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European Journal of Heart Failure 2002 4(5):577-582; doi:10.1016/S1388-9842(02)00096-X
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© 2002 European Society of Cardiology

Thyronin treatment in adult and pediatric heart surgery: clinical experience and review of the literature

Thierry Carrela,*, Friedrich Ecksteina, Lars Englbergera, Raymond Muryb and Paul Mohacsib

a Department of Cardiovascular Surgery, University Hospital CH-3010 Berne, Switzerland
b Division of Cardiology, University Hospital CH-3010 Berne, Switzerland

* Corresponding author. Tel.: +41-31-632-2375; fax: +41-31-632-4443. E-mail address: thierry.carrel{at}insel.ch


   Abstract
Top
 Abstract
1. Introduction
 2. Clinical experience
 3. Discussion
 4. Conclusions
 References
 
Thyroid hormone has multiple direct and indirect effects on the heart and the vasculature. Many signs and symptoms of thyroid dysfunction are manifest by the cardiovascular system. Furthermore, many cardiovascular diseases are adversely affected by the concomitant presence of either hyper- or hypothyroidism: it is still being debated whether these alterations are the consequence of increased cardiac workload alone or are due to the intrinsic properties of thyroid hormone. There are three potential mechanisms by which thyroid hormone might exert a cardiovascular action: (1) direct effects at the cellular level (inotropic and chronotropic effect); (2) interaction with the sympathetic nervous system; and (3) alteration of the peripheral circulation through changes in preload, afterload and energy metabolism. We treated 54 adult and seven pediatric patients suffering from severe low cardiac output in different clinical conditions with a mean bolus dosage of 2±1.5 µg h–1 of T3, followed by a continuous infusion of 0.4±0.3 µg h–1 for a mean duration of 48±12 h. In 45 patients, stabilization of the hemodynamic situation with a decrease in inotropic support requirement was observed; however, in 11 patients no beneficial effects were observed. From this experience we suggest that T3 treatment may improve hemodynamics in a substantial proportion of cardiac and cardiosurgical patients in whom more conventional treatment is unsuccessful.

Key Words: Thyronin • Heart surgery • Hemodynamics • Transplantation

Received May 22, 2001; Revised September 7, 2001; Accepted December 14, 2001


   1. Introduction
Top
 Abstract
 1. Introduction
2. Clinical experience
 3. Discussion
 4. Conclusions
 References
 
Thyroid hormone has multiple direct and indirect effects on the heart and the vasculature [1–10]. Many signs and symptoms of thyroid dysfunction are manifest by the cardiovascular system. The literature on these interrelations is voluminous and reflects ongoing clinical interest encountered in the fields of endocrinology, cardiology, cardiac surgery and intensive care medicine.

Hypothyroidism is associated with abnormal hemodynamic conditions characterized by a decreased heart rate, stroke volume, output and contractility, as well as by increased systemic vascular resistance. Several conditions have been identified, including surgical stress, severe illnesses (e.g. sepsis, renal failure, myocardial infarction) and cardiopulmonary bypass (CPB)—in addition to interaction by drugs—which induce a profound decrease in serum levels of triiodothyronine (T3) [11]. Therefore, the hemodynamic consequences of ‘stress-induced’ hypothyroidism and the potential effects of T3 supplementation have attracted increasing interest in cardiovascular medicine, but there is still concern about whether these abnormalities should be treated or not [12].

There are three potential mechanisms by which thyroid hormone might exert a cardiovascular action: (1) direct effects at the cellular level, which are mediated by stimulation of specific nuclear receptors (inotropic and chronotropic effect); (2) interaction with the sympathetic nervous system, with the consequence that the responsiveness to sympathetic stimulation is altered—presumably by modulating β-adrenergic receptor function or density [13]; and (3) alteration of the peripheral circulation through changes in preload, afterload and energy metabolism (increase in total body oxygen consumption). A variety of studies have shown that thyroid hormone, presumably acting through nuclear receptors, increases contractility and protein synthesis in heart muscle [7]. It also affects a number of events related to myocardial function, through effects on both efficiency of contractility and membrane function related to excitation–contraction coupling [14]. Basal TSH is usually normal in these patients [15].

Studies to date suggest that T3 replacement might be beneficial in certain patient populations, while in others no significant effects are observed [16–18]. We present our clinical experience with triiodothyronine treatment in different groups of adult and pediatric patients treated in a cardiac surgery department.


