Endocrine Abstracts

Introduction: Thyrotoxic cardiomyopathy is a rare but potentially fatal form of dilated cardiomyopathy caused by hyperthyroidism not timely diagnosed or inadequately treated. The first-line treatment is a treatment of the underlying thyroid disease as the structural and functional cardiac alterations are potentially reversible after achieving a euthyroid state.

Case presentation: A 41-year-old man was admitted to hospital due to the symptoms of heart failure and tachycardic atrial fibrillation. He complained of dyspnea, peripheral edema, and palpitations. Before admission, he had been treated for thyrotoxicosis caused by Graves’ disease in another country for seven months. Initially, he was given tiamazole, but it was replaced by propylthiouracil due to an allergic reaction (skin rash). Additionally, he had undergone electrocardioversion three times in the past six months, including the period of current hospitalization, to treat his tachycardic atrial fibrillation. His blood test results were as follows: TSH <0.01 mIU/l, FT4 3.71 pmol/l, FT3 – 7.8 pmol/l. His TRAb level was 13.03 IU/l and his NT-proBNP level was 2444 pg/ml . Echocardiography revealed a dilation of the left heart chambers. The global contractile ability of the left ventricle was moderately reduced, with an ejection fraction (Simpson method) of 35%. Additionally, global hypokinesia of all segments, moderately severe mitral regurgitation, and a diastolic dysfunction were observed. As other causes of cardiac dysfunction had been ruled out, his heart condition was concluded to be a consequence of unsatisfactory treatment of his thyroid disease. Therefore, his thyrostatic therapy was adjusted and the standard-of-care treatment for heart failure was initiated. He was also referred to the Multidisciplinary team for thyroid diseases, and it was decided that he would undergo a total thyroidectomy once his cardiac and thyroid status had stabilized. Four months later, a follow-up echocardiography showed that the global contractile ability of the left ventricle had improved significantly, with an ejection fraction (Simpson method) of 64%. There were no more signs of global hypokinesia. Due to the patient’s suppressed TSH levels with normal FT3 and FT4 levels, it was decided to administer Lugol’s Iodine solution prior to the total thyroidectomy, to achieve a preoperative euthyroid state. The total thyroidectomy procedure was successfully performed, and the patient was discharged as fully recovered. The patient’s follow-up visits with a cardiologist and an endocrinologist are scheduled.

Conclusions: Hyperthyroidism should be considered as an etiological factor for dilated cardiomyopathy in the absence of other causes of structural and functional cardiac alterations.