Use of levosimendan in cardiogenic shock

Fayçal Janen; Khaoula El Arayedh; Iheb Labbene; Chihebeddine Romdhani; Mustapha Ferjani

doi:10.12688/f1000research.5820.1

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Research Article

Use of levosimendan in cardiogenic shock

[version 1; peer review: peer review discontinued]

Fayçal Janen¹, Khaoula El Arayedh², Iheb Labbene³, Chihebeddine Romdhani³, Mustapha Ferjani³

Fayçal Janen¹, Khaoula El Arayedh², [...] Iheb Labbene³, Chihebeddine Romdhani³, Mustapha Ferjani³

PUBLISHED 05 Dec 2014

Author details Author details

¹ Pharmacy Department, Military Hospital of Tunis, Monfleury,Tunis, 1008, Tunisia
² Pharmacy Department, Basic Health Group of South Tunis, 90 Sayada Street Bellevue, Tunis, 1009, Tunisia
³ Université Tunis El Manar, Faculté de Médecine de Tunis, LR12DN01, Intensive Care Unit, Military Hospital of Tunis, Monfleury Tunis, 1008, Tunisia

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PEER REVIEW DISCONTINUED

Abstract

Cardiogenic shock (CS) is acute inadequate tissue perfusion caused by the heart's inability to pump an adequate amount of blood. Due to the failure of classic inotrope agents, a sensitizer agent, levosimendan, has been used as a rescue therapy in such situations. In order to assess the effectiveness of levosimendan to treat CS, we studied its hemodynamic effects on patients with CS. A retrospective study was conducted at the ICU of the Military Hospital of Tunis between January 2004 and December 2009, and between January 2011 and December 2013. Twenty-six patients with CS refractory to catecholamines were included in our study. When catecholamines failed to improve the hemodynamic condition, levosimendan was introduced. This treatment was administered in two steps: a loading dose of 12 µg/kg/min was infused for 30 min; and then continuous infusion was given for 24 h at a dose of 0.1 µg/kg/min. Levosimendan significantly increased mean arterial pressure to 76 ± 7 mmHg at 48 h and cardiac index to 3.19 ± 0.68 L/min/m²and decreased pulmonary wedge pressure to 17 ± 3 mmHg at 48 h. Pulmonary arterial systolic pressure, pulmonary arterial diastolic pressure, and mean pulmonary arterial pressure were significantly reduced at 24 h. A significant decrease in lactate from 3.77 ± 2.93 to 1.60 ± 1.32 mmol/L, by 72 h, was also noted. Levosimendan significantly reduced systemic vascular resistance and pulmonary vascular resistances. Administration of levosimendan also reduced the need for catecholamines. Our study confirms the efficacy of levosimendan to stabilize hemodynamic parameters in patients with CS.

Keywords

levosimendan, cardiogenic shock, hemodynamic variables, mortality

Corresponding author: Fayçal Janen

Competing interests: No competing interests were disclosed.

Grant information: Supported by a grant from the Research Laboratory LR12DN01 and The Military Hospital of Tunis.
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Copyright: © 2014 Janen F et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Data associated with the article are available under the terms of the Creative Commons Zero "No rights reserved" data waiver (CC0 1.0 Public domain dedication).

How to cite: Janen F, El Arayedh K, Labbene I et al. Use of levosimendan in cardiogenic shock [version 1; peer review: peer review discontinued]. F1000Research 2014, 3:296 (https://doi.org/10.12688/f1000research.5820.1) First published: 05 Dec 2014, 3:296 (https://doi.org/10.12688/f1000research.5820.1) Latest published: 05 Dec 2014, 3:296 (https://doi.org/10.12688/f1000research.5820.1)

Introduction

Cardiogenic shock (CS) is a clinical condition of acute inadequate tissue perfusion caused by the heart’s inability to pump an adequate amount of blood^1,2. Pharmacological treatment of CS is based on positive inotropic agents^3,4. Due to the failure of classic inotrope agents, a sensitizer agent, levosimendan, has been used as rescue therapy in such situations. This drug has both positive inotropic and myocardial relaxing properties, which increase the affinity of myofilaments within the myocardial cell to calcium without raising intracellular concentrations of calcium or AMPc^5–8. Levosimendan can improve the hemodynamic status of patients with CS without increasing the consumption of myocardial oxygen and without increasing the risk of arrhythmia^9,10; however, few studies have been conducted on the use of levosimendan to treat CS.

The purpose of our study was to assess the effectiveness of levosimendan to treat CS by studying its hemodynamic effects on 26 patients with CS and who were refractory to catecholamines.

Materials and methods

A retrospective study was conducted at the ICU in the Military Hospital of Tunis for two periods: between January 2004 and December 2009, and from January 2011 until December 2013. All patients had CS and were aged >18 years. Patients who died within 48 h were excluded from the study. The diagnosis of CS was made if hypotension was <90 mmHg for more than 30 min and there were signs of low perfusion in the absence of a hypovolemia or cardiac arrhythmia. These signs were associated with a cardiac index of <2.2 L/min/m², a pulmonary capillary wedge pressure of >18 mmHg, and high doses of catecholamines had been ineffective to restore mean arterial pressure to 65 mmHg (i.e., dobutamine at >15 µg/kg/min and noradrenaline at >0.6 µg/kg/min).

When catecholamines failed to improve the hemodynamic condition and there were persistent signs of low peripheral perfusion, levosimendan was introduced (Orion Pharma, Espoo, Finlande). This treatment was administered in two steps: a loading dose of 12 µg/kg/min was infused for 30 min; and then continuous infusion was given for 24 h at a dose of 0.1 µg/kg/min. The pulmonary artery was catheterized using a 7.5-Fr Swan Ganz catheter with continuous cardiac output and mixed venous saturation measurements (Edwards Life sciences, North Carolina, USA). This catheter allowed us to collect hemodynamic parameters from each patient at just before administration of levosimendan (i.e., T0), at 30 and 90 min, and at 2, 4, 8, 12, 24, and 48 h.

