Amiodarone/dobutamine/sotalol

Abstract

Various toxicity: case report A woman in her 50s developed supraventricular tachyarrhythmias and atrial flutter during treatment with dobutamine. She developed sinus bradycardia and dizziness during treatment with sotalol. Additionally, she developed hypothyroidism secondary to amiodarone [routes and times to reactions onsets; not all dosages and outcomes stated] The woman visited her general practitioner due to dry cough, understated pressure for her chest both in rest and activity and inadequate heart rate rise during activity. Her medical history was significant for migraines and slightly increased BP. She had been receiving candesartan cilexetil [candesartan]. She received unspecfieid steroids and unspecified beta-agonists on suspicion of obstructive pulmonary disease. However, after 2 weeks, no improvement was noted. Then, she was referred to hospital for further investigation. In subsequent outpatient hospital examination after 3 weeks, she was noted to have increased BP, sinus bradycardia and left branch block. Additionally, subclinical hypothyroidism was noted. On the following day, she was further investigated with stress echocardiography in the form of incremental increasing dobutamine infusion due to chest pain and left branch block. However, unsatisfactory sinus rate increased was noted. Subsequently, she received atropine. She developed atrial flutters with a rapid ventricular frequency of approximately 200 strokes/min. Later, dobutamine was stopped, and she received metoprolol. Eventually, ventricular frequency dropped to approximately 120 strokes/min. Then, she was electroconverted for 2 rounds. Eventually, her atrial flutter to stable sinus rhythm. Based on the findings, a diagnosis of dobutamine-associated supraventricular tachyarrhythmias and atrial flutter was made. She left the hospital with an increased dose of candesartan for increased BP. After 2 weeks, she was relapsed by rapid atrial flutter and was admitted. Then, she was electroconverted and received sotalol 80mg twice daily and rivaroxaban. She developed sotalol associated sinus bradycardia around 30 second/minute and dizziness. Therefore, sotalol was stopped. In the following weeks, she was admitted due to rapid atrial flutter and received electroconversion for 6 times. She was transferred to regional hospitals and treated with isthmus ablation. During the procedure, she developed transient sinus arrest and a total AV block, and the temporary pacemaker was added. This was later replaced by a permanent two-chamber pacemaker. Further, she was found to have heart failure NYHA II, which required several dose modifications. Subsequently, her heart failure worsen to heart failure NYHA III. Therefore, she received biventricular pacemakers. Eventually, she returned in NYHA Class II. Two weeks after changing the pacemaker, pulmonary hypertension was observed. She started receiving amiodarone 200mg daily. The dose of metoprolol was increased, and she received spironolactone. After further investigations, she was found to have cardiac sarcoidosis. Therefore, she underwent implantable cardioverter defibrillator as a preventive approach. She received prednisolone and amiodarone was discontinued. Further, she was admitted after 1 month due to ventricular tachycardia. Then, she started receiving amiodarone 200mg daily, and an improvement was noted. She received immuno-inhibiting therapy with methotrexate and infliximab. The dose of metoprolol was further increased. Candesartan was changed to sacubitril/valsartan. Later, prednisolone and infliximab were stopped. She developed a probable amiodaroneassociated clinical hypothyroidism, and received thyroxine substitution therapy.