Improved cardiac allograft function following triiodothyronine therapy to both donor and recipient.

Abstract

Brain death is associated with neuroendocrine changes, in particular with a significant reduction of plasma-free triiodothyronine (T3) that results in impaired aerobic metabolism. Myocardial energy stores are reduced and tissue lactate increased. Cardiac function deteriorates. Similar metabolic changes are seen in patients undergoing open-heart surgery on cardiopulmonary bypass, including those undergoing heart transplantation. Therapy with T3 leads to a reversal of these metabolic changes, resulting in improved cardiac function. One hundred and sixteen consecutive potential donors have been so treated, as have 70 of the recipients. Immediate posttransplant cardiac function was good in all but 3, and these hearts recovered to normal within a maximum of 24 hr of mechanical support. In 2 small randomized trials in patients undergoing myocardial revascularization on cardiopulmonary bypass, postoperative T3 therapy was associated with a reduced need for inotropic support and diuretic therapy in the first study and improved cardiac output in the second study.

• Authors: D Novitzky, D K Cooper, J S Chaffin, A E Greer, L E DeBault, N Zuhdi
• Journal: Transplantation (Transplantation) Vol. 49 Issue 2 Pg. 311-6 (Feb 1990) ISSN: 0041-1337 [Print] United States
• PMID: 2305461 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Phosphocreatine
• Triiodothyronine
• Adenosine Triphosphate

Topics

• Adenosine Triphosphate (metabolism)
• Animals
• Cardiac Output
• Energy Metabolism
• Heart Transplantation
• Humans
• Microscopy, Electron
• Myocardial Contraction
• Myocardium (metabolism, ultrastructure)
• Papio
• Phosphocreatine (metabolism)
• Swine
• Triiodothyronine (therapeutic use)