Doses of catecholamine and plasma-lactate concentrations were recorded on days 0, 1, 2, and 3. Values of the left-ventricular ejection fraction were collected on days 0, 1, 2, 7, and 15. The primary endpoints were the evolution of hemodynamic parameters (the cardiac index, pulmonary pressure, and SvO₂). Data were recorded and analyzed using Microsoft Excel (2007) software and Epi Info 6.0.4 (http://www.cdc.gov). Continuous variables were expressed as their means ± standard deviations and were compared between groups using Student’s two-tailed t-test. Non-parametric tests were also used where necessary (Mann–Whitney U test). Fisher’s exact (or the chi-squared) test was used to compare categorical variables, as appropriate. A p-value of <0.05 was considered statistically significant.

The local ethics committee approved the use of the patients’ data for this study.

Results

patient Number	age years	gender	weight Kg	etiology	Coronarography angioplasty	APACHE II	MOF	Evolution Dead : D. Survivor : S	length of stay	PAM 0 mmHg	PAM 30	PAM 90	PAM H2	PAM H4	PAM H8	PAM H12	PAM H24	PAM H48	HR 0 beat/min	HR 30	HR 90	HR H 2	HR H4	HR H8	HR H12	HR H24	HR H48	POD 0 mm Hg	POD 30	POD 90	POD H2	POD H4	POD H8	POD H12	POD H24	POD H48	IC 0 L/min/m2	IC 30	IC 90	IC H2	IC H4	IC H8	IC H12	IC H24	IC H48	PAPO 0 mm Hg	PAPO 30	PAPO 90	PAPO H2	PAPO H4	PAPO H8	PAPO H12	PAPO H24	PAPO H48	RVS 0 dyne/s/cm2	RVS 30	RVS 90	RVS H2	RVS H4	RVS H8	RVS H12	RVS H24	RVS H48	SVO2 0 (%)	SVO2 30	SVO2 90	SVO2 H2	SVO2 H4	SVO2 H8	SVO2 H12	SVO2 H24	SVO2 H48	PAP S 0 mmHg	PAP S 30	PAP S 90	PAP S H2	PAP S H4	PAP S H8	PAP S H12	PAP S H24	PAP S H48	PAP M 0 mmHg	PAP M 30	PAP M 90	PAP M H2	PAP M H4	PAP M H8	PAP M H12	PAP M H24	PAP M H48	PAP D 0 mmHg	PAP D 30	PAP D 90	PAP D H2	PAP D H4	PAP D H8	PAP D H12	PAP D H24	PAP D H48	RVP 0 dyne/s/cm2	RVP 30	RVP 90	RVP H2	RVP H4	RVP H8	RVP H12	RVP H24	RVP H48	type of catecholamines used	Noradre 0 ug/kg/min	Noradre H24	Noradre H48	Noradre H72	DOBU 0 ug/kg/min	DOBU H24	DOBU H48	DOBU H72	Adre 0 ug/kg/min	Adre H24	Adre H48	Adre H72	Lact 0 mmol/L	Lact H48	Lact H72	FE 0 (%)	FE H24	FE H48	FE J7	FE J 15
1	33	F	70	peripartum cardiomyopathy		13	4	D	2	56	56	58	59	64	65	63	66	77	132	133	123	128	127	119	118	111	86	14	11	8	14	17	22	15	15	12	1.7	1.8	1.9	1.9	2	2.1	2.3	2.3	2.4	32	21	23	22	24	19	18	19	17	1985	2017	2121	1890	1897	1654	1678	1432		55	56	55	61	63	66	69	67		46	40	38	36	35	36	34	35		37	29	30	28	29	25	25	26		29	24	26	20	24	21	19	21		235	356	295	253	200	229	243	243		ADRE									1.6	2			5.6	3.6		21	27
2	63	M	80	myocardial infarction	yes	23	4	D	43	61	72	72	86	73	75	75	73	75	100	118	123	110	103	92	98	100	95	18	14	11	27	22	14	14	25	24	2.2	2.6	2.8	3.3	3.1	3.2	3.3	3.2	3.4	30	18	18	14	14	19	16	16	16	2092	1771	1740	1440	1324	1523	1478	1212	1210	66	73	72	73	76	78	78	75	72	48	39	36	32	32	33	32	34	32	36	26	25	20	22	25	23	22	23	26	20	18	17	17	17	21	18	18	218	246	200	145	206	150	170	150	165	ADRE									1.7	0.7	0.3	0.02	3	3.3	2	25	33	37	46	58
3	35	F	72	peripartum cardiomyopathy		14	5	S	10	60	59	62	65	67	71	68	75	74	130	131	128	124	121	120	114	89	87	23	25	20	23	30	30	25	29	25	1.9	1.9	2.2	2.6	2.5	3	3.2	3.1	3.4	25	19	18	21	20	18	17	16	14	1546	1428	1511	1302	1179	1102	1065	1189	1155	57	61	59	67	72	75	76	74	73	42	39	38	39	37	38	33	32	32	32	26	25	28	27	27	23	24	22	23	17	18	19	22	20	17	18	16	295	295	255	215	224	240	150	206	188	NOR	0.58	0.23	0.1	0.01									2.2	1.6	1.1	29	35	47	60	60
4	19	M	55	dilated cardiomyopathy		11	4	D	8	54	57	61	61	65	65	64	67	69	126	128	126	119	121	117	99	104	99	22	21	15	14	12	12	11	10	12	2.0	2.3	2.7	2.6	2.8	3.0	3.0	3.0	3.2	28	23	22	22	21	20	19	19	19																																																							NOR:DOBU	0.4	0.1	0.05	0.02	10	5	4	4					17	11	6.5	16	22	28	27
5	67	M	75	myocardial infarction	yes	16	4	D	3	62	63	8	64	68	73	71	72	74	124	122	123	119	115	110	99	94	89	28	26	24	24	22	16	17	16	18	1.8	1.9	1.9	2.2	2.4	2.6	2.5	3	3.4	26	20	19	17	19	19	18	15	14	1810	1564	1224	1216	1300	1212	980	879	876	54	54	56	59	60	64	63	68	69	44	38	38	35	36	36	34	33	31	33	28	27	24	27	26	26	24	24	29	20	22	21	22	23	20	16	17	311	337	337	255	267	215	256	240	235	NOR:DOBU	0.51	0.21	0.1	0.05	9	6	6	4					4	4	2.2	22	30	28
