A New Treatment for Idiopathic Dilated Cardiomyopathy?
ABSTRACT & COMMENTARY
Synopsis: Although treatment with L-thyroxine is probably safe and cheap, there is scant evidence that it is truly effective for idiopathic dilated cardiomyopathy.
Source: Moruzzi P, et al. Am J Med 1996;101:461-467.
The aim of a recent study by moruzzi et al was to test the medium-term (3 months) efficacy of L-thyroxine (10 patients) compared with placebo (10 patients) and to find out whether later effects are obtainable in the treatment of dilated cardiomyopathy.
Echocardiographic parameters in the control state and during acute changes of left ventricular afterload, cardiopulmonary exercise test, and hemodynamic parameters, including cardiac b1 responses to dobutamine, were obtained before and at the end of treatment.
Significant (P < 0.05) changes were observed only with the active drug. After L-thyroxine, patients did not show evidence of chemical hyperthyroidism. Cardiac performance improved, as shown by the increase in the left ventricular ejection fraction and rightward shift of the slope of the relation of left ventricular ejection fraction/end-systolic stress. Resting cardiac output increased, and the left ventricular diastolic dimensions and systemic vascular resistances decreased. The responses of cardiac output and heart rate to dobutamine infusion were also enhanced. Functional capacity markedly improved, together with an increase in peak exercise cardiac output.
L-thyroxine does not lose its beneficial effects on cardiac and exercise performance on medium-term administration and does not induce adverse effects. In addition to the short-term study, the left ventricular diastolic dimensions were decreased. An up-regulation of b1 receptors might explain the cardiac response to dobutamine.
COMMENT BY RALPH R. HALL, MD
Does treating idiopathic dilated myocardiopathy with thyroid hormone improve the cardiac performance in patients with this disorder? I am a skeptic!
There are several theoretical reasons why thyroid hormone might improve cardiac performance. However, the data from this study fail to impress me or to confirm the effectiveness of thyroid hormone.
Why should we be skeptical? First off, this is a very small study. The authors present only the mean average changes of the group. Individual data on each patient would have allowed us to see if changes in one or two patients might significantly affect the mean of the group. Patients with idiopathic myocardiopathy do, on occasion, improve without medication. If there had been a significant improvement in one or two patients out of 10, which occurred spontaneously, this would affect the mean of the group.
It is difficult to see how replacing thyroid hormone made by the thyroid gland with what appears to be physiological replacement doses of thyroxine would change thyroid cellular metabolism. The only possibility that occurs to me is that changing the thyroid stimulating hormone levels might in some way be beneficial.
Initially, the statement, "In one case, after two months, laboratory tests showed subnormal plasma levels of thyroxine and thyroid stimulating hormone. The drug regime was considered inappropriate to the body size of the patient, and the daily dose was reduced to 50 micrograms," seems to be a misprint. However, the statement was repeated in the discussion that subnormal plasma levels of thyroxine were found to be present, but the plasma hormone levels were normalized in a few days after dosage reduction, without losing the improvement of cardio-circulatory and effort parameters. If this indeed occurred, the raising of plasma thyroxine by reducing the dose of thyroid hormone is unique, unreported, and in itself a reportable phenomenon.
The accompanying editorial hypothesized as to why this treatment might be effective;1 however, comparisons are made with studies using supernormal doses of thyroxin, which is inappropriate. The authors and the editorialist point to the effectiveness of tricodothyronine (T3) replacement therapy in patients undergoing coronary artery bypass surgery. However, we previously reviewed the studies in an earlier issue of Internal Medicine Alert2 which concluded that T3 was not effective in cardio pulmonary bypass patients.3
The patients in this study appear to have mean T3 levels at the lowest level of the normal range. This indicates that some of the patients were euthyroid sick in terms of their T3 levels. However, since the T3 are labeled in ng/mL, the numbers indicate that they should have been labeled in mol/L which, with the previously mentioned error, makes one wonder about the authors’ knowledge of thyroid function tests.
Although the treatment is probably safe and cheap, there is scant evidence that it is effective. The data from this study are poorly presented and, because of the small number of patients included, need further study.
The paper as presented did not warrant publication.
References
1. Klein I, Ojamaa K. Am J Med 1996;101:459-460.
2. Internal Med Alert 1996;18:19-20.
3. Klemper JD, et al. N Engl J Med 1995;333:1522-1529.
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