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Published: 4 June 2021
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1

Efentakis, Panagiotis, Aimilia Varela, Evangelia Chavdoula, Fragiska Sigala, Despina Sanoudou, Roxane Tenta, Katerina Gioti, et al. "Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy." Cardiovascular Research 116, no. 3 (June 22, 2019): 576–91. http://dx.doi.org/10.1093/cvr/cvz163.

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Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxide synthase (eNOS), and protein kinase-A and G (PKA/PKG) pathways emerged as contributors to the cardioprotection, converging onto phospholamban (PLN). To verify the contribution of PLN, phospholamban knockout (PLN−/−) mice were assigned to PLN−/−/Control (N/S-0.9%), PLN−/−/DXR (18 mg/kg), and PLN−/−/DXR+LEVO (ac) for 14 days. Furthermore, female breast cancer-bearing (BC) mice were divided into: Control (normal saline 0.9%, N/S 0.9%), DXR (18 mg/kg), LEVO, and DXR+LEVO (LEVO, 24 μg/kg-bolus) for 28 days. Echocardiography was performed in all protocols. To elucidate levosimendan’s cardioprotective mechanism, primary cardiomyocytes were treated with doxorubicin or/and levosimendan and with N omega-nitro-L-arginine methyl ester (L-NAME), DT-2, and H-89 (eNOS, PKG, and PKA inhibitors, respectively); cardiomyocyte-toxicity was assessed. Single bolus administration of levosimendan abrogated DXR-induced cardiotoxicity and activated Akt/eNOS and cAMP-PKA/cGMP-PKG/PLN pathways but failed to exert cardioprotection in PLN−/− mice. Levosimendan’s cardioprotection was also evident in the BC model. Finally, in vitro PKA inhibition abrogated levosimendan-mediated cardioprotection, indicating that its cardioprotection is cAMP-PKA dependent, while levosimendan preponderated over milrinone and dobutamine, by ameliorating calcium overload. Conclusion Single dose levosimendan prevented doxorubicin cardiotoxicity through a cAMP-PKA-PLN pathway, highlighting the role of inotropy in doxorubicin cardiotoxicity.
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2

&NA;. "Levosimendan." Reactions Weekly &NA;, no. 1272 (October 2009): 21–22. http://dx.doi.org/10.2165/00128415-200912720-00073.

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3

&NA;. "Levosimendan." Reactions Weekly &NA;, no. 1314 (August 2010): 27. http://dx.doi.org/10.2165/00128415-201013140-00086.

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4

Figgitt, David P., Peter S. Gillies, and Karen L. Goa. "Levosimendan." Drugs 61, no. 5 (2001): 613–27. http://dx.doi.org/10.2165/00003495-200161050-00006.

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5

Aronow, Wilbert S. "Levosimendan." Drugs 61, no. 5 (2001): 628–29. http://dx.doi.org/10.2165/00003495-200161050-00007.

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6

Nieminen, Markku S. "Levosimendan." Drugs 61, no. 5 (2001): 628–29. http://dx.doi.org/10.2165/00003495-200161050-00008.

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7

Innes, Carmen A., and Antona J. Wagstaff. "Levosimendan." Drugs 63, no. 23 (2003): 2651–71. http://dx.doi.org/10.2165/00003495-200363230-00009.

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8

&NA;. "Levosimendan." Inpharma Weekly &NA;, no. 1136 (May 1998): 7. http://dx.doi.org/10.2165/00128413-199811360-00013.

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9

Mason, Paula. "Levosimendan." Intensive and Critical Care Nursing 19, no. 6 (December 2003): 370–71. http://dx.doi.org/10.1016/s0964-3397(03)00074-0.

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10

Levin, Asher, and Gideon Paret. "Levosimendan." Journal of Pediatric Intensive Care 02, no. 03 (July 28, 2015): 095–103. http://dx.doi.org/10.3233/pic-13057.

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11

Michels, G., S. Herzig, and U. C. Hoppe. "Levosimendan." DMW - Deutsche Medizinische Wochenschrift 130, no. 43 (October 2005): 2444–46. http://dx.doi.org/10.1055/s-2005-918588.

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12

&NA;. "Levosimendan." Reactions Weekly &NA;, no. 1432 (December 2012): 32. http://dx.doi.org/10.2165/00128415-201214320-00112.

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13

Toller, W. G., P. S. Pagel, J. R. Kersten, and D. C. Warltier. "Levosimendan." Drugs of the Future 25, no. 6 (2000): 563. http://dx.doi.org/10.1358/dof.2000.025.06.580665.

