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Cardiovascular Anesthesia

The Effects of Triiodothyronine on Hemodynamic Status and Cardiac Function in Potential Heart Donors

Goarin, Jean-Pierre MD; Cohen, Sophie MD; Riou, Bruno MD, PhD; Jacquens, Yves MD; Guesde, Richard MD; Le Bret, Francoise MD; Aurengo, Andre PhD; Coriat, Pierre MD

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Successful organ transplantation depends on optimal management of organ donors and a better understanding of the physiological consequences of brain death [1]. Several experimental studies have demonstrated that hemodynamic instability during brain death could be due to severe myocardial dysfunction [2]. Using transesophageal echocardiography (TEE), we reported a relatively high incidence (30%) of severe myocardial dysfunction [3]. Severe myocardial dysfunction in the donor has been reported to be an important prognosis factor in heart transplantation [4].

The mechanisms of this myocardial dysfunction remain debatable [5]. After brain death, brainstem ischemia is followed by a sudden reduction in free circulating pituitary hormones [6]. Some authors have suggested that a reduction in plasma free triiodothyronine (T3) concentrations could be responsible for impairment in myocardial cell metabolism and myocardial contractility [7]. Furthermore, some studies have demonstrated that hormonotherapy could reverse some of these metabolic impairments [8] and reduce hemodynamic instability [9]. This hypothesis was supported by experimental studies in the baboon that demonstrated a beneficial effect of T3 on myocardial function [10]. However, these results have not been confirmed by other experimental [11] and clinical studies [12].

Thus, we conducted a prospective study to determine the hemodynamic and myocardial effects of T3 administration in brain-dead organ donors. In the present study, we used TEE to precisely assess left ventricular function in brain-dead patients [3,5].



After ethical approval had been obtained, this prospective, randomized, blinded, placebo-controlled study was conducted according to the French legislation concerning organ procurement. Brain death was certified by: 1) a neurological examination demonstrating the absence of brainstem reflexes; 2) an apnea test performed with intratracheal continuous high flow (15 L/min) of oxygen and after 15 min of mechanical ventilation under a fraction of inspired oxygen of 100%, with the absence of spontaneous ventilatory activity after 15 min of apnea at an arterial PCO2 above 60 mm Hg; 3) no electrical activity over a 20-min period of electroencephalographic recording; and 4) absence of hypothermia (>35 degrees C) and drugs known to depress central nervous system function. Patients with a history of cardiovascular disease were excluded.


All patients had invasive hemodynamic assessment, including the continuous measurement of arterial pressure with an indwelling radial artery catheter and right heart catheterization (Swan-Ganz catheter SP5507 S; Viggo-Spectramed, Montigny le Bretonneux, France) connected to an HP 78354 hemodynamic monitor (Hewlett-Packard, Andover, MA). The following hemodynamic parameters were recorded: heart rate, mean arterial blood pressure, systolic arterial blood pressure, mean pulmonary arterial pressure, pulmonary artery occlusion pressure (PAOP), and right atrial pressure. Cardiac output determination was performed using the thermodilution method, the mean calculated from three measurements.

Arterial and mixed venous blood were withdrawn to measure the following biological variables: hemoglobin levels, pH, PO2, PCO2, and oxygen saturation. The following variables were calculated: cardiac index, stroke volume, systolic left ventricular stroke work index, arteriovenous difference in oxygen content, oxygen consumption, and pulmonary and systemic vascular resistances, according to standard formulae.

Left ventricular function was assessed using TEE (HP Sonos 1500; Hewlett-Packard). TEE examination was performed by two trained echocardiographers. TEE was used on-line for guiding fluid therapy and to stratify the patients into two groups according to their left ventricular function (normal versus decreased). During the study, TEE images were recorded on a videotape and analyzed retrospectively by a blinded observer. Using the transgastric short-axis view of the left ventricle at the midpapillary level, the left ventricular end-diastolic area (LVEDa) and end-systolic area (LVESa) were manually traced using a light pen system, as previously reported [13]. Three measures of left ventricle areas at three consecutive beats were performed and averaged. The left ventricular fractional area change (FAC) is an ejection phase index of left ventricular systolic performance and was calculated using the following equation: Equation 1

