In heart failure, cardiac output is insufficient to meet the needs of the body 
for oxygen delivery. Available data suggest that alterations in thyroid hormone 
metabolism may contribute to defective myocardial performance. Accordingly, 
thyroid hormone or a thyroid hormone analogue that improves cardiac performance 
might be useful in the treatment of heart failure and has been studied. 
Experimental and theoretical results of these studies are reviewed and indicate 
that thyroid hormone increases cardiac output by a combination of effects on the 
heart and peripheral circulation, specifically by increasing myocardial 
contractile performance and decreasing venous compliance. In the rat 
postinfarction model of heart failure, treatment with low doses of thyroxine 
(1.5 micrograms/100 g) for 3 days produced a positive inotropic response, 
including an increase in rate of change of left ventricular pressure and a 
decrease in left ventricular end-diastolic pressure. These changes could be 
attributed to conversion to triiodothyronine, the active intracellular form of 
thyroid hormone. When treatment with thyroxine was continued at the same or 
higher doses (3 to 15 micrograms/100 g) for 10 to 12 days, heart rate increased 
and improvement in left ventricular end-diastolic pressure was not sustained. 
More favorable results were obtained with 3,5-diiodothyropropionic acid, a 
cardiotonic thyroid hormone analogue administered at doses of 375 microgram/100 
g, given in combination with captopril. Thus, triiodothyronine or a thyroid 
hormone analogue may be a useful adjunct to other measures in the treatment of 
heart failure.