Context: Low-T 3 syndrome is a predictor of poor outcome in patients with cardiac dysfunction. The study aimed to assess the short-term effects of synthetic L-T 3 replacement therapy in patients with low-T 3 syndrome and ischemic or nonischemic dilated cardiomyopathy (DC).Design: A total of 20 clinically stable patients with ischemic (n ϭ 12) or nonischemic (n ϭ 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-T 3 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-T 3 (initial dose: 20 g/m 2 body surface⅐d) or placebo infusion.Results: After T 3 administration, free T 3 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 ϭ 0.03) without side effects. Heart rate decreased significantly after T 3 infusion (63, 60 -66 vs. 69, 60 -76 beats per minute; P ϭ 0.008). Plasma noradrenaline (347; 270 -740 vs. 717, 413-808 pg/ml; P ϭ 0.009), N-terminal pro-B-Type natriuretic peptide (3000, 438-4005 vs. 3940, 528-5628 pg/ml; P ϭ 0.02), and aldosterone (175, 152-229 vs. 231, 154 -324 pg/ml; P ϭ 0.047) significantly decreased after T 3 administration. Neurohormonal profile did not change after placebo infusion in the control group. After synthetic L-T 3 administration, left-ventricular end-diastolic volume (142, 132-161 vs. 133, 114 -158 ml/m 2 body surface; P ϭ 0.02) and stroke volume (40, 34 -44 vs. 35, 28 -39 ml/m 2 body surface; P ϭ 0.01) increased, whereas external and intracardiac workload did not change. Conclusions:In DC patients, short-term synthetic L-T 3 replacement therapy significantly improved neuroendocrine profile and ventricular performance. These data encourage further controlled trials with more patients and longer periods of synthetic L-T 3 administration. (J Clin Endocrinol

Background— Clinical and experimental data have suggested a potential negative impact of low-T3 state on the prognosis of cardiac diseases. The aim of the present prospective study was to assess the role of thyroid hormones in the prognosis of patient population with heart disease. Methods and Results— A total of 573 consecutive cardiac patients underwent thyroid function profile evaluation. They were divided in two subgroups: group I, 173 patients with low T3, ie, with free T3 (fT3) <3.1 pmol/L, and group II, 400 patients with normal fT3 (≥3.1 pmol/L). We considered cumulative and cardiac death events. During the 1-year follow-up, there were 25 cumulative deaths in group I and 12 in group II (14.4% versus 3%, P <0.0001); cardiac deaths were 13 in group I and 6 in group II (7.5% versus 1.5%, P =0.0006). According to the Cox model, fT3 was the most important predictor of cumulative death (hazard ratio [HR] 3.582, P <0.0001), followed by dyslipidemia (HR 2.955, P =0.023), age (HR 1.051, P <0.005), and left ventricular ejection fraction (HR 1.037, P =0.006). At the logistic multivariate analysis, fT3 was the highest independent predictor of death (HR 0.395, P =0.003). A prevalence of low fT3 levels was found in patients with NYHA class III-IV illness compared with patients with NYHA class I-II (χ 2 5.65, P =0.019). Conclusions— Low-T3 syndrome is a strong predictor of death in cardiac patients and might be directly implicated in the poor prognosis of cardiac patients.

Hyperthyroidism is associated with prolonged QTc that normalizes once the patient becomes euthyroid. The strong positive correlation between FT3 and QTc supports the hypothesis of an important role of thyroid hormone on modulation of QTc lengthening.

In this report we show that human endothelial cells (EC) can be detected in circulating blood by means of the EC-specific monoclonal antibody (MoAb) designated as CLB-HEC 19 and expressed quantitatively as number of cells per milliliter of whole blood. We first developed a method that was able to recover cultured human EC added to whole blood by Percoll density gradient centrifugation. The final recovery of the EC was 91.6% (SE = 0.65%). The EC were identified in the gradient subfractions by indirect immunofluorescence with the MoAb CLB-HEC 19. This method was then applied to the separation and characterization of EC or EC remnants from the whole arterial and venous blood taken from two groups of patients subjected to heart catheterization. Firstly, a preliminary blood screening of random samples was performed in a group of eight patients (group I) using a scoring evaluation for the presence of EC and the results were expressed as positivity index. Secondly, the complete blood screening of a group of ten patients (group II) was performed for the detection of immunofluorescent cells and the results were expressed as number of EC per milliliter of whole blood. Our results show in both group I and II a significant presence of EC in the blood after catheterization compared with their basal values. The minimal detectable concentration of EC was 0.06 cells/mL (SE = 0.057) of whole blood. We consider this technique as a suitable clinical test for the detection of EC injury in cardiovascular pathology.