6	77	M	79	dilated cardiomyopathy	yes	23	2	D	10	55	56	57	60	62	65	65	69	68	108	130	102	100	99	91	97	89	91	19	20	22	18	15	17	15	17	17	1.7	1.8	1.9	2.2	2.3	2.2	2.5	2.5	2.7	28	20	19	18	20	16	18	17	17	1723	1204	1199	1203	1100	1012	917	921	861	56	55	59	62	64	64	71	75	72	62			69	70		50	59	55	40			47	43		28	35	40	35			42	28		17	21	18	384			133	436		348	237	412	NOR/DOBU	0.69	0.33	0.12	0.07	15	8	5	0					4.1	3.5	2.2	21	32	33	36
7	55	F	78	myocardial infarction	yes	14	2	S	16	61	67	81	84	70	95	90	82	89	136	140	109	99	98	110	99	89	90	24	26	16	22	19	15	17	16	16	2.3	3.8	6.6	4.2	3.9	4.4	4.7	4.7	4.6	24	15	17	21	19	18	17	20	17	1274	630	800	702	767	1042	890	719	930	54	65	68	71	75	69	71	73	75	45	42	43	40	38	37	37	35	34	34	26	29	31	29	25	26	28	25	28	17	19	22	20	21	18	19	19	348	232	145	190	205	127	153	136	139	NOR/DOBU	0.5	0.3	0.2	0.02	10	4	0	0					2.9	1.9	1.2	30	36	46	47	50
8	69	M	80	myocardial infarction	yes	37	4	D	10	65	64	66	70	71	72	73	73	74	98	103	108	92	87	92	97	88	87	24	23	19	20	18	21	16	16	17	2.2	2.8	3.5	3.3	3.6	3.4	3.3	3.4	3.5	31	24	20	26	25	24	25	23	22	1466	1355	1046	1046	998	969	901	850	734	58	57	59	64	65	71	69	72	71	55	47	46	47	48	44	43	43	39	42	38	36	37	37	33	34	34	30	33	27	20	24	25	27	26	25	22	367	400	366	267	257	212	218	259	183	NOR	0.47	0.44	0.21	0.13									2.9	1.8	1.3	28	35	47	47
9	62	F	90	mitral valvulopathy		28	3	S	18	70	74	73	73	72	78	74	75	72	46	44	45	50	47	69	68	60	63	22	28	16	12	13	8	15	16	15	1.6	1.7	1.9	2.2	2.5	2.9	2.9	3.1	3.4	27	22	22	18	16	15	15	15	9	2250	2153	2418	2223	1890	1927	1631	1532	1335	57	64	64	65	71	73	74	78	73	39	37	34	35	32	28	26	26	33	32	27	27	25	25	19	18	19	16	25	19	17	19	19	13	13	14	11	235	235	211	255	288	110	83	103	165	NOR/DOBU	0.45	0.15	0.01	0.02	8	5	3	0					2.5	1.6	1.4	38	45	50	50	56
10	28	F	77	peripartum cardiomyopathy		18	3	S	9	62	62	76	77	78	78	80	76	80	110	112	122	108	112	109	98	96	96	22	21	15	14	12	12	11	10	12	2.0	2.3	2.7	2.6	2.8	3.0	3.0	3.0	3.4	28	23	22	22	21	20	19	19	19																																																							NOR	0.15	0.15	0.15	0.07									1.9	1.2	0.5	21	23	28	49	52
11	35	M	68	myocardial infarction	no	24	4	S	11	64	64	68	67	75	77	76	84	84	100	108	110	100	98	100	88	100	85	20	27	22	25	11	8	16	11	11	1.7	1.6	2.1	2	3.8	4.5	3.9	3.6	3.4	22	24	21	22	18	17	19	19	16	2092	1854	1740	1671	1340	1220	1235	1626	1422	57	61	60	68	65	68	70	72	70	42			39	34	35		34	35	30			29	25	26		25	25	24			23	20	22		19	19	376			280	147	160		133	176	NOR/DOBU	0.36	0.36	0.3	0.24	9	6	6	6					2.3	1.6	0.9	28	35	38	40	51
12	44	F	74	viral cardiomyopathy		35	4	S	28	58	55	59	70	74	71	70	71	72	140	140	140	135	135	135	135	122	110	19	13	21	14	16	14	15	20	21	1.6	2.6	2.5	2.3	2.2	2.4	2.3	2.4	2.5	34	34	27	29	30	30	28	30	27	1970	1293	1210	1940	2091	1907	1910	1708	1636	48	58	60	59	61	57	49	62	64	55	51	51	42	48	44	43	43	40	39	38	36	33	35	35	33	34	32	30	28	24	22	28	27	25	27	25	250	123	288	139	182	167	174	133	160	ADRE	1.5				20				8	6	6	2	5.2	3	1.5	25	33	42	40	52
13	69	M	69	myocardial infarction	no	29	4	D	2	65	60	66	69	70	68	71	70		102	110	88	89	95	105	100	89	87	17	13	23	16	26	18	8	26		1.8	1.7	1.7	1.7	1.6	1.6	1.7	1.6	1.7	23	24	22	24	22	22	19	14	14	2116	2224	2028	2500	2223	2500	2985	2200		61	63	59	60	54	55	54	58		42	40	38	42	36	33	30	26		30	29	28	30	27	25	23	17		25	23	23	22	21	19	18	12		311	235	282	282	250	150	188	150		ADRE	1.4				15				6.5	8			4.5	8.7		21	23	28	49	52
14	50	M	78	myocardial infarction	yes	17	3	S	56	81	72	73	77	77	81	70	78	83	87	96	98	96	86	87	77	89	93	18	14	14	10	11	12	14	14	11	3.1	3.4	3.3	3.4	2.8	3.1	2.8	3.5	4.1	25	20	19	18	18	19	19	22	21	1626	1367	1435	1584	1872	1781	1600	1463	1405	64	72	75	74	71	73	70	74	72	46	41	40	38	36	38	36	40	39	34	28	28	26	25	25	24	30	29	25	23	21	20	20	19	20	23	23	232	188	218	188	200	155	143	183	156	NOR/DOBU	0.3	0.2			17	6							2	0.9		32	40	42	55	52
