

Publisher: John Wiley & Sons Inc
E-ISSN: 2055-5822|2|1|5-11
ISSN: 2055-5822
Source: ESC HEART FAILURE, Vol.2, Iss.1, 2015-03, pp. : 5-11
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
AbstractObjectivesThe present study assessed the changes in functional, biochemical, and echocardiographic measures following long‐term liothyronine therapy in heart failure (HF) patients with low‐triiodothyronine (T3) syndrome (LT3S).MethodsIn the present placebo‐controlled, double‐blind study, adult patients with clinically stable New York Heart Association functional class I–III systolic HF and LT3S receiving standard HF therapy were randomly assigned 1:1 to receive oral liothyronine or placebo for 6 weeks. Low‐T3 syndrome was defined as a serum free T3 of less than the lower limit of normal (<2.4 pg/mL) with normal thyroid‐stimulating hormone (thyrotropin) and free thyroxin values.ResultsFifty patients, including 39 (78%) men with a mean ± standard deviation age of 60 ± 15 years were included. The 6‐min walk distance increased in the liothyronine group by 93 ± 16 m and in the placebo group by 67 ± 28 m, resulting in a treatment effect of 26 m (P = 0.003). A higher decrease of high‐sensitivity C‐reactive protein level was seen in the liothyronine group than in the placebo group (P = 0.009). Liothyronine markedly decreased serum N‐terminal pro‐brain natriuretic peptide level compared with the placebo (P = 0.01). A significant increase was also seen in the left ventricular ejection fraction by liothyronine as compared with the placebo (<0.001).ConclusionTriiodothyronine replacement by chronic liothyronine therapy seems to safely benefit stable HF patients with LT3S receiving optimal HF medications.
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