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Long-term L-Triiodothyronine (T3) treatment in stable systolic heart failure patients: a randomised, double-blind,
Pernille Holmager1, Ulla Schmidt1, Peter Mark1
1Department of Medicine, Endocrine Unit, Herlev University Hospital, Herlev, Denmark.
Insights
Long-term triiodothyronine (T3) treatment did not improve cardiac function or neurohormonal markers in patients with chronic systolic heart failure (HF). This study found no benefit for T3 therapy in this patient group.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Chronic heart failure (HF) is associated with reduced serum triiodothyronine (T3) and increased T3 degradation.
- This hormonal imbalance may create a hypothyroid-like intracellular state in cardiomyocytes.
- Previous short-term studies suggested potential benefits of T3 administration in HF patients.
Purpose of the Study:
- To investigate the long-term effects of T3 treatment on cardiac function and neurohormonal activation.
- To assess the efficacy of T3 in chronic systolic HF patients with low-normal serum T3 levels (below 1.6 nmol/l).
Main Methods:
- A randomized, double-blind, cross-over, placebo-controlled study.
- Oral T3 treatment administered twice daily for 3 months, with dose titration to avoid suppressed TSH.
- Primary endpoint: Left-ventricular ejection fraction (LVEF) assessed by MUGA-SPECT; secondary endpoints included neurohormonal markers and arrhythmias.
Main Results:
- Thirteen patients completed the study; mean LVEF was 43% and mean serum T3 was 1.4 nmol/l.
- T3 treatment (mean dose 20 μg/day) did not significantly alter LVEF, cardiac volumes, or cardiac output.
- No significant changes were observed in neurohormonal markers, and no cardiac arrhythmias or adverse effects were reported.
Conclusions:
- Long-term oral T3 treatment does not appear to benefit patients with chronic systolic HF and low-normal T3 levels.
- The study did not support the hypothesis that T3 improves cardiac contractility or reduces neurohormonal activation in this population.
- Further research may be needed to explore T3's role in specific HF subpopulations or with different therapeutic strategies.
Background:
Chronic heart failure (HF) is characterized by reduced serum T3 levels and increased activity of the T3 degrading enzyme deiodinase D3. This may result in an intracellular composition of the cardiomyocyte mimicking that of hypothyroidism. Short-term T3-administration to systolic HF patients might be beneficial.
Question:
Does long-term treatment with T3 have a beneficial effect on cardiac function and neurohormonal activation in chronic systolic HF patients with serum T3 levels below 1·6 nmol/l?
Design:
A randomized, double-blind, cross-over, placebo-controlled intervention study with oral T3 treatment twice daily for 3 months. The T3 dose was uptitrated to a final dose avoiding reduced TSH levels.
Primary End-Point:
Left-ventricular ejection fraction (LVEF).
Methods:
Cardiac imaging was performed using multiple gated tomographic radionuclide ventriculography (MUGA-SPECT). Neurohormonal stimulation was evaluated by plasma measurements of natriuretic peptides, aldosterone, renin, noradrenalin and copeptin levels. The patients were monitored for potential cardiac arrhythmias at the start of each treatment period.
Results:
Thirteen patients completed the protocol. Mean LVEF was 43%, range: 37-52 and serum T3 levels 1·4 nmol/l (0·9-1·6). The T3 dose was 20 μg per day (10-40). TSH levels did not change between groups, whereas serum T3 levels increased in the active arm. Cardiac function as measured by LVEF, end-diastolic and end-systolic volumes and cardiac output did not change during T3-treatment and neither did the neurohormonal profile. There were no side-effects in terms of cardiac arrhythmias and no change in resting heart rate.
Conclusions:
This study does not support the hypothesis that oral T3 treatment might be beneficial to patients with chronic, stable systolic HF with a modest degree of reduced LVEF and low-normal serum T3 concentrations. The study included both functional studies of heart contractility as well as measures of the neurohormonal activation.
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