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    Abstract
   Introduction
   Case Report
   Discussion
   Conclusion
    References
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Table of Contents
CASE REPORT  
Year : 2013  |  Volume : 16  |  Issue : 3  |  Page : 212-214
Levosimendan in a neonate with severe coarctation of aorta and low cardiac output syndrome


1 Department of Pediatric Cardiac Anesthesiology and Intensive Care, Necker-Sick Children Hospital, Paris, France; Department of Anesthesiology, University Hospital Centre, Lausanne, Switzerland
2 Department of Pediatric Cardiac Anesthesiology and Intensive Care, Necker-Sick Children Hospital, Paris, France
3 Department of Pediatric Cardiac Surgery, Necker-Sick Children Hospital, Paris, France; Department of Cardiovascular Surgery, University Hospital Centre, Lausanne, Switzerland

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Date of Submission03-Dec-2012
Date of Acceptance28-Apr-2013
Date of Web Publication29-Jun-2013
 

   Abstract 

We report successful use of levosimendan after failed balloon angioplasty in a critically ill neonate with coarctation of aorta (CoA) and severe low cardiac output syndrome (LCOS). Treatment with levosimendan improved left heart function, and decreased lactate and brain natriuretic peptide levels. To our knowledge, this is the first report on the safe and successful use of levosimendan in the management of LCOS due to severe CoA in a neonate awaiting surgical repair.

Keywords: Coarctation of aorta, Balloon angioplasty, Brain natriuretic peptide, Levosimendan, Low cardiac output syndrome

How to cite this article:
Boegli YO, Gioanni S, van Steenberghe M, Pouard P. Levosimendan in a neonate with severe coarctation of aorta and low cardiac output syndrome. Ann Card Anaesth 2013;16:212-4

How to cite this URL:
Boegli YO, Gioanni S, van Steenberghe M, Pouard P. Levosimendan in a neonate with severe coarctation of aorta and low cardiac output syndrome. Ann Card Anaesth [serial online] 2013 [cited 2019 Jul 22];16:212-4. Available from: http://www.annals.in/text.asp?2013/16/3/212/114254



   Introduction Top


Coarctation of the aorta (CoA) represents 5-7% of congenital heart diseases with an incidence of 0.3-0.4 per 1000 live births. [1] Cardiac failure with metabolic acidosis and multiorgan dysfunction is a major cause of death in these patients which may be attributed to premature closure of the patent ductus arteriosus (PDA). Prostaglandins are the first line pharmacologic agent in the management of CoA; however, in the neonates, response to them is unpredictable. [2] In these critical situations, the outcome is often unfavourable unless the aortic obstruction is released as soon as possible by angioplasty or by surgical repair. [3] We describe the use of levosimendan after failure of balloon angioplasty for CoA in a neonate complicated by low cardiac output syndrome (LCOS) awaiting surgical repair.


   Case Report Top


A 9-day-old, 3.5 kg, term-born child was referred to the emergency room for poor feeding. On clinical examination, the baby was lethargic and the femoral pulses were absent. Transthoracic echocardiography (TTE) showed a severely hypokinetic left ventricle corresponding to LCOS due to severe CoA (ejection fraction < 20%). During TTE, a small PDA with a bidirectional shunt was also identified. The X-ray chest showed an enlarged heart [Figure 1]. The patient was transferred to the intensive care unit. Arterial blood gas analysis showed metabolic acidosis with a pH 7.13 and lactate 15 mmol/l; the child was oligo-anuric. The liver function test showed elevated L-aspartate aminotransferase 75 U/l; and L-aspartate aminotransferase 224 U/l. After placement of a central venous and an arterial catheter (arterial pressure −42/25 mmHg), the child was intubated and ventilated using FiO2: 50%, positive end-expiratory pressure PEEP: 8 cmH 2 O, respiratory rate: 35/min; the peak inspiratory airway pressure was 23 mmHg; simultaneously, an infusion of alprostadil 25 ng/kg/min and epinephrine 0.05 μg/kg/min was started. In spite of support with epinepherine and the increase of prostaglandin dose, the pH was 7.38 and the lactate and NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels were high at 20 mmol/l and > 5000 pg/ml, respectively. A repeat TTE was performed, which showed a hypokinetic left ventricle with an ejection fraction (LVEF) less than 30%. Gradient across the CoA was high in spite of heart failure (gradient max: 38 mmHg). Balloon angioplasty was attempted in the catheterization laboratory, but was unsuccessful because the angioplasty catheter could not be passed beyond the stenosis. The left ventricular function did not improve (gradient max: 32 mmHg and LVEF < 30%). BNP remained at 5000 pg/ml while lactate decreased to 13 mmol/l. Then, an infusion of levosimendan 0.2 μg/kg/min was started and epinepherine infusion was weaned. The treatment with alprostadil was continued until surgery to maintain patency of the PDA. After 24 h of levosimendan infusion an improvement of the left heart function (LVEF 58%) was observed with a decrease of the lactate and BNP levels to 1.8 mmol/l and to 508 pg/ml, respectively [Figure 2]. Urine output and liver functions also improved.
Figure 1: Chest X-ray at admission, showing moderate cardiomegaly

