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.