A FAC of below 50% was considered abnormal. We have previously determined that the interobserver variability in the measurement of FAC is 4.7% +/- 3.6% and the intraobserver variability is 6.0% +/- 4.2% in brain-dead patients [14]. On the same transgastric short-axis view of the left ventricle, M-mode echocar-diograms were recorded for measurement of the left ventricular end-diastolic (LVEDD) and end-systolic (LVESD) diameters, the anterior end-systolic (ESWT) and end-diastolic (EDWT) wall thicknesses, left ventricular ejection time (LVET) from the peak of the R wave on electrocardiogram recording to the maximal thickening of the anterior wall, and the RR interval (RR). The rate-corrected mean velocity of fiber short-ening (mean Vcfc) is another ejection phase index of left ventricular systolic performance and was calculated according to the following formula: Equation 2

The loading conditions were assessed using the LVEDa indexed on the body surface area (LVEDai) and using the meridonial end-diastolic wall stress (EDWS) using the following formula [15]: Equation 3

The meridonial end-systolic wall stress (ESWS) was calculated on the basis of the following formula with the peak systolic left ventricular pressure estimated by the systolic arterial pressure (SAP): Equation 4

The noninvasive methods of calculating ESWS and the velocity of fiber shortening have been validated [16]. The fiber shortening-stress relation is considered a load-independent measure of myocardial contractility [17].

Hormone Dosages

Arterial blood samples were withdrawn for free serum T3, thyroxine (T4), and thyroid stimulating hormone (TSH) concentration measurements. Blood was withdrawn into dry tubes and immediately centrifuged, and serum was stored at -40 degrees C until assayed. Determination of free serum thyroid hormone concentrations was performed using an immunoluminometric assay (Berilux FT3, FT4, hTSH; Behring Laboratory, Marburg, Germany). Normal ranges of serum concentrations were as follows: T3: 2.9-8.9 pmol/L; T4: 9-25 pmol/L; TSH: 0.1-3.2 mUI/mL).

Experimental Protocol

Before the onset of the study, hypovolemia was corrected by fluid loading using colloids. Hypovolemia was diagnosed when the LVEDai was lower than 5.5 cm2/m2, as previously reported [13]. Moreover, fluid loading was also administered in patients with a normal LVEDa but virtual obliteration of the left ventricular cavity at end-systole, resulting in supranormal value of FAC (i.e., greater than 75%), which could be considered to reflect mild hypovolemia [18]. Subsequently, hemodynamic stability was ensured with dopamine administration. The dose of dopamine was the lowest dose resulting in a mean arterial pressure greater than 65 mm Hg. During the study period, mechanical ventilation variables were maintained constant (tidal volume, ventilatory rate, and end-expiratory pressure), as was dopamine infusion rate. No colloid was administered, and the amount of crystalloids administered was determined according to our resuscitation protocol, i.e., according to diuresis.

Patients were randomized into two groups, a placebo group and a T3 group. After all variables had been recorded in control conditions, patients blindly received either placebo (saline) or 0.2 micro gram/kg T3 (Thyrotardin Inject; Henning Laboratory, Berlin, Germany) as an intravenous bolus. In order to obtain the same proportion of patients with a low FAC between the two groups, randomization was stratified according to initial FAC, i.e., <50% or >50%.

All hemodynamic, echocardiographic, and biological parameters were determined before and 30 min after T3 or placebo administration. Moreover, whenever possible, TEE was performed again 6 h after T3 or placebo administration.

Statistical Analysis

Data are expressed as mean +/- SD. Comparison of means was performed using Student's t-test or repeated measures analysis of variance and Newman-Keuls test. Comparison of proportion was performed using the Fisher's exact method. Correlation between two variables was performed using the least square method. Randomization was performed using a random number table. All P values were two-tailed, and a P value of less than 0.05 was considered significant. Statistical analysis was performed using PCSM software (Deltasoft, Meylan, France).