15	52	M	75	myocardial infarction	yes	25	4	D	6	83	87	90	85	85	87	83	75	88	85	88	90	99	102	100	96	80	75	25	28	28	22	23	22	16	15	23	2.0	2.3	3	2.9	3.3	3.3	3	3.2	3.3	40	36	34	32	34	32	24	19	21	2191	2042	1655	1744	1495	1564	1793	1500	1580	61	63	66	70	75	66	68	72	70	58	56		53	52		39	36		45	42		38	41		29	24		36	32		29	33		24	16		190	209		166	170		133	125		ADRE									3.6	3.4	2.5	0.5	3.8	0.3	0.4	21	25	33
16	74	F	120	myocardial infarction	yes	22	4	D	16	67	55	57	56	58	56	65	61	67	60	60	60	60	60	60	60	60	60	25	28	23	23	23	20	18	17	23	2.2	2.3	2.4	2.3	2.5	2.8	2.9	2.8	2.4	23	22	23	24	18	18	16	17	16	1533	953	1148	1162	1021	1020	1288	1257	1456	61	60	63	64	58	67	65	59	64	39	38	37	39	35	35	32	33	33	31	29	29	31	26	26	25	25	24	23	24	23	25	20	19	18	19	19	291	243	200	243	256	229	248	229	267	NOR/DOBU	1.2	1.1	1.2	0.8	18	15	15	8					2.2	1.1	1.6	28	27	35	42	41
17	73	F	88	myocardial infarction	yes	21	3	D	10	58	56	58	59	64	65	63	66	89	100	108	110	100	98	100	88	100	85	14	11	8	14	17	22	15	15	12	2.4	2.8	3.5	3.3	3.6	3.4	3.3	3.4	3.6	27	22	22	18	16	15	15	15	15										55	56	55	61	63	66	69	72	74	52	49	44	44	40	38	37	37	37										31	26	26	22	20	19	19	19	19										DOBU					14	8	5	4					2.5	1.6		25	33	37
18	66	M	76	myocardial infarction	yes	19	4	D	12	66	64	66	70	71	72	73	73	74	140	140	140	135	135	135	135	122	110	18	14	11	27	22	14	14	14	16	1.7	1.8	1.9	1.9	2	2.1	2.3	2.3	2.3	24	15	17	21	19	18	17	18	17										66	73	72	73	76	78	78	75	72	48	47	45	40	44	42	41	40	41										28	26	21	25	23	22	21	22	21										NOR	0.65	0.66	0.18	0.02									1.9	2.2		29	35	37
19	33	F	101	peripartum cardiomyopathy		20	3	S	6	62	67	81	84	70	95	90	82	89	60	62	65	68	62	61	74	63	66	23	25	20	23	30	30	25	23	25	2.1	2.6	2.8	3.3	3.1	3.2	3.3	3.2	3.3	28	20	19	18	20	16	18	16	18										57	61	59	67	72	75	76	74	73	53	50	44	41	40	42	38	40	38										32	26	23	22	24	20	22	20	22										DOBU					12	7	3	0					2.3	1.6	0.9	30	36	46	47	50
20	32	F	65	peripartum cardiomyopathy		22	3	S	5	57	56	57	60	62	65	65	69	68	102	110	88	89	95	105	100	89	87	22	21	15	14	12	12	11	10	12	2.3	3.8	6.6	4.2	3.9	4.4	4.7	4.7	4.6	26	20	19	17	19	19	18	19	18										61	63	66	70	75	66	68	72	70	48	46	40	39	37	39	39	38	39										30	24	23	21	23	23	22	23	22										DOBU					20	15	10	10					5.2	3	1.5	28	35	46	49	49
21	52	F	49	viral cardiomyopathy		18	4	S	12	63	63	8	64	68	73	71	72	74	87	96	98	96	86	87	77	89	93	28	26	24	24	22	16	17	16	18	1.7	1.8	1.9	2.2	2.3	2.2	2.5	2.5	2.8	28	23	22	22	21	20	19	20	19										54	54	56	59	60	64	63	68	69	49	47	42	41	40	40	39	37	39										32	27	26	25	25	24	22	24	22										NOR	0.77	0.55	0.33	0.16									4.5	8.7	2.3	38	45	50	50	56
22	65	M	76	myocardial infarction	yes	21	3	S	6	63	72	72	86	73	75	75	73	75	85	88	90	99	102	100	96	80	75	19	20	22	18	15	17	15	17	17	1.8	1.9	1.9	2.2	2.4	2.6	2.5	3	3	32	21	23	22	24	19	18	17	17										56	55	59	62	64	64	71	75	72	56	55	44	46	45	43	42	41	40										36	25	27	26	24	23	22	21	21										DOBU					15	10	5	2					2	0.9	0.9	28	35	38	40	51
23	29	F	66	peripartum cardiomyopathy		13	2	S	4	62	59	62	65	67	71	68	75	74	110	112	122	108	112	109	98	96	96	24	26	16	22	19	15	17	16	16	1.8	2.3	2.7	2.6	2.8	3.0	3.0	3.0	3.0	30	18	18	14	14	19	16	17	16										54	65	68	71	75	69	71	73	75	55	51	39	39	35	35	40	37	38										34	22	22	18	18	23	20	21	20										DOBU					12	12	5	7					3.8	1.3	1.4	25	33	42	40	52
24	68	M	62	mitral valvulopathy		22	4	D	3	52	57	61	61	65	65	64	67	69	46	44	45	50	47	69	68	60	63	24	23	19	20	18	21	16	16	17	1.9	1.9	2.2	2.6	2.5	3	3.2	3.1	3.2	25	19	18	21	20	18	17	16	17										58	57	59	64	65	71	69	72	71	48	47	41	40	40	39	40	39	38										29	23	22	22	21	22	21	20	21										NOR	0.90	0.75	0.66	0.33									2.2	2.1		32	38	39
25	39	F	78	mitral valvulopathy		15	2	S	15	54	57	61	60	64	66	68	68	69	130	132	118	115	117	105	100	100	90	25	25	24	23	23	24	22	19	20	2.2	2.3	2.4	2.3	2.5	2.8	2.9	2.8	2.4	26	20	19	17	19	19	18	19	18										55	58	60	59	61	57	49	62	64	42	40	38	42	40	37	37	39	42										25	23	26	23	21	21	19	19	18										NOR/DOBU	0.55	0.40	0.12	0.05	14	10	7	5					2.2	1.1	1.6	24	30	35	40	45
This is a portion of the data; to view all the data, please download the file.

