fig. 1A,B). As the patient’s vital signs were not affected, he was transferred to the intensive care unit after the operation. Follow-up TEE again showed a space on the back of the left atrium, which at that time obstructed the left ventricle inflow. Enhanced computed tomography (CT) revealed a non-enhanced space on the back of the left atrium (Fig. 1C). We established the diagnosis of LAD. Because there was no connection between the LAD cavity and the left atrium on CT, we did not administer anticoagulant drugs to prevent expansion of the LAD cavity. However, the patient developed atrial fibrillation (AF) and his hemodynamics deteriorated. We considered that the LAD stimulated the left atrium and triggered AF. Therefore, we administered a beta-blocker (under intubation, landiolol hydrochloride was administered intravenously at 0–5 μg/kg/min, while after extubation, bisoprolol fumarate was given orally at a dose of 1.25–7.5 mg; the dose at discharge was 1.25 mg) and amiodarone, which successfully managed the AF, and the patient’s hemodynamics improved.
The patient was extubated on postoperative day (POD) 5. Amiodarone administration was discontinued on POD 29, and he was started on anticoagulation therapy with a direct oral anticoagulant. We used warfarin potassium, with the dose adjusted so that the INR was approximately 2. There was residual paroxysmal AF rhythm, but the patient was hemodynamically stable. Follow-up enhanced CT performed on POD 37 showed LAD reduction (Fig. 2). The patient was discharged on POD 40.