Manifestation of latent Graves’ disease in patient with paroxysmalform of atrial fibrillation

Introduction. Thyroid dysfunction often develops in cardiac patients received amiodarone (up to 20 % of cases) and is an important clinical problem. Amiodarone-induced thyrotoxicosis type 1 develops in conditions of thyroid diseases (Graves' disease, nodular goiter). Amiodarone-induced thyrotoxicosis type 2 develops without any thyroid disease. Differential diagnosis and treatment of thyrotoxic syndrome in such patients is a complex clinical task. Patient T., 56 years old, entered the clinic of the Research Institute of Cardiovascular Diseases with complaints of frequent paroxysms of atrial fibrillation, periodic increases in blood pressure, increased fatigue in normal physical activity, trembling in the hands. It is known that the patient has a multinodular goiter in her anamnesis. Paroxysms of atrial fibrillation were stopped by intravenous administration of amiodarone in a hospital. At the time of admission to the cardiology department, the level of thyroid-stimulating hormone is reduced to 0.011 mlU/l, the detection of antibodies to the thyroid-stimulating hormone receptor (30.4 IU/L), the increase in free triiodothyronine and thyroxine levels. Objectively, the patient showed an increase in the thyroid gland (volume by the results of ultrasound of 29 cm³) and manifestations of Graves’ ophthalmopathy (bilateral periorbital edema). Thus, the manifestation of Graves’ disease due to the amiodarone administration is not in doubt. The sinus rhythm was restored on therapy with thyreostatics and beta-blockers. Conclusion. Thyrotoxic syndrome is a frequent cause of atrial fibrillation, therefore before the appointment of antiarrhythmic therapy, it is recommended to determine the level of TSH and the volume of the thyroid gland.

amiodarone-induced thyrotoxicosis, Graves’ disease, atrial fibrillation, amiodarone

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