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Figure 2: Trends of lactatemia and N-terminal pro-B-type natriuretic peptide level at baseline, after balloon angioplasty, after treatment with levosimendan, and after surgery

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Two days after admission in the paediatric intensive care unit (PICU), a Crafoord procedure (excision of CoA segment and end-to-end anastomosis) was successfully performed. Nevertheless, the BNP level increased to 5000 pg/ml in spite of the clinical improvement. The child was extubated 23 h after surgery and left the PICU 3 days later. Follow-up TTE showed a LVEF of 72%. The BNP and lactate levels decreased to 2470 pg/ml and 1.5 mmol/l.


   Discussion Top


The present case report underscores the successful use of levosimendan in a critically ill neonate with CoA and severe LCOS. The severity of the cardiac failure was documented by echocardiography and by NT-proBNP and lactate levels. The initial management of CoA complicated with LCOS remains debatable. [4] In our center, in neonates with CoA and LCOS, the initial treatment is to attempt balloon angioplasty in the catheterization laboratory. Because of failed balloon angioplasty, we started levosimendan as a bridge to surgical repair. In France, nominative temporary authorization for the off-label use of levosimendan is granted by the national agency of drugs safety (Agence National de Sécurité du Médicament et des Produits de Santé). Levosimendan was preferred over milrinone because of its more pronounced inotropic effects and for its anti-stunning and anti-ischemic properties. [5] Furthermore, because of its calcium-sensitizing properties, levosimendan is an ideal therapeutic for the immature myocardium, characterized by a highly calcium-dependent contractility. [6],[7] The administration of levosimendan in paediatric patients has been described since 2004. In the neonatal population; however, only a few case reports discuss the use of levosimendan for heart failure, pulmonary hypertension or after cardiac surgery. The improvement of left-ventricular function was highlighted and no side-effects were reported in these isolated cases. [8],[9] Nevertheless, no controlled clinical trial exist to verify this observation. Based on our report, we propose the use of levosimendan as cardiac conditioning agent before surgery in the neonates presenting with severe CoA and acute left-ventricular failure. We believe that the favorable properties of the levosimendan (positive inotropism, peripheral vasodilatation, preservation of the consumption of oxygen) could be useful in these conditions. In our patient, the efficacy of the treatment was assessed by repeated echocardiography and assessment of biomarkers NT-proBNP and lactate as markers of cardiac failure and multiorgan failure. In this case, we noted that the level of BNP correlated with the clinical observations as well as with the echocardiographic findings. After the failed attempt at balloon dilatation, BNP did not decrease and the ventricular and multiorgan dysfunction persisted. After 12 h, of the onset of treatment with levosimendan, the significant fall in BNP was accompanied with an improvement of cardiac function with a LVEF reaching 58% on TTE. The drop in lactate and the progressive restoration of diuresis also correlated with the efficacy of levosimendan treatment. After 24 h of treatment with levosimendan, and stabilization of the clinical status, the child was successfully operated. During the procedure, we observed an increase of NT-proBNP. It has been shown that the level of NT-proBNP increases significantly 6 h after surgery for congenital heart diseases, to reach a plateau between 12 h and 48 h. [10],[11] However, these studies only concern cardiac surgery using the cardiopulmonary bypass (CPB) and their results may not be applicable for surgery without CPB. We, however, extrapolated these conclusions in view of the aortic cross clamping during the surgical repair of CoA.