   2. Clinical experience
Top
 Abstract
 1. Introduction
 2. Clinical experience
3. Discussion
 4. Conclusions
 References
 
2.1. Heart transplant candidates with severe heart failure
We administered triiodothyronine (Thyrotardine®, Merck, Dietikon, Switzerland) to eight transplant candidates (mean age 55±7.5 years, coronary artery disease in three, dilated idiopathic cardiomyopathy in three and valvular heart disease in two patients, mean ejection fraction 0.24±0.06). The patients all presented with severely compromised hemodynamics during the waiting period for transplantation (Table 1), despite full treatment for advanced heart failure and additional intravenous inotropic support. In these patients, bridging to transplant using a ventricular assist device was considered to be the next logical step.


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  		Table 1 Pre- and post-T3 treatment hemodynamics in patients with advanced heart failure (data from 7 patients)

 
Triiodothyronine treatment consisted of an intravenous bolus of thyronine hormone (2–4 µg within one hour. Thereafter, triiodothyronine was administered at a mean dosage of 2–4 µg h–1 (range 2–5 µg). The mean duration of treatment was 60±12 h. During treatment or shortly after discontinuation of T3, intravenous inotropic support could be reduced within hours. Bolus doses and continuous infusion were well tolerated and no significant adverse events attributable to T3 were observed. There were no significant changes in heart rate, global left ventricular function and end-diastolic volume, but within 12 h, the blood pressure showed an increasing trend. No deaths occurred in this group of patients in the period before transplantation.

2.2. Brain-dead multiorgan donors
We prospectively analyzed a consecutive series of 32 multi-organ donors treated in the intensive care unit of our institution (age 15–61 years). The majority (20/32) were receiving moderate to high doses of inotropic support (e.g. >10–20 µg kg–1 dopamine combined or not with epinephrine or norepinephrine >1–3 µg k–1). Echocardiography performed shortly after brain death was diagnosed showed a global impairment of the LV function (mean EF 0.45±0.07) without signs of regional wall abnormalities in 14 patients. T3 substitution combined with a cortisol bolus (500 mg of solumedrol) was started immediately after echocardiography with a maximal dosage of 1–2 µg h–1 until organ procurement. In all patients, hemodynamic stabilization (increasing systolic pressure, decreasing filling pressure) was observed and inotropic support could be reduced to 5 µg kg–1 dopamine in two and stopped in 12 patients. During multiorgan procurement, there was no visual impairment of LV contractility, while filling pressures (left atrial and central venous pressure) were normal. All cardiac allografts showed a normal early postoperative function in the recipients.

2.3. Immediate allograft dysfunction following cardiac transplantation
In a consecutive series of 60 patients who received cardiac transplantation, a severely compromised allograft function was observed in the immediate postoperative period during or following weaning from cardiopulmonary bypass (CPB) in five patients, despite considerable inotropic support (Table 2). In two patients a LVAD was implanted, but both patients died, one due to multiorgan failure and the other due to bleeding. In three patients T3 supplementation (2 µg intravenous bolus followed by 0.6 µg h–1 infusion during 12 h) was started intra-operatively. Hemodynamic improvement was observed in all three patients, while inotropic support, which included dobutamine, epinephrine and milrinone, as well as nitric oxide (NO), could be reduced to dobutamine and nitric oxide within 24–48 h after transplantation. All three patients had an uneventful recovery.


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  		Table 2 Pre- and post-T3 treatment hemodynamics in cardiac recipients with compromised allograft function; two patients died despite maximal medical support and assist device (data from three patients)

 
2.4. Low cardiac output following myocardial revascularization
We have occasionally administered T3 in patients with severely compromised postoperative hemodynamics following CABG or valvular surgery. In a consecutive series of 1780 CABG and valvular cases operated with extra corporial circulation, 11 patients (mean pre-operative LV function 0.26±0.05) received triiodothyronine treatment substitution when substantial difficulty to wean from CPB was encountered under inotropic support. All patients had intra-aortic balloon conterpulsation. Pre-treatment T3 levels were lower than 40 ng dl–1 in all patients. T3 dosage included a bolus injection of 2–3 µg during reperfusion, followed by an infusion of 0.2–0.6 µg h–1 for 6–12 h. In two instances, this infusion was repeated on post-operative day 1. Two patients died from low cardiac output. In the remaining nine patients, inotropic support could be reduced within 48 h in five, while IABP was left during 48–72 h in two other patients. These patients recovered from surgery.

