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.