Triiodothyronine repletion in infants during cardiopulmonary bypass for congenital heart disease

Citation
Ma. Portman et al., Triiodothyronine repletion in infants during cardiopulmonary bypass for congenital heart disease, J THOR SURG, 120(3), 2000, pp. 604-608
Citations number
23
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
ISSN journal
00225223 → ACNP
Volume
120
Issue
3
Year of publication
2000
Pages
604 - 608
Database
ISI
SICI code
0022-5223(200009)120:3<604:TRIIDC>2.0.ZU;2-U
Abstract
Objective: Cardiopulmonary bypass suppresses circulating thyroid hormone le vels. Although acute triiodothyronine repletion has been evaluated in adult patients after cardiopulmonary bypass, triiodothyronine pharmacokinetics a nd effects have not previously been studied in infants undergoing operation s for congenital heart disease. We hypothesized that triiodothyronine defic iency in the developing heart after bypass may adversely affect cardiac fun ction reserve postoperatively, Methods: Infants less than 1 year old undergoing ventricular septal defect or tetralogy of Fallot repair were randomized into 2 groups. Group T (n = 7 ) received triiodothyronine (0.4 mu g/kg) immediately before the start of c ar diopulmonary bypass and again with myocardial reperfusion, Control (NT, n = 7) patients received saline solution placebo or no treatment. Results: These groups underwent similar ischemic and bypass times and recei ved similar quantities of inotropic agents after the operation, The NT grou p demonstrated significant depression in circulating levels, compared with prebypass levels, for free triiodothyronine and total triiodothyronine at 1 , 24, and 72 hours after bypass. Group T demonstrated similar low thyroxine values, but free and total triiodothyronine levels were maintained at preb ypass levels for 24 hours and remained elevated over those of group NT (P < .05) at 72 hours. Heart rate was transiently elevated in group T compared with group NT (P < .05), and peak systolic pressure-rate product increased after 6 hours. Conclusion: These data imply that (1) triiodothyronine in the prescribed do se prevents circulating triiodothyronine deficiencies and (2) triiodothyron ine repletion promotes elevation in heart rate without concomitant decrease in systemic blood pressure. Elevation of peak systolic pressure-rate produ ct implies that triiodothyronine repletion improves myocardial oxygen consu mption and may enhance cardiac function reserve after cardiopulmonary bypas s in infants.