Objectives: A low T3 syndrome was described in patients with heart failure (HF), and it appears to be associated with adverse outcome, representing an independent predictor of mortality. However, it is not known if low T3 levels contribute to the pathophysiology of HF. On the other hand, it has been seen that an elevation of brain natriuretic peptides (BNP and NT-proBNP) may represent a warning signal for future cardiovascular disease and may be an early marker of diastolic dysfunction. Therefore we tested the hypothesis that low levels of free-triiodothyronine (FT3) are sufficient to determine an increased concentration of the amino-terminal fragment of pro-brain natriuretic peptide (NT-proBNP), as the result of an initial and asymptomatic cardiac impairment.
Methods: A total of 52 consecutive non-cardiac patients underwent thyroid function profile evaluation and NT-proBNP determination. On the basis of FT3 values they were divided in two subgroups: a low T3 group (19 patients) and a normal T3 group (33 patients).
Results: The median NT-proBNP concentration of patients with low T3 syndrome was significantly higher than in those with normal FT3 (370 vs. 120 pg/ml, P = 0.002). There is a strong and inverse correlation between FT3 and Log NT-proBNP (R = -0.47, P < 0.001); this relation persists in a multivariable regression analysis, after adjustment for other potentially confounding variables (P = 0.008).
Conclusion: In absence of overt cardiovascular disease, patients with low T3 syndrome present an increased concentration of NT-proBNP. These data suggest that low FT3 levels may be a contributing factor for the development of cardiac dysfunction.