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14

&NA;. "Levosimendan." Reactions Weekly &NA;, no. 1416 (August 2012): 28. http://dx.doi.org/10.2165/00128415-201214160-00091.

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15

Pisano, Antonio, Giacomo Monti, and Giovanni Landoni. "Levosimendan." Current Opinion in Anaesthesiology 29, no. 4 (August 2016): 454–61. http://dx.doi.org/10.1097/aco.0000000000000357.

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16

Braun, J. P., U. D�pfmer, M. Kastrup, I. Roots, A. Borges, M. Schneider, P. Dohmen, W. Kox, and C. Spies. "Levosimendan." Der Anaesthesist 53, no. 2 (February 1, 2004): 163–67. http://dx.doi.org/10.1007/s00101-003-0637-1.

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17

Li, Ling-Li, Li Wei, Ning Zhang, Wen-Ying Wei, Can Hu, Wei Deng, and Qi-Zhu Tang. "Levosimendan Protects against Doxorubicin-Induced Cardiotoxicity by Regulating the PTEN/Akt Pathway." BioMed Research International 2020 (June 8, 2020): 1–11. http://dx.doi.org/10.1155/2020/8593617.

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Background and Aims. Myocyte apoptosis plays a critical role in the development of doxorubicin- (DOX-) induced cardiotoxicity. In addition to its cardiotonic effect, laboratory evidence indicates that levosimendan can inhibit apoptosis, but its role in DOX-induced cardiac injury remains unclear. Therefore, the present study is aimed at exploring whether levosimendan could attenuate DOX-induced cardiotoxicity. Methods. Levosimendan (1 mg/kg) was administered to mice through oral gavage once daily for 4 weeks, and the mice were also subjected to an intraperitoneal injection of DOX (5 mg/kg) or saline, once a week for 4 weeks, to create a chronic model of DOX-induced cardiotoxicity. A morphological examination and biochemical analysis were used to evaluate the effects of levosimendan. H9C2 cells were used to verify the protective role of levosimendan in vitro. And an Akt inhibitor was utilized to verify the cardioprotection of levosimendan. Results. Levosimendan reduced the cardiac dysfunction and attenuated the myocardial apoptosis induced by DOX in vivo and in vitro. Levosimendan also inhibited the activation of phosphatase and tensin homolog (PTEN) and upregulated P-Akt expression both in vivo and in vitro. And inhibition of Akt abolished the cardioprotection of levosimendan in vitro. Conclusion. Levosimendan may protect against DOX-induced cardiotoxicity via modulation of the PTEN/Akt signaling pathway.
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18

Dhaliwal, Vikramjit Singh, Manpreet Singh Gill, and Monika . "Levosimendan: a remedy for treating the patients of decompensated heart failure." International Journal of Advances in Medicine 7, no. 8 (July 21, 2020): 1280. http://dx.doi.org/10.18203/2349-3933.ijam20203129.

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Background: Levosimendan is a new-fangled calcium based sensitizer which is used to treat the patients with congestive or decompensated heart failure. The empirical study reveals that it intensifies myocardial contractility and expands coronary and peripheral vessels without affecting the diastolic function adversely. Levosimendan also performs as an opener of ATP-based K channels in vascular smooth muscle. The empirical research study shows the benefits of usage of levosimendan over other drugs in the treatment of decompensated and congestive heart failure.Methods: Levosimendan has been administered to patients with decompensated heart failure conditions. Infusion of levosimendan started with a dose of 0.1 µg/kg/min and titrated to 0.2 µg/kg/min. The systolic BP has been monitored after the administration of levosimendan to maintain stability in the patient’s BP for the initial 2-3 hours. The suggested duration of infusion of levosimendan in critical heart failure is twenty-four hours. Initially levosimendan is infused in the patients with systolic BP is more than hundred mmHg and diastolic BP is more than sixty mmHg.Results: The outcomes of the usage of Levosimendan have been studied on 80 patients with decompensated heart problems and the comparative study has also been made with other inotropes, respectively. We have also performed a trial on two groups of people named as LIVO and NON-LIVO groups. The research study proves that the usage of levosimendan is better than other inotropes. Levosimendan can be recommended in the standard treatment of patients with acute heart conditions.Conclusions: Levosimendan is offering an effective remedy to treat the patients with decompensated heart failure. In comparison to other inotropes available for the treatment of patients suffering from congestive heart ailments, levosimendan can be considered to be a safe and efficient sensitizer.
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19

Brixius, Klara, Sebastian Reicke, and Robert H. G. Schwinger. "Beneficial effects of the Ca2+ sensitizer levosimendan in human myocardium." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 1 (January 1, 2002): H131—H137. http://dx.doi.org/10.1152/ajpheart.2002.282.1.h131.

