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Bradycardia in sinus rhythm and corneal disturbances: case report A 54-year-old man developed bradycardia in sinus rhythm during treatment with amiodarone and bisoprolol, and corneal disturbances during treatment with amiodarone for heart failure [routes and duration of treatments to reactions onsets not stated]. The man presented to emergency department due to several month history of dyspnoea and reduced effort tolerance (current presentation). Three years prior to the current presentation, he had undergone implantable cardioverter-defibrillator (ICD) implantation for dilated cardiomyopathy with normal coronary arteries. After one year (2 years prior to the current presentation), he reported five accesses to the emergency department for persistent atrial fibrillation, which were treated with electrical cardioversions. At this time, he was suggested electrical insulation of pulmonary veins by radiofrequency ablation, but he denied. Therefore, he was started on slow release flecainide, substituted 12 months before the last access with amiodarone 200mg once daily due to clear contraindication, in absence of left ventricular reverse remodeling. His other medications included bisoprolol 5mg along with apixaban, ramipril and canrenone. His CHADS-VASC score was 2 (due to underlying hypertension and heart failure). Following the current presentation, examinations showed low ejection fraction of 35%. Despite the low ejection fraction, his medications were not titrated further because of bradycardia. An ECG showed atrial fibrillation with an average ventricular response of 130 beats/min. Device interrogation revealed high burden of atrial fibrillation during therapy with amiodarone, sometimes with high ventricular frequency for 9 months. Additionally, it was noted that at two instances, the device had delivered therapy with antitachycardia pacing (ATP) without inappropriate shocks. He was unable to tolerate higher doses of beta blocker(bisoprolol) due to bradycardia in sinus rhythm. Amiodarone therapy, which also shows some beta blocking effect, was also considered as a contributing agent in the development of bradycardia. However, he continued to refuse electrical insulation of pulmonary veins. As chest x-ray showed signs of heart failure, he was admitted to the department of cardiology. The man’s treatment was started with furosemide, which showed some improvement. After that, due to normal renal function and adequate BP of 120/75mmHg, his ongoing ramipril and canrenone therapies were stopped, and sacubitril/valsartan was started. He was explained the risk of bradycardia, and was suggested a device upgrade to a dual-chamber anti-bradycardia (DDD) pacing, but he refused. Three days later, he was discharged in atrial fibrillation with an average ventricular frequency of 90 bpm. During follow-up examination after 1 month, subjective improvement was noted in his condition. Subsequently, during an ophthalmologic evaluation, development of amiodarone therapy related corneal disturbances was noted. Therefore, his amiodaron