thyronines and Heart-Failure

Thyroid hormone has multiple direct and indirect effects on the heart and the vasculature. Many signs and symptoms of thyroid dysfunction are manifest by the cardiovascular system. Furthermore, many cardiovascular diseases are adversely affected by the concomitant presence of either hyper- or hypothyroidism: it is still being debated whether these alterations are the consequence of increased cardiac workload alone or are due to the intrinsic properties of thyroid hormone. There are three potential mechanisms by which thyroid hormone might exert a cardiovascular action: (1) direct effects at the cellular level (inotropic and chronotropic effect); (2) interaction with the sympathetic nervous system; and (3) alteration of the peripheral circulation through changes in preload, afterload and energy metabolism. We treated 54 adult and seven pediatric patients suffering from severe low cardiac output in different clinical conditions with a mean bolus dosage of 2+/-1.5 microg h(-1) of T(3), followed by a continuous infusion of 0.4+/-0.3 microg h(-1) for a mean duration of 48+/-12 h. In 45 patients, stabilization of the hemodynamic situation with a decrease in inotropic support requirement was observed; however, in 11 patients no beneficial effects were observed. From this experience we suggest that T(3) treatment may improve hemodynamics in a substantial proportion of cardiac and cardiosurgical patients in whom more conventional treatment is unsuccessful.

Topics: Adolescent; Adult; Cardiac Surgical Procedures; Child; Heart Failure; Humans; Switzerland; Thyronines

Thyroid hormone metabolites might affect the heart. The endogenous aminergic metabolite 3-iodothyronamine (T1am) reduces left ventricular ejection fraction (LVEF) in rodents.. To investigate concentration of T1am and its association with LVEF and biomarkers of heart function in patients with chronic heart failure (CHF) without thyroid disease, including patients with cardiac cachexia (nonedematous weight loss >5% over 6 months).. Cross-sectional study. CHF was characterized by LVEF <45% and symptoms. Three groups were included (n = 19 in each group, matched on age, sex, and kidney function): patients with cachexia (CAC), patients without (non-CAC), and control (C) patients with prior myocardial infarction and LVEF >45%. T1am was measured by a monoclonal antibody-based chemiluminescence immunoassay. N-amino terminal pro-BNP (NT-proBNP) concentrations were also analyzed.. Mean (SD) LVEF: CAC, 32 ± 9%; non-CAC, 38 ± 8%; and C, 60 ± 8% (P < 0.0001). TSH, T4, and T3 levels did not differ between groups and did not correlate to T1am. Serum T1am (nmol/L) concentrations were higher in CHF: CAC (mean ± SD), 12.4 ± 6.6; non-CAC, 9.1 ± 5; and C, 7.3 ± 2.9. A negative association between T1am and LVEF was present after adjusting for sex, age, T3, and estimated glomerular filtration rate (P = 0.03). Further, serum T1am levels tended to be associated with NT-proBNP (P = 0.053).. Serum T1am levels were increased in patients with CHF and numerically highest (although nonsignificant) in patients with cardiac cachexia. Increasing T1am concentrations were independently associated with reduced LVEF, suggesting a direct effect on the human heart.

Topics: Aged; Aged, 80 and over; Biomarkers; Cachexia; Chronic Disease; Cohort Studies; Cross-Sectional Studies; Female; Heart; Heart Failure; Humans; Male; Thyronines; Ventricular Function, Left