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Levosimendan has been reported to increase cardiac Ca2+ sensitivity, thereby not enhancing intracellular Ca2+ or diastolic tension. This may be advantageous for the treatment of heart failure patients. Therefore, the present study investigates the mode of action of levosimendan in both failing and nonfailing (NF) human myocardium. The effects of levosimendan on contractile force, Ca2+ transient (fura 2), and the force-frequency relationship (0.5–3 Hz) were studied in left ventricular terminally failing [dilated cardiomyopathy (DCM; n = 18)] and nonfailing (NF) myocardium (donor hearts, n = 6). Levosimendan (0.03–10 μmol/l) increased contractile force in NF (EC50: 0.38 μmol/l). In left ventricular failing myocardium, levosimendan only increased force after prestimulation with isoprenaline (0.1 μmol/l, EC50levosimendan: 0.062 μmol/l) or after elevation of the extracellular Ca2+ concentration from 1.8 to 3.2 mmol/l. After application of isoprenaline, levosimendan shortened relaxation and contraction kinetics. Levosimendan did not change the systolic Ca2+ transient but it improved the force-frequency relationship in DCM. In conclusion, levosimendan improves contraction in failing human myocardium under conditions with already increased intracellular Ca2+.
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20

Rababa'h, Abeer M., Karem H. Alzoubi, Sandy Baydoun, and Omar F. Khabour. "Levosimendan Prevents Memory Impairment Induced by Diabetes in Rats: Role of Oxidative Stress." Current Alzheimer Research 16, no. 14 (January 28, 2020): 1300–1308. http://dx.doi.org/10.2174/1567205017666200102153239.

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Background: Levosimendan is a calcium sensitizer and phosphodiesterase inhibitor that has potent antioxidant and anti-inflammatory activities. Objectives: The aim of the current study is to investigate the potential protective effect of levosimendan on learning and memory impairment induced by diabetes. Methods: Adult Wister rats were randomly divided into four groups (n=15 rats/group): control, levosimendan, streptozotocin (STZ) induced diabetes, and levosimendan-STZ diabetes. Upon confirmation of the success of the STZ diabetic model, intraperitoneal levosimendan (100µg/kg/week) was administrated to the assigned groups for 4 weeks. Then, the radial arm water maze was used to evaluate spatial learning and memory. Oxidative stress biomarkers and brain-derived neurotrophic factor were evaluated in hippocampal tissues. Results: The results showed that Diabetes Mellitus (DM) impaired both short- and long- term memory (P<0.01), while levosimendan protected the animals from memory impairment. In addition, levosimendan prevented DM-induced reduction in the hippocampal levels of superoxide dismutase and glutathione peroxidase (P<0.05). Moreover, the administration of levosimendan prevented DM-induced increases in hippocampal thiobarbituric acid reactive substances level (P<0.05). Furthermore, levosimendan restored the ratio of reduced/oxidized glutathione (GSH/GSSG) in DM rats to that observed in the control group (P<0.05). Conclusions: In summary, DM induced learning and memory impairment, and treatment with levosimendan impeded this impairment probably through preventing alterations in the antioxidant system in the hippocampus.
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21

Grossini, Elena, Serena Farruggio, Daniele Pierelli, Virginia Bolzani, Lidia Rossi, Piero Pollesello, and Carolina Monaco. "Levosimendan Improves Oxidative Balance in Cardiogenic Shock/Low Cardiac Output Patients." Journal of Clinical Medicine 9, no. 2 (January 30, 2020): 373. http://dx.doi.org/10.3390/jcm9020373.

