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J Thorac Cardiovasc Surg 2006;131:505-506
© 2006 The American Association for Thoracic Surgery
Letter to the Editor |
Paediatric Cardiac Intensive Care, The Prince Charles Hospital, Brisbane, Queensland, Australia
We congratulate Mackie and colleagues
1
on their randomized study on triiodothyrodine (T3) treatment in neonatal heart surgery. In their study group the authors correctly enrolled a homogenous group of infants at highest risk of postoperative low cardiac output syndrome and marked thyroid hormone suppression.
2
As already shown by several other authors, the thyroid hormone levels are suppressed after cardiopulmonary bypass (CPB), decreasing to a nadir at around 48 hours after CPB and recovering over approximately 1 week. Logically, treatment with T3 after CPB raises the T3 plasma concentrations to normal levels, and no negative effects have been demonstrated so far. Previous studies, as well as the study presented, had relatively small subject numbers, thereby limiting the ability to determine a clinical effect. This led to the initiation of the Triiodothyronine for Infants and Children Undergoing Cardiopulmonary Bypass (TRICC) study, a randomized, multicenter clinical trial designed to determine safety and efficacy of T3 supplementation in children less than 2 years of age undergoing surgical procedures for congenital heart disease.
3
We would, however, counsel some caution in the interpretation of the main results of this study mainly for two reasons:
First, to our knowledge many centers worldwide would use in these patients peritoneal dialysis (PD) in the early postoperative phase to minimize the effects of systemic inflammatory response and achieve adequate fluid balance.
4
Usually peritoneal catheters are placed at the end of the operation to drain excess fluid as a routine institutional procedure, and PD is started after admission to the intensive care unit either on a prophylactic basis or after oliguria, anuria, fluid overload, hyperkalemia, or acidosis. PD is able to achieve adequate negative fluid balance in nearly all instances and treat other underlying causes simultaneously. Thus the positive achievement of negative fluid balance at day 2 versus day 2.5 may be clinically negligible under most given circumstances.
Second, the authors quote the effect of the T3 infusion on the cardiac output, systolic blood pressure and, herewith, indirectly on the requirements of catecholamines. Unfortunately, no information is provided on the absolute use of vasodilators (such as phenoxybenxzamine, sodium nitroprusside, and milrinone), nor is there differentiation in the catecholamine use with regard to dopamine. It is widely known that dopamine has a direct negative effect on thyroid function and thyroid hormone levels in infants and children.
5
Other factors such as the use of amiodarone should be discussed too. Finally, the overall dropout rate of cardiac output measurements in both groups (14/42) seems relatively high and unbalanced between the two small study groups. This additional information seems crucial to enable a more objective assessment of the study.
Despite these limitations, we believe that the study by Mackie and associates adds valuable information to the controversial dispute on the efficiency of T3 as an inotropic agent after CPB. However, we hope some of the questions may be answered by the results of the TRICC study.
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