Dataset 1.Data used for retrospective analysis of the effects of levosimendan for cardiogenic shock.

Data was collected at the ICU in the Military Hospital of Tunis between Jan 2004 and Dec 2009, and between Jan 2011 and Dec 2013. PAM: Mean Arterial Pressure (mmHg); HR: Heart Rate (beat/min); POD: Right Atrial Pressure (mmHg); IC: Cardiac Index (L/min/m²); PAPO: Pulmonary Wedge Pressure (mmHg); RVS: Systemic Vascular Resistance (dyne/s/cm²); SVO2: Mixed Venous Oxygen Saturation (%); PAP: Pulmonary arterial systolic pressure (mmHg); Mean Pulmonary Arterial Pressure (mmHg); PAP D: Pulmonary arterial diastolic pressure (mmHg); RVP: Pulmonary Vascular Resistance (mmHg); Noradre: Norepinephrine (ug/kg/min); DOBU: Dobutamine (ug/kg/min); Adre: Epinephrine (ug/Kg/min); Lact: Arterial Lactate (mmol/L); FE: Left Ventricular Ejection fraction (%).

Twenty-six patients who were hospitalized for CS met our criterion for inclusion in this study. The status of CS was mainly secondary to myocardial infarction (in 42% of cases) and to cardiomyopathy of the peripartum (in 31% of cases). The demographic data are shown in Table 1.

Table 1. Distribution of demographic parameters.

Parameters	Value
Number of patients	26
Age (years)	51 ± 18
Gender ratio (male/female)	0.85
APACHE II medium	20 ± 7
Multiple organ-failure score	3.4 ± 1
Average length of stay in ICU (days)	13 ± 12
Etiology of CS
- Myocardial infarction	12
- Peripartum cardiomyopathy	6
- Dilated myocardiopathy	3
- Other pathology	5
History of patients
- Coronary-artery disease	5
- Diabetes	5
- Arteritis ischemic lower limbs	3
- Smoking	4
Evolution
- Survival	14
- Death	12

The hemodynamic data at inclusion showed a mean arterial pressure of 63 ± 7 mmHg, a cardiac index of 1.96 ± 0.29 l/min/m², and a pulmonary capillary wedge pressure of 28 ± 4 mmHg.

Levosimendan resulted in significantly improved mean arterial pressure to 76 ± 7 mmHg at 48 h (p=0.001 compared to T0) and cardiac index to 3.19 ± 0.68 L/min/m² (p<0.0001 compared to T0) (Figure 1) without any significant modification to either heart rate (101 ± 28 to 86 ± 13, p=0.26) or the emergence of rhythm disturbance.

Figure 1. Data are expressed as mean values of cardiac index of all our patients.

Levosimendan decreased pulmonary wedge pressure to 17 ± 3 mmHg at 48h (p=0.001 compared to T0). Pulmonary arterial systolic pressure was significantly reduced to 38 ± 5 mmHg after 48 h, compared to 49 ± 6 mmHg at inclusion (p=0.016 compared to T0). Pulmonary arterial diastolic pressure was significantly reduced to 20 ± 4 mmHg at 24 h, compared to 29 ± 4 mmHg at inclusion (p<0.001 compared to T0). Mean pulmonary arterial pressure was significantly reduced to 26 ± 5 mmHg after 24 h compared to 35 ± 5 mmHg at inclusion (p=0.001 compared to T0).

There was a significant decrease in lactate from 3.77 ± 2.93 to 1.60 ± 1.32 mmol/L after 72 h. Levosimendan significantly reduced systemic vascular resistance (1834 ± 308 to 1321 ± 304 dyne/s/cm², p<0.0001) and pulmonary vascular resistances (289 ± 64 to 204 ± 78 dyne/s/cm², p=0.001). Administration of levosimendan also reduced the need for catecholamines (Figure 2), thus leading to a gradual reduction in the need for catecholamines in six patients.

Figure 2. Data are expressed as mean values from 15 patients who received norepinephrine, 15 patients who received Dobutamine and 5 patients who received epinephrine.

Administration of levosimendan improved SvO2 to 70 ± 5% after 24 h of infusion. The evolution of the left-ventricle ejection fraction showed bottom-up kinetics as a function of time, which ranged from 26 ± 5% at inclusion to 54 ± 5% by day 15.

Discussion

Levosimendan is a calcium sensitizer. Its main mechanism of action is to increase the binding affinity of troponin C to Ca²⁺ and to stabilize its conformation. It also directly increases cardiac contractility without raising intracellular concentrations of calcium or AMPc. This makes levosimendan one of the best inotropic agents and causes least arrhythmia. In addition to its positive inotropic affects, levosimendan can caused vasodilatation of many vascular areas by opening ATP-dependent potassium channels. This increased coronary blood flow without increasing consumption of myocardial oxygen, thus explains the good tolerance of levosimendan in cases of coronary syndrome and also its effects as an anti-ischemic and a cardio-protector.

Many clinical studies have been conducted to assess the effects of levosimendan on hemodynamic parameters. The first studies focused on patients with decompensated heart failure. The main aim of these authors was to compare levosimendan with dobutamine (i.e., the main type of catecholamine used during low cardiac output). Three main studies have been published: the LIDO, SURVIVE, and CASINO studies.

In the LIDO study, 203 patients were hospitalized for severe cardiac failure and received either levosimendan (a loading dose of 24 µg/kg/min infused for 10 min; and then continuous infusion for 24 h at a dose of 0.1 µg/kg/min, n=103) or dobutamine (a dose of 5 µg/kg/min was given without a loading dose, n=100). Levosimendan increased the cardiac index by ≥30% and decreased pulmonary capillary wedge pressure by ≥25% in 29 patients compared to only 15 patients receiving dobutamine (hazard ratio=1.9, CI= of 95%, p=0.022)^11,12. A decline in the need for catecholamines and the resumption of beta blockers occurred more frequently in patients that received levosimendan¹⁴. Mortality rate was also lower in patients that received levosimendan compared to dobutamine after 1 month (7.8% vs. 17%, p=0.045) and at 6 months (26% vs. 38%, p=0.029)^9,11–13.