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The beneficial effects exerted by levosimendan against cardiac failure could be related to the modulation of oxidative balance. We aimed to examine the effects of levosimendan in patients with cardiogenic shock or low cardiac output on cardiac systo-diastolic function and plasma oxidants/antioxidants (glutathione, GSH; thiobarbituric acid reactive substances, TBARS). In four patients undergoing coronary artery bypass grafting or angioplasty, cardiovascular parameters and plasma GSH and TBARS were measured at T0 (before levosimendan infusion), T1 (1 h after the achievement of the therapeutic dosage of levosimendan), T2 (end of levosimendan infusion), T3 (72 h after the end of levosimendan infusion), and T4 (end of cardiogenic shock). We found an improvement in the indices of systolic (ejection fraction, cardiac output, cardiac index) and diastolic (E to early diastolic mitral annular tissue velocity, E/’; early to late diastolic transmitral flow velocity, EA) cardiac function at early T2. A reduction of central venous pressure and pulmonary wedge pressure was also observed. Plasma levels of GSH and TBARS were restored by levosimendan at T1, as well. The results obtained indicate that levosimendan administration can regulate oxidant/antioxidant balance as an early effect in cardiogenic shock/low cardiac output patients. Modulation of oxidative status on a mitochondrial level could thus play a role in exerting the cardio-protection exerted by levosimendan in these patients.
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22

Kalam, Yasmean, and Andis Graudins. "Levosimendan Does Not Improve Cardiac Output or Blood Pressure in a Rodent Model of Propranolol Toxicity When Administered Using Various Dosing Regimens." International Journal of Toxicology 31, no. 2 (March 2012): 166–74. http://dx.doi.org/10.1177/1091581811435366.

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Background: Levosimendan (CAS: 141505-33-1) is a myocardial calcium sensitizer that improves myocardial contractility in various forms of heart failure. It produces a moderate improvement in cardiac output (CO) without an improvement in blood pressure (BP) in verapamil and metoprolol poisoned rodents. Aim: To assess the effect of various levosimendan dosing regimens on hemodynamics in a rodent model of propranolol poisoning. Method: Male Wistar rats (350-450 g) were anesthetized, ventilated, and instrumented to record BP, heart rate (HR), and CO. Propranolol was infused continually. When BP dropped to 50% of baseline rats received 1 of 7 treatments: (1) 0.9% saline (control), (2) levosimendan 36 μg/kg loading dose then 0.6 μg/kg per min, (3) levosimendan 0.6 μg/kg per min, (4) epinephrine 0.5 μg/kg per min, (5) levosimendan 70 μg/kg loading dose then 1.2 μg/kg per min, (6) levosimendan 1.2 μg/kg per min, and (7) levosimendan 70 μg/kg loading dose alone. Hemodynamics were recorded every 10 minutes for 70 minutes. Cardiac output, mean arterial pressure, and HR for each group were compared with control. Results: All groups had comparable baseline and maximal toxicity hemodynamics prior to initiation of treatment. Levosimendan did not improve CO or BP with any dosing regimen. Blood pressure tended to be lower than control for all doses of levosimendan. Epinephrine significantly improved BP but not CO compared to all other treatment groups. Survival did not differ between groups. Conclusions: Unlike in verapamil and metoprolol poisoning models, levosimendan did not improve CO or survival in propranolol poisoning. Epinephrine improved BP, but not CO, suggesting that its actions were due to peripheral vasoconstriction.
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23

Abacilar, Ahmet Feyzi, and Omer Faruk Dogan. "Levosimendan Use Decreases Atrial Fibrillation in Patients after Coronary Artery Bypass Grafting: A Pilot Study." Heart Surgery Forum 16, no. 5 (November 15, 2013): E287—E294. http://dx.doi.org/10.1532/hsf98.2013190.

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Background: Atrial fibrillation (AF) often occurs after coronary artery bypass grafting (CABG) and can result in increased morbidity and mortality due to complications. In the present study, our goal was to investigate whether the use of levosimendan can reduce the frequency of AF after coronary artery bypass grafting in patients with poor left ventricle function. Material and Methods: To investigate the effectiveness of levosimendan in the prophylaxis of AF, we conducted a prospective, randomized, placebo-controlled clinical study on 200 consecutive patients in whom we performed elective CABG operations. Baseline characteristics were similar in both groups. A control group of 100 patients were treated with placebo (500 mL saline solution), whereas the levosimendan group (n = 100 patients) was treated with levosimendan. High-sensitivity C-reactive protein, cardiac troponin, and creatine kinase–MB levels were measured before surgery and 5 days postoperatively. Results: AF occurred in 12% of the levosimendan group and 36% of the control group. The occurrence of AF was significantly lower in the levosimendan group (P < 0.05). The duration of AF in the levosimendan group was significantly shorter than that in the control group (4.83 ± 1.12 and 6.50 ± 1.55 hours, respectively; P = 0.028). Our research showed that C-reactive protein was higher postoperatively in the control group than in the levosimendan group (P < 0.05). Conclusions: The incidence of postoperative AF in the levosimendan group was reduced significantly in patients with poor left ventricle function after CABG operations.
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24

Earl, Grace L., and James T. Fitzpatrick. "Levosimendan: A Novel Inotropic Agent for Treatment of Acute, Decompensated Heart Failure." Annals of Pharmacotherapy 39, no. 11 (November 2005): 1888–96. http://dx.doi.org/10.1345/aph.1g128.