Forty patients were randomized, and three patients were excluded because hormone determination was not performed. Thus, 37 patients were included in the study, with a mean age of 35 +/- 12 yr (range 15-55 yr). The cause of brain death was head trauma in 21 cases (57%), cerebrovascular disease in 10 cases (27%), and cerebral anoxia related to cardiac arrest in 6 cases (16%). Mean concentration of T3 was 1.86 +/- 1.55 pmol/L. Only six patients had normal values of T3 in control conditions Figure 1. Mean T4 concentration was 11.97 +/- 4.02 pmol/L. T4 concentration was normal or above normal values in all patients. Mean value of TSH concentration was 0.56 +/- 0.84 mUI/mL. Only two patients had a low TSH concentration. In control conditions, there were no significant differences between the two groups in regard to physical characteristics and dopamine doses Table 1, hemodynamic and echocardiographic parameters Table 2, and serum hormone concentrations Table 3. There was no significant difference between the two groups of patients with normal and decreased FAC in age (34 +/- 13 yr vs 36 +/- 11 yr) or cause of brain death (head trauma: 47% vs 40%, cerebrovascular disease: 24% vs 30%; cerebral anoxia: 12% vs 20%).

Figure 1
Figure 1:
Correlation between triiodothyronine (T3) serum concentrations and left ventricular fractional area change (FAC) in control condition. No significant correlation was found (r = 0,17, NS). Dotted lines indicate normal range of T3.
Table 1
Table 1:
Comparison of Patients' Characteristics and Dopamine Dose in Placebo and Triiodothyronine (T3) Groups
Table 2
Table 2:
Comparison of Hemodynamic Variables Before (Control) and 30 Min After Administration of Triiodothyronine (T3) or Placebo
Table 3
Table 3:
Comparison of Hormonal Concentrations Before (Control) and 30 Min After Administration of T3 or Placebo

In control conditions, there was no significant correlation between individual values of T3 concentration and FAC (R = 0.17, not significant) Figure 1. After 30 min, all patients receiving T3 had normalized serum T3 concentration Table 3. No significant differences in hemodynamic and echocardiographic parameters were observed between the placebo and T3 groups Table 2. Indeed, hemodynamic and echocardiographic parameters remained unchanged after either T3 or placebo administration in the whole study population as well as in the group of subjects with low FAC. There were no significant changes in preload (LVEDai, EDWS), afterload (ESWS), or ejection phase indices of left ventricular systolic performance (mean Vcfc, FAC). There was no significant difference in FAC before and after administration of either placebo (47% +/- 18% vs 48% +/- 16%, not significant) or T3 (45% +/- 17% vs 47% +/- 17%) in the whole population.

In 20 patients with impaired left ventricular function (FAC < 50%), FAC remained unchanged after T3 (n = 10; 34% +/- 12% vs 30% +/- 10%) or placebo (n = 10; 38% +/- 12% vs 35% +/- 13%) administration. Figure 2 shows the velocity of myocardial fiber shortening-ESWS relation before and after T3 administration in patients with a normal or a decreased FAC. In patients with a normal FAC, a decrease in mean Vcfc was observed even when this parameter was matched with the ESWS, suggesting that some patients in this group had a mild or moderate impairment of myocardial contractility Figure 2.

Figure 2
Figure 2:
Evolution of the fiber shortening-stress relation before and after injection of triiodothyronine (T3) in the group of patients with a normal left ventricular fractional area change (FAC) (A) and the group of patients with a decreased FAC (B). Values are mean +/- SD. ESWS = end-systolic wall stress; mean Vcfc = mean velocity of fiber shortening. The lines indicate the normal fiber-shortening stress relation (solid line) +/- 2 SD (dotted lines).

Ten patients did not require dopamine administration, 5 in the placebo group and 5 in the T3 group. In these patients, FAC remained unchanged after T3 (53% +/- 3% vs 57% +/- 9%) or placebo (46% +/- 11% vs 39% +/- 15%) administration.