The SURVIVE study was a multicenter study that included 1327 randomized patients with severe cardiac failure and who had a left-ventricle ejection fraction of <30%. This study chose mortality as the main criterion for judgment and assessed the effectiveness of levosimendan compared to dobutamine¹¹. When the analyses focused on early mortality rates during the first 5 days, levosimendan was more effective than dobutamine (4.4% vs. 6%), indicating that levosimendan could be an alternative to dobutamine for patients with acute cardiac insufficiency. However, this favorable trend was not found in the longer term¹¹. During the 180 days of follow-up, there were 173 deaths (26%) in the group receiving levosimendan (n=664) compared to 185 (28%) in the group receiving dobutamine (n=663)¹⁵. However, the main criterion of mortality at 6 months may not be appropriate to judge the effectiveness of this treatment when its main benefits were observed at an early stage¹⁶.

The CASINO study was a randomized, controlled, double-blind study that included 299 patients with decompensated congestive heart failure. The study compared levosimendan therapy with dobutamine, and with a placebo. The study showed positive results for its first assessment criterion: i.e., mortality rate at 6 months. The authors reported that improved survival was associated with the use of levosimendan¹⁶. In the light of these results, levosimendan represents a significant advance in the treatment of cardiac insufficiency. These studies have helped to expand levosimendan’s indications and have also assessed its contribution to treat CS.

Many authors have evaluated the hemodynamic effects of levosimendan in the course of CS. Delle et al. concluded that administration of levosimendan to 10 patients with CS led to a significant increase in the cardiac index and significantly decreased vascular resistance¹⁷.

Russ et al. obtained similar results when they prescribed levosimendan to 56 patients with CS. They reported a significant increase in the cardiac index (from 2.1 ± 0.56 to 3.0 ± 1.11 l/min/m² at 24 h, p<0.01) associated with a significant decrease in systemic vascular resistance (from 1208 ± 333 to 858 ± 299 dynes/s/mm^-4 at 24 h, p<0.01), whereas mean arterial pressure and pulmonary wedge pressure were slightly but non-significantly decreased. An improved SOFA score was found after 72 h of levosimendan treatment, suggesting improved organic function¹⁸.

Labriola et al. also reported the same variations in hemodynamic parameters as described by Delle et al. and Russ et al., which were distinguished by the development of a significant increase in the left-ventricle ejection fraction¹⁹.

According to the study of Berry et al., a continuous decrease in noradrenalin, dobutamine, and milrinone was associated with improved hemodynamic parameters in 93 patients with CS who received a continuous infusion of levosimendan for 26 h at a dose of 0.096 µg/kg/min²⁰.

Labbene et al. analyzed the hemodynamic effects of levosimendan in 16 patients hospitalized with CS and who were refractory to catecholamine²¹. The evolution of hemodynamic parameters after infusion of levosimendan was marked by a significant increase in the cardiac index (from 2.01 ± 0.4l to 3.4 ± 0.65 l/min/m² at 48 h) of SvO₂ (from 57% ± 5% to 70% ± 3%) and the left-ventricular ejection fraction (from 26 ± 6% to 52 ± 5%). There was also a significant decrease in pulmonary wedge pressure from 28 ± 5 to 17 ± 5 mmHg, and of pulmonary arterial systolic pressure, of diastolic arterial systolic pressure, of average arterial systolic pressure of systemic vascular resistance (from 1833 ± 308 to 1216 ± 304 dyne/s/cm² at 48 h), and of pulmonary vascular resistances (from 289 ± 64 at T0 to 179 ± 44 dyne/s/cm² at 4 h)²¹. Our results agree with those from the literature and show the effectiveness of levosimendan to treat CS when it is refractory to catecholamines. At the recommended dose, levosimendan improves hemodynamic parameters by increasing the cardiac index and SvO₂. It is responsible for the drop in systemic vascular resistance and pulmonary vascular resistances, and reduces the need for catecholamines. Other studies have also confirmed the efficacy of levosimendan to stabilize hemodynamic parameters in patients with CS^22–25.

Conclusion

Our results show that levosimendan was efficacious at treating CS, and that it has several advantages compared to other isotropic agents. However, it is expensive (compared to dobutamine) and the absence of a net profit on long-term survival represents a limit to its wide-spread use in pathologies with a poor prognosis, such as CS. Further randomized studies that include a placebo and a larger patient population with CS are needed to precisely determine the indications for levosimendan and to assess its cost in relation to patient survival.

Data availability

F1000Research: Dataset 1. Data used for retrospective analysis of the effects of levosimendan for cardiogenic shock, 10.5256/f1000research.5820.d40172²⁶

Author contributions

IL and MF conceived the study. IL and FJ designed the experiments. KEA, CR and IL carried out the research. KEA and FJ prepared the first draft of the manuscript. IL, FJ and KEA contributed to the experimental design and preparation of the manuscript. All authors were involved in the revision of the draft manuscript and have agreed to the final content.

Competing interests

No competing interests were disclosed.

Grant information

Supported by a grant from the Research Laboratory LR12DN01 and The Military Hospital of Tunis.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Acknowledgments

The authors thank Newmed Publishing Services for language editing and submission support, provided on a pro bono basis.