   Conclusion Top


Neonates presenting for emergency surgery with LCOS and multiorgan failure are prone to an increased rate of adverse outcome. Levosimendan is an inodilator and doesn't increase myocardial oxygen consumption. It is a myofilament calcium sensitizer without alpha or beta receptor agonist effects. It allows decreasing beta adrenergic inotropes, and may induce pharmacological pre-conditioning. In this neonate, myocardial recovery assessed by echocardiography, blood lactate and NT-proBNP levels showed gradual recovery of myocardial function during the levosimendan treatment. No side-effects were noticed during the levosimendan administration. Although controlled trials concerning the safety of levosimendan in neonates have not yet been performed, we suggest its cautious use as a bridge to surgery in neonates with a LCOS due to CoA. Prospective trials are needed to confirm our findings.

 
   References Top

1.Jenkins NP, Ward C. Coarctation of the aorta: Natural history and outcome after surgical treatment. QJM 1999;92:365-71.  Back to cited text no. 1
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2.Fesseha AK, Eidem BW, Dibardino DJ, Cron SG, McKenzie ED, Fraser CD Jr, et al. Neonates with aortic coarctation and cardiogenic shock: Presentation and outcomes. Ann Thorac Surg 2005;79:1650-5.  Back to cited text no. 2
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3.Alaei F, Moghadam MY, Mortaezaian H, Alaei M, Bakhshandeh H. Balloon Angioplasty versus Surgical Repair of Coarctation of Aorta in Infants. J Tehran Heart Cent 2011;6:134-7.  Back to cited text no. 3
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4.Francis E, Gayathri S, Vaidyanathan B, Kannan BR, Kumar RK. Emergency balloon dilation or stenting of critical coarctation of aorta in newborns and infants: An effective interim palliation. Ann Pediatr Cardiol 2009;2:111-5.  Back to cited text no. 4
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5.De Luca L, Colucci WS, Nieminen MS, Massie BM, Gheorghiade M. Evidence-based use of levosimendan in different clinical settings. Eur Heart J 2006;27:1908-20.  Back to cited text no. 5
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6.Caresta E, Papoff P, Benedetti Valentini S, Mancuso M, Cicchetti R, Midulla F, et al. What's new in the treatment of neonatal shock. J Matern Fetal Neonatal Med 2011;24:17-9.  Back to cited text no. 6
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7.Lechner E, Moosbauer W, Pinter M, Mair R, Tulzer G. Use of levosimendan, a new inodilator, for postoperative myocardial stunning in a premature neonate. Pediatr Crit Care Med 2007;8:61-3.  Back to cited text no. 7
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8.Braun JP, Schneider M, Kastrup M, Liu J. Treatment of acute heart failure in an infant after cardiac surgery using levosimendan. Eur J Cardiothorac Surg 2004;26:228-30.  Back to cited text no. 8
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9.De Carolis MP, Piastra M, Bersani I, Pardeo M, Stival E, Tempera A, et al. Levosimendan in two neonates with ischemic heart failure and pulmonary hypertension. Neonatology 2012;101:201-5.  Back to cited text no. 9
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10.Pérez-Piaya M, Abarca E, Soler V, Coca A, Cruz M, Villagrá F, et al. Levels of N-terminal-pro-brain natriuretic peptide in congenital heart disease surgery and its value as a predictive biomarker. Interact Cardiovasc Thorac Surg 2011;12:461-6.  Back to cited text no. 10
    
11.Walsh R, Boyer C, LaCorte J, Parnell V, Sison C, Chowdhury D, et al. N-terminal B-type natriuretic peptide levels in pediatric patients with congestive heart failure undergoing cardiac surgery. J Thorac Cardiovasc Surg 2008;135:98-105.  Back to cited text no. 11
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Correspondence Address:
Yann Olivier Boegli
Department of Paediatric Cardiac Anaesthesiology and Intensive Care, Necker - Sick Children Hospital, Paris, France and Department of Anaesthesiology, University Hospital Centre, Lausanne, Switzerland

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.114254

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