Case report
A 79-year-old male was referred to our hospital because of dyspnea on
exertion in May 2019. His CHA2DS2-VASc
score was 3 points and he had moderate aortic valve stenosis. AF was
found on 12-lead electrocardiography. We performed a radiofrequency
catheter ablation with pulmonary vein isolation and cavo-tricuspid
isthmus ablation in May 2019. AF recurred at 4 months post ablation.
After confirming there was no thrombus in the left atrial appendage by
transesophageal echocardiography, we performed a second AF ablation in
November 2019.
The patient had been taking apixaban 5 mg twice daily before the
procedure. On the day of the procedure,
the
morning dose
was
withheld and the evening dose was administered.
The procedure was performed under intravenous conscious sedation with
dexmedetomidine and fentanyl. Electrophysiological studies and catheter
ablation were performed using an electro-anatomical mapping catheter
(Rhythmia™, Boston Scientific, Boston MA, USA) and an open-irrigated
linear ablation catheter with a 3.5-mm tip (INTELLATIP MiFi™, Boston
Scientific).
The cardiac rhythm at the beginning of the procedure was atrial
tachycardia, and electrophysiological study revealed that the atrial
tachycardia was perimitral flutter. Ablation creating left atrial
anterior line changed perimitral flutter into biatrial tachycardia.
After that, lateral mitral isthmus linear ablation including both
endocardial and epicardial radiofrequency application terminated the
biatrial tachycardia.
After linear ablation of the left atrium, no atrial tachyarrhythmia was
induced by atrial burst stimuli. Reconnections of the pulmonary vein and
cavo-tricuspid isthmus were not found. In this case, the body mass index
was high and glossoptosis with conscious sedation tended to occur
irrespective of using noninvasive positive pressure ventilation. The
procedural time was 209 minutes. We used heparin and set target
activated clotting time at 300 s during the procedure (Figure 1).
Baseline and procedural characteristics of the patient are shown in
Table 1.
The patient was asymptomatic until visual loss in the left eye occurred
3.5 h after the procedure. Eyesight in the left lower quadrant was
limited to counting fingers, and eyesight in the rest of the left eye
was light perception only. There was no identifiable ischemic stroke or
hemorrhage which caused visual loss on brain computed tomography or
magnetic resonance imaging. We consulted with ophthalmology. A fundus
examination revealed a cherry red spot in the left eye and he was
diagnosed with CRAO (Figure 2).
Ocular massage was performed, and nitroglycerine and 5000 units of
heparin sodium were infused. However, eyesight did not improve. An
infusion of 10 µg/h of alprostadil was also initiated 4 h after the
symptoms onset, and continued for 3 d. Carotid artery ultrasound
performed on the day after the procedure showed no mobile plaque.
Although peripheral vision was improved, central visual field loss of
the left eye persisted. Because the patient needed physical therapy, he
was discharged 8 d after the procedure.