Organ harvesting was delayed in 17 patients and TEE was performed again 6 h later. Eight patients belonged to the T3 group and nine to the placebo group. No significant changes in FAC were noted in either the placebo group (51% +/- 18% vs 47% +/- 18%) or the T3 group (49% +/- 17% vs 44% +/- 17%). Individual values are depicted in Figure 3. Plasma T3 concentrations were measured 6 h later in nine patients (five in the T3 group and four in the placebo group). The plasma T3 concentration remained in the normal range 6 h after T3 administration (6.05 +/- 1.90 vs 8.25 +/- 2.20 pmol/L).

Figure 3
Figure 3:
Evolution of the left ventricular fractional area change (FAC) determined using transesophageal echocardiography in brain-dead patients before and after administration of triiodothyronine (T3) (n = 19). In eight of these patients, FAC was determined again 6 h later.


In the present study, we did not observe any beneficial effects of T3 administration on hemodynamic variables or left ventricular systolic function. The administration of T3 did not improve any conventional hemodynamic variables or echocardiographic variables of cardiac systolic function, whereas the injected dose of T3 normalized the serum T3 concentration.

Several studies have highlighted hemodynamic instability, myocardial injury, and impairment in cardiac function after brain death [2,3,5,14,19]. The mechanisms involved in brain-death-induced myocardial dysfunction are not yet fully understood and may involve several possible etiologies. High levels of catecholamines related to Cushing reflex, which appears in the early phase of brain death, may lead to direct myocardial injury, coronary vasospasm, or both [14]. A change from aerobic to anaerobic metabolism, because of hemodynamic deterioration with low perfusion pressure, which occurs immediately after brain death, may lead to a stunned myocardium. In addition, a reduction in circulating T3 may result in a reduction in oxidative metabolism [8]. In the present study, we confirmed a high incidence of low serum free T3 concentration in brain-dead patients. Some of our patients had a marked decrease in circulating T3 concentration, whereas the serum T4 and TSH concentrations were in the normal range in most of them. Despite brainstem ischemia, TSH concentration was normal in most of our patients at the early stage of brain death. This hormonal status suggests the presence of a euthyroid sick syndrome in brain-dead organ donors [6]. Euthyroid sick syndrome is due to the transformation of T4 into reverse T3, the inactive form of T3, and has been largely described during fasting and critical illness [20]. In the present study, we found no significant correlation between serum T3 concentration and FAC. These results suggest that serum T3 concentration was not a major determinant of cardiac function in our brain-dead patients.

The action of thyroid hormone on myocardial contractility is complex and involves immediate and delayed effects. An increase in the transsarcolemnal calcium entry and in the sarcoplasmic reticulum calcium uptake is detectable 24 hours after administration of a single dose of T4 [21] and seems to be nondependent on catecholamine activity [21,22]. The long-term administration of T4 significantly increases myocardial myosine and ATPase activity after eight days of T4 administration [22]. Thus, delayed T4 effects on myocardial contractility could not be detectable during the acute phase of brain death. However, some authors have described an acute inotropic effect of T3 related to different and not fully understood mechanisms [23]. In isolated cardiac muscle, Ririe et al. [24] showed a rapid inotropic effect of T3 not mediated by beta-adrenergic receptors. Moreover, Novitsky et al. [25] have described a positive inotropic effect of T3 in cardiac surgery patients with post-cardiopulmonary bypass myocardial dysfunction. These immediate effects were thought to be involved in the beneficial hemodynamic effect of T3 in brain-dead patients [9,10].

