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Acute Effects of Triiodothyronine (T₃) Replacement Therapy in Patients with Chronic Heart Failure and Low-T₃ Syndrome: A Randomized, Placebo-Controlled Study

Institute of Clinical Physiology (A.P., A.I., M.S., D.N., G.I.), Consiglio Nazionale delle Ricerche, 56124 Pisa, Italy; Cardiothoracic Department (E.G., A.B., R.M.), University of Pisa, 43-56126 Pisa, Italy; and Scuola Superiore Sant’Anna (A.L.), 34 56025 Pisa, Italy

Address all correspondence and requests for reprints to: Giorgio Iervasi, M.D., Clinical Physiology Institute, Consiglio Nazionale delle Ricerche, Via Moruzzi 1 Località la Fontina, 56124 Pisa, Italy. E-mail: iervasi{at}ifc.cnr.it.

Context: Low-T₃ syndrome is a predictor of poor outcome in patients with cardiac dysfunction. The study aimed to assess the short-term effects of synthetic L-T₃ replacement therapy in patients with low-T₃ syndrome and ischemic or nonischemic dilated cardiomyopathy (DC).

Design: A total of 20 clinically stable patients with ischemic (n = 12) or nonischemic (n = 8) DC were enrolled. There were 10 patients (average age 72 yr, range 66–77; median, 25–75th percentile) who underwent 3-d synthetic L-T₃ infusion (study group); the other 10 patients (average age 68 yr, range 64–71) underwent placebo infusion (control group). Clinical examination, electrocardiography, cardiac magnetic resonance, and bio-humoral profile (free thyroid hormones, TSH, plasma renin activity, aldosterone, noradrenaline, N-terminal-pro-B-Type natriuretic peptide, and IL-6) were assessed at baseline and after 3-d synthetic L-T₃ (initial dose: 20 µg/m² body surface·d) or placebo infusion.

Results: After T₃ administration, free T₃ concentrations increased until reaching a plateau at 24–48 h (3.43, 3.20–3.84 vs. 1.74, 1.62–1.93 pg/ml; P = 0.03) without side effects. Heart rate decreased significantly after T₃ infusion (63, 60–66 vs. 69, 60–76 beats per minute; P = 0.008). Plasma noradrenaline (347; 270–740 vs. 717, 413–808 pg/ml; P = 0.009), N-terminal pro-B-Type natriuretic peptide (3000, 438-4005 vs. 3940, 528-5628 pg/ml; P = 0.02), and aldosterone (175, 152–229 vs. 231, 154–324 pg/ml; P = 0.047) significantly decreased after T₃ administration. Neurohormonal profile did not change after placebo infusion in the control group. After synthetic L-T₃ administration, left-ventricular end-diastolic volume (142, 132–161 vs. 133, 114–158 ml/m² body surface; P = 0.02) and stroke volume (40, 34–44 vs. 35, 28–39 ml/m² body surface; P = 0.01) increased, whereas external and intracardiac workload did not change.

Conclusions: In DC patients, short-term synthetic L-T₃ replacement therapy significantly improved neuroendocrine profile and ventricular performance. These data encourage further controlled trials with more patients and longer periods of synthetic L-T₃ administration.

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