2.5. Low cardiac output following surgery for complex congenital disease
In a consecutive series of 495 neonates and infants who underwent surgical correction of congenital heart defects using CPB. Among these children, a severe low cardiac output refractory to any conventional drug treatment occurred in seven patients presenting with a complex diagnosis: double-inlet left ventricle (n=1); double-outlet right ventricle (n=2); tricuspid atresia with mitral regurgitation (n=1); multiple muscular ventricular septum defects (n=1); and complete AV canal (n=2). All children received high-dose inotropic support and those with pulmonary hypertension received NO (Table 4).


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  		Table 4 Pre- and post-T3 treatment hemodynamics in pediatric patients with severe low cardiac output following surgical repair (data from 5 patients)

 
Metabolic acidosis was present in all children, the highest base excess being –14 mmol l–1. Inclusion criteria to proceed with T3 treatment are summarized in Table 3. Hormone supplementation was performed when T3 levels were lower than 60 ng dl–1 in neonates and <40 ng dl–1 in infants. A bolus injection of 0.5 µg was administered, followed by a continuous infusion at a dosage of 0.1 µg h–1 for 24–48 h. One patient received LVAD (Medos, Starnberg, Germany) pediatric size 9-ml ventricle, but unfortunately died from cerebral hemorrhage 2 days later. Another patient died from intractable right ventricular failure; the parents refused therapeutic escalation with RVAD. In the remaining five patients, a continuous improvement in hemodynamics could be observed within 48–96 h. These five patients recovered well.


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  		Table 3 Empirical inclusion criteria for pediatric patients to receive T3 treatment

 

   3. Discussion
Top
 Abstract
 1. Introduction
 2. Clinical experience
 3. Discussion
4. Conclusions
 References
 
Hemodynamic benefit following T3 treatment is much more difficult to demonstrate clinically than experimentally [19–33]. In the experimental setting, minor changes in contractility may be registered with a high sensitivity, while inter-subject variability remains problematic within clinical trials, especially as the degree of myocardial injury is difficult to quantify and to control.

Depressed T3 serum levels are commonly observed in patients suffering from severe heart failure, while norepinephrine serum level is generally elevated [19] in those having undergone cardiopulmonary bypass and in multi-organ donors. This may contribute to cardio-respiratory dysfunction and prolonged postoperative recovery.

The hypothesis that T3 supplementation might improve contractility after ischemic injury has been confirmed by numerous studies performed in different experimental models. Hearts exposed to a T3-depleted environment and subjected to ischemia showed improved left ventricular performance following T3 administration. This effect appears very rapidly, and therefore rules out the classical, nuclear-mediated pathway of thyroid hormone interaction with contractility, which takes more time. In an isolated porcine myocytes model, T3 was demonstrated to improve the myocyte contractile process through a cyclic-adenosine monophosphate (c-AMP)-independent mechanism. Furthermore, T3 potentiates the effects of β-adrenergic-receptor stimulation transduction by increasing c-AMP production, Ca2+-channel current and Ca2+ availability to the myocyte contractile apparatus; knowledge of these mechanisms may have implications regarding calcium homeostasis in the myocardial tissue [36].

3.1. Multi-organ donors and cardiac transplant recipients
A significant percentage of potential donor hearts are not used because of diminished hemodynamic performance or poor LV function prior to organ procurement [24]. In addition to transient but massive increases in catecholamine levels, brain death is associated with significant changes in blood levels of a number of hormones, including T3, cortisol and insulin. These abnormalities have been linked to impairment of cellular oxygen utilization and a shift from aerobic to anaerobic metabolism. Anaerobic metabolism is associated with an enhanced need for inotropic support, a further predictor of poor organ viability. Several authors have shown that repletion of thyroid hormone in these donors may improve cardiac performance and decrease the need for inotropic support [25–27]. Jeevanandam et al. described a series of six organ donors, two of whom had cardiac arrest for up to 10 min, presenting with hemodynamic instability despite high doses of inotropes. After intravenous administration of T3, LV filling pressures decreased, hemodynamic condition stabilized and inotropic support could be reduced. All subsequent recipients survived and were shown to have normal LV function at 1 week on echocardiography [27].

At present, the supply of donor hearts is so limited that the majority of patients with advanced heart failure will not undergo transplantation, and those who are accepted frequently experience long waiting periods. The varying degrees of cardiac, circulatory and neurohumoral disorders will influence prognosis in these patients. Thyroid hormone metabolism is frequently altered in advanced heart failure. Triiodothyronine levels are low and reverse T3 levels high in a majority of patients, with thyroxine and thyroid-stimulating hormone levels remaining normal [20]. Hamilton and co-authors have recently shown that short-term intravenous triiodothyronine is well tolerated in patients with advanced heart failure [20]. In a series of 21 patients who received different dosages, there was no evidence of ischemia or clinical arrhythmia and no significant increase in heart rate. In most patients who received a high dose (2 µg h–1 during 12 h) there was an increase in cardiac output and a reduction in systemic vascular resistance. An investigation by Hamilton and associates published in 1990 concluded that a low T3 and elevated reversed T3 state was associated with poor ventricular function and was the strongest predictor for short-term outcome and survival (37 vs. 100% for patients with preserved thyroid metabolism) [21]. In another trial, Salter and colleagues showed that hormonal disturbance was correlated with hemodynamic compromise [22,23].

