Reversal of donor myocardial dysfunction by triiodothyronine replacement therapy.

Triiodothyronine deficiency after brain death can result in progressive deterioration of cardiac function in potential organ donors. We report on the use of triiodothyronine replacement in improving myocardial function, allowing the use of donor hearts that might have been considered unsuitable for transplantation. From July to September 1992, of 24 organ procurements and transplantations, six donors were receiving high doses of inotropes with elevated left-sided filling pressures. Donor characteristics were as follows: five were male donors and one was a female donor, with mean age 16.50 +/- 7.50 years (8 to 30 years), mean weight 49.17 +/- 13.64 kg (25 to 63 kg), average time from clinical brain death to procurement 94.50 +/- 73.53 hours (49 to 240 hours), and two donors had arrest periods of up to 10 minutes. Despite large inotrope infusions, echocardiograms showed depressed left ventricular function (mean ejection fraction 39.17 +/- 5.85) and hemodynamic instability was present with elevated ventricular filling pressures. Triiodothyronine replacement (maximal dose 0.6 microgram/kg) was initiated an average of 139.17 +/- 32.00 minutes (115 to 185 minutes) before procurement. At the time of procurement, ventricular filling pressures were lower, hemodynamic condition stabilized, and pressor requirements decreased. Hearts were preserved in University of Wisconsin solution with a mean ischemic time of 188.83 +/- 36.86 minutes (149 to 237 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)