Faculty Opinions recommended

References

1. Leurent G: [Ischaemic cardiogenic shock. Where do we stand in 2012?]. Ann Cardiol Angeiol (Paris). 2012; 61: 417–422. PubMed Abstract | Publisher Full Text
2. Lambert Y, Boutout F: Etat de choc cardiogénique dans les premières heures. Encycl Méd Chir. Elsevier, Masson, Paris. Médecine d’urgence, 25-020-A-20, 2007; 14. Reference Source
3. Pirracchio R: Etat de choc cardiogénique. Encycl Méd Chir. Elsevier, Masson, Paris, Anesthésie-Réanimation, 36-840-C-10, 2012; 9. Reference Source
4. Salem JE, Aissaoui A: Choc cardiogénique. Encycl Méd Chir. Elsevier, Masson, Paris, Cardiologie, 11-038-B-10, 2014; 10. Reference Source
5. Pathak A, Lebrin M, Vaccaro A, et al.: Pharmacology of levosimendan: inotropic, vasodilatory and cardioprotective effects. J Clin Pharm Ther. 2013; 38(5): 341–349. PubMed Abstract | Publisher Full Text
6. Parissis JT, Rafouli-Stergiou P, Paraskevaidis I, et al.: Levosimendan: from basic science to clinical practice. Heart Fail Rev. 2009; 14(4): 265–275. PubMed Abstract | Publisher Full Text
7. Robertson IM, Sun YB, Li MX, et al.: A structural and functional perspective into the mechanism of Ca2+-sensitizers that target the cardiac troponin complex. J Mol Cell Cardiol. 2010; 49(6): 1031–1041. PubMed Abstract | Publisher Full Text | Free Full Text
8. Papp Z, Édes I, Fruhwald S, et al.: Levosimendan: molecular mechanisms and clinical implications: consensus of experts on the mechanisms of action of levosimendan. Int J Cardiol. 2012; 159(2): 82–87. PubMed Abstract | Publisher Full Text
9. Rami L, Giunti C, Mebazaa A, et al.: Choc cardiogénique: quel inotrope choisir? In: Conférences d’actualisation. Elsevier-SFAR, 2004; 425–440. Reference Source
10. Fotbolcu H, Duman D: A promising new inotrope: levosimendan. Anadolu Kardiyol Derg. 2010; 10(2): 176–82. PubMed Abstract | Publisher Full Text
11. De Luca L, Colucci WS, Nieminem MS, et al.: Evidence-based use of levosimendan different clinical settings. Eur Heart J. 2006; 27(16): 1908–1920. PubMed Abstract | Publisher Full Text
12. Follah F, Celand JG, Just H, et al.: Efficacy and safety of intravenous levosimendan compared with dobutamine in severe low-output heart failure (the LIDO study): a randomized double-blind trial. Lancet. 2002; 360(9328): 196–202. PubMed Abstract | Publisher Full Text
13. Nieminen MS, Fruhwald S, Heunks LM, et al.: Levosimendan: current data clinical use and future development. Heart Lung Vessel. 2013; 5(4): 227–245. PubMed Abstract | Free Full Text
14. Labbene I, Belhadj AM, Lebbi A, et al.: Intérêt du lévosimendan dans les défaillances myocardiques aigues. J Magh A Réa Méd Urg. 2006; 8: 34–38. Reference Source
15. Mebazaa A, Nieminen MS, Packer M, et al.: Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE Randomized Trial. JAMA. 2007; 297(17): 1883–1891. PubMed Abstract | Publisher Full Text
16. Ferjani M: Le lévosimendan une révolution dans la prise en charge des défaillances myocardiques aigue? J Magh A Réa Méd Urg. 2006; 8: 2. Reference Source
17. Delle Karth G, Buberl A, Geppert A, et al.: Hemodynamic effects of a continuous infusion of levosimendan in critically ill patients with cardiogenic shock requiring catecholamines. Acta Anaesthesiol Scand. 2003; 47(10): 1251–1256. PubMed Abstract | Publisher Full Text
18. Russ MA, Prondzinsky R, Christoph A, et al.: Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock. Crit Care Med. 2007; 35(12): 2732–2739. PubMed Abstract | Publisher Full Text
19. Labriola C, Siro-Brigiani M, Carrata F, et al.: Hemodynamic effects of levosimendan in patients with low-output heart after cardiac surgery. Int J Clin Pharmacol Ther. 2004; 42(4): 204–211. PubMed Abstract
20. Berry WT, Hewson RW, Langrish CJ, et al.: Levosimendan: a retrospective single-center case series. J Crit Care. 2013; 28(6): 1075–1078. PubMed Abstract | Publisher Full Text
21. Labbene I, Hichri N, Thabet S, et al.: Hemodynamic Effects of levosimendan during cardiogenic shock. Ann Fr Anesth Reanim. 2007; 26: S167–S170.
22. Lehmann A, Lang J, Boldt J, et al.: Levosimendan in patients with cardiogenic shock undergoing surgical revascularization: a case series. Med Sci Monit. 2004; 10(8): MT89–93. PubMed Abstract
23. Katsytadze I, Amosova E, Purdkyi I, et al.: Long term effects of levosimendan therapy in patients with cardiogenic shock. Resuscitation. 2013; 84(Supplement 1): S8–S98. Publisher Full Text
24. Zobel C, Reuter H, Schwinger RH: [Treatment of cardiogenic shock with the Ca2+ sensitizer levosimendan]. Med Klin (Munich). 2004; 99(12): 742–746. PubMed Abstract | Publisher Full Text
25. Greif M, Zwermann L, Reithumann C, et al.: Levosimendan as rescue therapy in severe cardiogenic shock after ST-elevation myocardial infarction. Acute Card Care. 2008; 10(3): 185–190. PubMed Abstract | Publisher Full Text
26. Janen F, El Arayedh K, Labbene I, et al.: Dataset 1 in: Use of levosimendan in cardiogenic shock. F1000Research. 2014. Data Source

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¹ Pharmacy Department, Military Hospital of Tunis, Monfleury,Tunis, 1008, Tunisia
² Pharmacy Department, Basic Health Group of South Tunis, 90 Sayada Street Bellevue, Tunis, 1009, Tunisia
³ Université Tunis El Manar, Faculté de Médecine de Tunis, LR12DN01, Intensive Care Unit, Military Hospital of Tunis, Monfleury Tunis, 1008, Tunisia

Competing interests

No competing interests were disclosed.

