Background Previous studies suggest that thyroid hormone supplementation alters fetal gene expression while improving left ventricular systolic function and exercise capacity in heart failure. Our objective was to test the hypothesis that administration of thyroid hormone to patients with idiopathic dilated cardiomyopathy (IDC) would reverse myocardial fetal gene expression, improve cardiac hemodynamics, and improve exercise capacity.
Methods 6 adults from University of Colorado Hospital with IDC with ejection fractions less than 35% received thyroid hormone (1.33 mcg/kg/day, mean dose 129 ±16 mcg/day) for 3 months. All subjects were on standard medical therapy for heart failure. We measured myocardial fetal gene expression using reverse transcriptase PCR at baseline and after thyroid hormone therapy. We also measured exercise capacity and right heart catheterization hemodynamics at baseline and after thyroid hormone therapy. Data were analyzed using a paired t-test of the means.
Results Mean TSH levels decreased from 2.24 ± 1.39 mU/L to 0.072 ± 0.066 mU/L (p=0.34). There was no significant change in fetal gene expression of alpha myosin heavy chain, beta myosin heavy chain, atrial naturetic peptide, or SRCa++ ATPase from baseline to post-thyroid therapy. There was no significant change in right heart catheterization measurements of cardiac output (5.12 ± 1.89 L/min pre, 5.18 ± 0.84 L/min post, p=0.94), pulmonary capillary wedge pressure (12.2 ± 9.1 mmHg pre, 13.7 ± 6.2 mmHg post, p=0.42), systemic vascular resistance (1579 ± 418 dynes.sec/cm^5 pre, 1431 ± 260 dynes.sec/cm^5 post, p=0.59). There was also no significant change in exercise capacity measured by the 6 minute walk test (1486 ± 327 feet pre, 1430 ± 284 feet post, p =0.62), ventilatory efficiency slope (32.8 ± 6.38 pre, 33.3 ± 5.76 post, p=0.32), VO2 at anerobic threshold (15.3 ± 3.6 pre, 14.1 ± 5.61 post, p=0.45), or peak VO2 (19.0 ± 4.9 ml/kg/min pre, 19.6 ± 4.1 ml/kg/min post, p=0.43).
Conclusion Short-term thyroid hormone at a dose of 1.33 mcg/kg/day does not reverse fetal gene expression or significantly improve hemodynamics or exercise capacity in patients with idiopathic dilated cardiomyopathy receiving standard heart failure therapy.
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