OBJECTIVE: To review cardiac manifestations in the syndrome of resistance to 
thyroid hormone (RTH) and to question the general recommendation that the 
thyroid-stimulating hormone (TSH) value be the guide to thyroid hormone 
replacement.
METHODS: The syndrome of RTH is caused by mutations in the carboxy-terminal 
portion of the β isoform of the thyroid hormone receptor, resulting in variable 
clinical manifestations. It is generally recommended that the replacement of 
thyroid hormone in patients with RTH be guided by the serum TSH concentration. 
The variable responsiveness of tissues to thyroid hormone, however, makes it 
difficult to balance the correct replacement dose. We present a case that brings 
into question the conventional wisdom about the replacement dose of thyroid 
hormone in this scenario, and we review the pertinent literature.
RESULTS: A 54-year-old man with RTH was treated with levothyroxine and 
increasing doses of liothyronine sodium as part of an evaluation of RTH. On day 
10 of the protocol, he developed atrial fibrillation despite a normal level of 
TSH (1.1 mIU/L). Administration of liothyronine was discontinued, and 
cardioversion was planned; however, the patient's heart rhythm converted 
spontaneously to normal sinus rhythm.
CONCLUSION: Replacement of thyroid hormone in patients with RTH should include 
careful monitoring of thyrotoxic cardiac side effects in addition to 
consideration of normalization of the TSH level.