Grant information

Supported by a grant from the Research Laboratory LR12DN01 and The Military Hospital of Tunis.
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Janen F, El Arayedh K, Labbene I et al. Use of levosimendan in cardiogenic shock [version 1; peer review: peer review discontinued]. F1000Research 2014, 3:296 (https://doi.org/10.12688/f1000research.5820.1)

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[1] 1. Leurent G: [Ischaemic cardiogenic shock. Where do we stand in 2012?]. Ann Cardiol Angeiol (Paris). 2012; 61: 417–422. PubMed Abstract | Publisher Full Text

[2] 2. Lambert Y, Boutout F: Etat de choc cardiogénique dans les premières heures. Encycl Méd Chir. Elsevier, Masson, Paris. Médecine d’urgence, 25-020-A-20, 2007; 14. Reference Source

[3] 3. Pirracchio R: Etat de choc cardiogénique. Encycl Méd Chir. Elsevier, Masson, Paris, Anesthésie-Réanimation, 36-840-C-10, 2012; 9. Reference Source

[4] 4. Salem JE, Aissaoui A: Choc cardiogénique. Encycl Méd Chir. Elsevier, Masson, Paris, Cardiologie, 11-038-B-10, 2014; 10. Reference Source

[5] 5. Pathak A, Lebrin M, Vaccaro A, et al.: Pharmacology of levosimendan: inotropic, vasodilatory and cardioprotective effects. J Clin Pharm Ther. 2013; 38(5): 341–349. PubMed Abstract | Publisher Full Text

[6] 6. Parissis JT, Rafouli-Stergiou P, Paraskevaidis I, et al.: Levosimendan: from basic science to clinical practice. Heart Fail Rev. 2009; 14(4): 265–275. PubMed Abstract | Publisher Full Text

[7] 7. Robertson IM, Sun YB, Li MX, et al.: A structural and functional perspective into the mechanism of Ca2+-sensitizers that target the cardiac troponin complex. J Mol Cell Cardiol. 2010; 49(6): 1031–1041. PubMed Abstract | Publisher Full Text | Free Full Text

[8] 8. Papp Z, Édes I, Fruhwald S, et al.: Levosimendan: molecular mechanisms and clinical implications: consensus of experts on the mechanisms of action of levosimendan. Int J Cardiol. 2012; 159(2): 82–87. PubMed Abstract | Publisher Full Text

[9] 9. Rami L, Giunti C, Mebazaa A, et al.: Choc cardiogénique: quel inotrope choisir? In: Conférences d’actualisation. Elsevier-SFAR, 2004; 425–440. Reference Source

[10] 10. Fotbolcu H, Duman D: A promising new inotrope: levosimendan. Anadolu Kardiyol Derg. 2010; 10(2): 176–82. PubMed Abstract | Publisher Full Text

[11] 11. De Luca L, Colucci WS, Nieminem MS, et al.: Evidence-based use of levosimendan different clinical settings. Eur Heart J. 2006; 27(16): 1908–1920. PubMed Abstract | Publisher Full Text

[12] 12. Follah F, Celand JG, Just H, et al.: Efficacy and safety of intravenous levosimendan compared with dobutamine in severe low-output heart failure (the LIDO study): a randomized double-blind trial. Lancet. 2002; 360(9328): 196–202. PubMed Abstract | Publisher Full Text

[13] 13. Nieminen MS, Fruhwald S, Heunks LM, et al.: Levosimendan: current data clinical use and future development. Heart Lung Vessel. 2013; 5(4): 227–245. PubMed Abstract | Free Full Text

[14] 14. Labbene I, Belhadj AM, Lebbi A, et al.: Intérêt du lévosimendan dans les défaillances myocardiques aigues. J Magh A Réa Méd Urg. 2006; 8: 34–38. Reference Source

[15] 15. Mebazaa A, Nieminen MS, Packer M, et al.: Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE Randomized Trial. JAMA. 2007; 297(17): 1883–1891. PubMed Abstract | Publisher Full Text

[16] 16. Ferjani M: Le lévosimendan une révolution dans la prise en charge des défaillances myocardiques aigue? J Magh A Réa Méd Urg. 2006; 8: 2. Reference Source

[17] 17. Delle Karth G, Buberl A, Geppert A, et al.: Hemodynamic effects of a continuous infusion of levosimendan in critically ill patients with cardiogenic shock requiring catecholamines. Acta Anaesthesiol Scand. 2003; 47(10): 1251–1256. PubMed Abstract | Publisher Full Text

[18] 18. Russ MA, Prondzinsky R, Christoph A, et al.: Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock. Crit Care Med. 2007; 35(12): 2732–2739. PubMed Abstract | Publisher Full Text

[19] 19. Labriola C, Siro-Brigiani M, Carrata F, et al.: Hemodynamic effects of levosimendan in patients with low-output heart after cardiac surgery. Int J Clin Pharmacol Ther. 2004; 42(4): 204–211. PubMed Abstract

[20] 20. Berry WT, Hewson RW, Langrish CJ, et al.: Levosimendan: a retrospective single-center case series. J Crit Care. 2013; 28(6): 1075–1078. PubMed Abstract | Publisher Full Text

[21] 21. Labbene I, Hichri N, Thabet S, et al.: Hemodynamic Effects of levosimendan during cardiogenic shock. Ann Fr Anesth Reanim. 2007; 26: S167–S170.

[22] 22. Lehmann A, Lang J, Boldt J, et al.: Levosimendan in patients with cardiogenic shock undergoing surgical revascularization: a case series. Med Sci Monit. 2004; 10(8): MT89–93. PubMed Abstract

[23] 23. Katsytadze I, Amosova E, Purdkyi I, et al.: Long term effects of levosimendan therapy in patients with cardiogenic shock. Resuscitation. 2013; 84(Supplement 1): S8–S98. Publisher Full Text

[24] 24. Zobel C, Reuter H, Schwinger RH: [Treatment of cardiogenic shock with the Ca2+ sensitizer levosimendan]. Med Klin (Munich). 2004; 99(12): 742–746. PubMed Abstract | Publisher Full Text

[25] 25. Greif M, Zwermann L, Reithumann C, et al.: Levosimendan as rescue therapy in severe cardiogenic shock after ST-elevation myocardial infarction. Acute Card Care. 2008; 10(3): 185–190. PubMed Abstract | Publisher Full Text

[26] 26. Janen F, El Arayedh K, Labbene I, et al.: Dataset 1 in: Use of levosimendan in cardiogenic shock. F1000Research. 2014. Data Source

Use of levosimendan in cardiogenic shock

Abstract

Keywords

Introduction

Materials and methods

Results

Table 1. Distribution of demographic parameters.

Figure 1. Data are expressed as mean values of cardiac index of all our patients.

Figure 2. Data are expressed as mean values from 15 patients who received norepinephrine, 15 patients who received Dobutamine and 5 patients who received epinephrine.

Discussion

Conclusion

Data availability

Author contributions

Competing interests

Grant information

Acknowledgments

References

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