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Low triiodothyronine and cardiovascular disease.

To the Editor: Iervasi et al1 report a strong correlation between low free biologically active triiodothyronine (fT3), a thyroid hormone, and all-cause and cardiovascular mortality in 573 consecutive patients with heart disease. The observations in this study are stimulating and may be of major clinical interest. However, the following points deserve to be clarified for better appreciating the implications of this study. (1) Neither creatinine nor other markers of renal function were considered as potential confounders of the relationship between fT3 and the outcomes. This is an important omission because fT3 is frequently reduced in patients with renal failure.2 Because it is likely that some patients with heart disease included in the Iervasi et al1 study had some degree of renal insufficiency, fT3 may be just a proxy of renal dysfunction. (2) Cox survival analysis and logistic regression analysis do not seem to provide coherent results. In fact, the fT3 hazard ratio of 3.582 (see Cox regression model in Table 3 of Iervasi et al1) implies that an increase of 1 pmol/L in fT3 is associated with a 258% excess risk for all-cause mortality. In contrast, in the multivariate logistic regression analysis (Table 41), the authors report a fT3 hazard ratio of 0.395, implying that an increase of 1 pmol/L in fT3 is associated with a 60.5% risk reduction in the hazard ratio of all-cause mortality. Finally, with just 19 cardiac deaths during the follow-up, only 2 covariates can be entered into the Cox model (ie, 1 covariate every 10 events),3 whereas data reported in Table 31 apparently include 4 covariates. This model is overfitted, and, therefore, the independence of the fT3–cardiovascular outcomes link requires confirmation in a more powerful study, or requires testing in more parsimonious statistical models.