A Clinical Case of Cordarone-Induced Thyrotoxicosis in a Patient With Paroxysm of Ciliary Arythmia

Abstract

Objective. To discuss the clinical study of the development of cordarone-associated thyrotoxicosis. Results and discussion. The female patient D., born in 1956, had been under observation since 2007 on ciliary arythmia and artery hypertension. Sinus rhythm (SR) was restored and maintained by the application of cordarone. In March 2010 due to recrudescence the patient was hospitalized into the Department of Immunopathology and Allergology, Republican Research Center for Radiation Medicine and Human Ecology. After the clinical examination she was diagnosed with «cordarone-induced» thyrotoxicosis, probably, of type 2. It was recommended to stop using cordarone. Thyrotoxicosis was managed with methylprednisolone, and antiarythmic therapy was conducted with sotalex, propranolol, propafenone, strofantine (with no effect), also electropulse therapy was provided (rhythm was restored). To administer supporting antiarythmic therapy, it was recommended to take alapenin and bisoprolol. In the sequel, the patient revealed euthyroidism, the level of thyroidal hormones was at a norm. However, later there were frequent paroxysms of atrium fibrillation, short-term paroxysm of ventricular tachycardia. The patient was sent to have a consultation at the Laboratory for Heart Rhythm Disturbances of the Republican Research Center «Cardiology». Conclusion. Thus, the above-mentioned clinical observation makes it possible to draw a conclusion that long-term intake of cordarone can change metabolism of thyroidal hormones and, possibly, the electrophysiological properties of heart.