The effects of T3 administration in brain-dead patients remain controversial. Many studies have evaluated the combined effects of global hormonotherapy, such as T3 plus vasopressin [26] or T3 plus cortisol [9], but they could not discriminate the specific actions of these different hormones. Some experimental studies have suggested that T3 administration could reverse the change from aerobic to anaerobic metabolism at the tissue level after brain death [8]. Moreover, in a retrospective study, Novitsky et al. [9] reported a beneficial effect of T3 administration on hemodynamic stability in brain-dead patients. In this retrospective clinical study, cardiac function was assessed by using only simple hemodynamic parameters such as arterial blood pressure, cardiac output, or dopamine dose required to maintain a normal arterial pressure [9]. Moreover, some experimental [11] and clinical studies [12,27] have failed to confirm these results, suggesting that T3 has no important effect on hemodynamics and myocardial function during brain death. In the present randomized, placebo-controlled study, we made an accurate analysis of hemodynamic and cardiac function using TEE, and we observed no significant effect of T3 administration in brain-dead patients. TEE enabled us to obtain a more precise and reliable evaluation of cardiac function than that achievable with a pulmonary artery catheter alone. It should be pointed out that a similar controversy exists concerning the effects of T3 administration after coronary-artery by-pass surgery and that a large, controlled study has recently concluded that T3 does not change outcome or alter the need for standard therapy, despite the use of very high doses of T3, which significantly decreased systemic resistance and increased cardiac index [28].

In isolated heart, Dyke et al. [29] have observed enhanced left ventricular systolic function after ischemic injury and T3 administration that could not be detected in nonischemic hearts. This result suggests that T3 had no direct inotropic effect but could have a beneficial effect on postischemic left ventricular dysfunction. Novitsky et al. [19] have described cardiac histopathological changes after brain death in the baboon, affecting smooth muscle in coronary arteries and contractile myocardium, related to severe spasm and ischemic injury. Moreover, we have recently reported that high levels of circulating cardiac troponin T were associated with decreased cardiac function in brain-dead patients, suggesting that myocardial ischemia occurred [14]. Nevertheless, we did not observe any significant changes in hemodynamic variables or echocardiographic data even in brain-dead patients with decreased FAC.

Some of our brain-dead patients received dopamine, which could have interfered with T3 effects. Indeed, T3 has been reported as increasing the beta-adrenoceptor sensitivity [30], while other studies have failed to demonstrate any modification in heart sensitivity to adrenoceptor stimulation during either hypo- or hyperthyroidism [31]. Furthermore, the acute inotropic effect of T3 administration seems independent of beta-adrenergic receptors [27]. Therefore, the presence of dopamine should not have precluded an accurate analysis of the effects of T3 on cardiac function, but should be considered rather as an important design of the study. However, while dopamine dose was maintained constant, no significant changes in hemodynamic and echocardiographic variables were noted between the two groups of patients. Moreover, no changes occurred in patients with or without dopamine administration. Thus, we believe that dopamine administration did not modify the fundamental conclusion of the present therapeutic trial.

Some limitations of the study should be considered when assessing the clinical relevance of our findings. First, myocardial contractility is difficult to assess precisely in the clinical setting and left ventricular FAC is not considered to be a reliable measure of myocardial contractility because it is load dependent. Nevertheless, the loading conditions were assessed and there were no significant changes in preload as assessed by the LVEDAi and EDWS or in afterload as assessed by ESWS before and after injection of T3. Moreover, the velocity-stress relation, which is considered to be a relatively load-independent parameter of myocardial contractility [17], also did not change significantly. Second, the study duration could be considered too short to observe some of the delayed thyroid hormone metabolic action. Nevertheless, some of the T3 effects (beta-adrenoceptor sensitization, direct positive inotropic effect) have been shown to occur rapidly. Moreover, in some of the brain-dead patients, FAC was measured six hours later and remained unchanged. Third, we did not assess the effects of T3 administration on early cardiac function in the recipients and/or on cardiac allograft survival. Thus, we cannot rule out the hypothesis that T3 administration may have some delayed beneficial effects on recipient cardiac function. However, Garcia-Farges et al. [32] did not observe a significantly higher intracellular nucleotide level in heart biopsies immediately after organ retrieval from patients receiving T3. Fourth, the present study only dealt with hemodynamic status and cardiac function, and some clinical studies have suggested that T3 administration may increase intracellular nucleotide levels in the kidneys and the pancreas.

In conclusion, we confirmed that serum T3 is reduced in brain-dead patients, but we observed no significant correlation between serum T3 concentration and cardiac function, suggesting that the euthyroid sick syndrome was not a significant determinant of myocardial dysfunction in these patients. Furthermore, we observed that T3 administration had no detectable effects on hemodynamic status and cardiac function in potential heart donors.


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