The interesting report of a myxedema-associated cardiogenic shock treated with intravenous triiodothyronine [1] raised several questions.

Intravenous triiodothyronine rapidly normalizes both myocardial performance and metabolic abnormalities [2]; on the other hand, although most thyroxine-treated patients may respond clinically within 48 hours [3], it may take up to 1 week before beneficial effects are seen [1, 2]. Finally, a low-dose (25 µg) triiodothyronine regimen for 1 week is equivalent to an equipotent (100 µg) dose of thyroxine in reversing cardiac and metabolic abnormalities, although such a regimen is significantly less effective in lowering serum thyroid-stimulating hormone (TSH) levels [2].

The patient described by Mackerrow and colleagues [1] was started on triiodothyronine after having been on thyroxine for 1 week and continued to be on both for the rest of his hospitalization. Thus, it is unclear whether the hemodynamic improvement of this patient was attributable to a rapid effect of triiodothyronine, a late effect of thyroxine, or both.

Hypothyroidism may not only coexist with coronary artery disease [4], its associated symptoms and laboratory findings may be similar to those seen with a cardiovascular event [5]. Although triiodothyronine proved to be a rapidly effective and safe treatment for the major organ system consequences of hypothyroidism in a limited group of patients without evidence of ischemic heart disease [2], patients with clinically or electrocardiographically evident ischemic heart disease may require a course of gradual hormone replacement.

Because case reports support the effectiveness of both thyroxine and triiodothyronine for the treatment of myxedematous patients [1, 5] and because any controlled clinical study to define the treatment of choice for such patients would be extremely difficult [2], the recommendation for intravenous triiodothyronine therapy for all hypothyroid patients with severe heart failure seems to be premature.