The scarcity of cardiac donors has influenced donor selection and great efforts have been made to use as many donors as possible. The number of potential organ donors could be increased by enlarging the acceptance criteria, but the evaluation of these potential donors in terms of appropriateness for heart transplantation is critical. The medical management of these donors, maintaining stable organ perfusion and metabolic homeostasis up to multi-organ procurement, is also critical.

One of the most common causes of early death following cardiac transplantation is acute graft failure leading to low cardiac output syndrome. In cases of immediate early postoperative left or biventricular allograft dysfunction, the cause is likely to be myocardial stunning due to ischemia or sub-optimal myocardial protection and usually resolves within 48 h. In most cases, inotropic support is adequate to maintain cardiac output. Otherwise, T3 treatment should be advocated. Our data confirmed those reported by Novitzky et al., who were able to demonstrate improved cardiac allograft function following T3 supplementation in both donor and recipient [26].

3.2. Low cardiac output following cardiac surgery
Cardiopulmonary bypass (CPB) has been shown to produce functional hypothyroidism, characterized by low levels of circulating T3 and elevated levels of reversed T3 [28–30]. In a number of experimental models, evidence has accumulated suggesting that T3 supplementation to the ischemically injured myocardium enhances contractile performance [31–33].

The mechanisms by which serum T3 concentration decreases in patients undergoing CPB is uncertain, but is probably associated with hypothermia, hemodilution and the activation of inflammatory response mediators. Acute abnormalities of thyroid metabolism may be a manifestation of the stress response, along with complement activation, cytokine production and the release of other inflammatory mediators—which might be induced by CPB, in a similar way to sepsis and other critical illnesses [11].

T3 supplementation in CABG surgery was initiated by Novitzky et al. and mainly focused on high-risk patients with severely impaired left ventricular function [16]. However, these studies have only demonstrated a trend to beneficial effects. Only two placebo-controlled, double-blind studies have investigated the efficacy of T3 in the setting of myocardial revascularization. Klemperer and co-authors administered T3 or placebo to 142 patients with depressed LV function undergoing CABG [17,34]. T3 was administered as a bolus before declamping the aorta, during the reperfusion and then continuously for 6 h. Although the authors observed an increase in cardiac output and a decrease in systemic vascular resistance, the need for inotropic support and the final outcome did not differ with or without T3 supplementation. Bennett-Guerrero and the Duke T3 study group enrolled 211 patients undergoing CABG and likely to require inotropic support [35]. At release of aortic cross-clamp, patients were randomized to receive either T3 infusion for 6 h or placebo. Intravenous T3 did not significantly influence hemodynamic variables or inotropic drug requirements.

There are few data concerning T3 supplementation after complex congenital operations in the pediatric population. In cases of severe low cardiac output, these patients are generally difficult to manage and there is much more reluctance to implant assist devices in children compared with adults. Portman and co-authors investigated the action of triiodothyronine repletion following cardiopulmonary bypass in children [37]. Their results demonstrated that T3 substitution prevented deficiency in circulating T3 and promoted elevation in heart rate without concomitant decrease in systolic blood pressure. Myocardial oxygen consumption was improved and cardiac function reserve enhanced following extracorporeal circulation.

More recently, Chowdhury showed that T3 levels are more likely to fall in children after cardiac surgery and that the magnitude of the fall in serum T3 predicts greater therapeutic requirements in the post-operative period [38]. T3 treatment in neonates leads to a significant improvement in therapeutic measures.


   4. Conclusions
Top
 Abstract
 1. Introduction
 2. Clinical experience
 3. Discussion
 4. Conclusions
References
 
Despite a large number of experimental studies showing a benefit of thyroid hormone in compromised hearts, only a few reports describe clinical experience. Our data give some additional evidence that T3 treatment might be beneficial in multi-organ donors and in some subsets of adult and pediatric cardiosurgical patients


   References
Top
 Abstract
 1. Introduction
 2. Clinical experience
 3. Discussion
 4. Conclusions
 References
 

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