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OBJECTIVE To review the literature on a novel calcium sensitizer, levosimendan. DATA SOURCES Articles were identified through searches of MEDLINE (1966–June 2005), International Pharmaceutical Abstracts (1970–June 2005), and EMBASE (1992–June 2005) using the key words levosimendan, simendan, calcium sensitizer, calcium sensitiser, and congestive heart failure. STUDY SELECTION AND DATA EXTRACTION Clinical trials and pharmacokinetic studies evaluating the safety and efficacy of levosimendan were selected. DATA SYNTHESIS Levosimendan 6–24 μg/kg intravenous bolus followed by a 24-hour continuous infusion of 0.05—0.2 μg/kg/min improved cardiac output and reduced pulmonary capillary wedge pressure in a dose-dependent manner. Dose-ranging and randomized clinical trials have demonstrated improvement in symptoms and hemodynamics and short-term survival outcomes in the treatment of acute, decompensated heart failure. Clinical trials evaluating retrospective mortality data and combined endpoints (mortality, rehospitalization) have demonstrated better outcomes with levosimendan compared with dobutamine. The incidence of hypotension with levosimendan is not significantly different than with dobutamine, but there is a dose-related increase in heart rate. CONCLUSIONS Levosimendan is useful in moderate to severe low-output heart failure in patients who have failed to respond to diuretics and vasodilators. Based on current studies, levosimendan appears to be a safe alternative to dobutamine for treatment of acute, decompensated heart failure. Prospective clinical trials are needed to confirm the effect of levosimendan on long-term survival and its role in heart failure in the setting of myocardial infarction.
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25

Banfor, Patricia N., Lee C. Preusser, Thomas J. Campbell, Kennan C. Marsh, James S. Polakowski, Glenn A. Reinhart, Bryan F. Cox, and Ryan M. Fryer. "Comparative effects of levosimendan, OR-1896, OR-1855, dobutamine, and milrinone on vascular resistance, indexes of cardiac function, and O2 consumption in dogs." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (January 2008): H238—H248. http://dx.doi.org/10.1152/ajpheart.01181.2007.

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Levosimendan enhances cardiac contractility via Ca2+ sensitization and induces vasodilation through the activation of ATP-dependent K+ and large-conductance Ca2+-dependent K+ channels. However, the hemodynamic effects of levosimendan, as well as its metabolites, OR-1896 and OR-1855, relative to plasma concentrations achieved, are not well defined. Thus levosimendan, OR-1896, OR-1855, or vehicle was infused at 0.01, 0.03, 0.1, and 0.3 μmol·kg−1·30 min−1, targeting therapeutic to supratherapeutic concentrations of total levosimendan (62.6 ng/ml). Results were compared with those of the β1-agonist dobutamine and the phosphodiesterase 3 inhibitor milrinone. Peak concentrations of levosimendan, OR-1896, and OR-1855 were 455 ± 21, 126 ± 6, and 136 ± 6 ng/ml, respectively. Levosimendan and OR-1896 produced dose-dependent reductions in mean arterial pressure (−31 ± 2 and −42 ± 3 mmHg, respectively) and systemic resistance without affecting pulse pressure, effects paralleled by increases in heart rate; OR-1855 produced no effect at any dose tested. Dobutamine, but not milrinone, increased mean arterial pressure and pulse pressure (17 ± 2 and 23 ± 2 mmHg, respectively). Regarding potency to elicit reductions in time to peak pressure and time to systolic pressure recovery: OR-1896 > levosimendan > milrinone > dobutamine. Levosimendan and OR-1896 elicited dose-dependent increases in change in pressure over time (118 ± 10 and 133 ± 13%, respectively), concomitant with reductions in left ventricular end-diastolic pressure and ejection time. However, neither levosimendan nor OR-1896 produced increases in myocardial oxygen consumption at inotropic and vasodilatory concentrations, whereas dobutamine increased myocardial oxygen consumption (79% above baseline). Effects of the levosimendan and OR-1896 were limited to the systemic circulation; neither compound produced changes in pulmonary pressure, whereas dobutamine produced profound increases (74 ± 13%). Thus levosimendan and OR-1896 are hemodynamically active in the anesthetized dog at concentrations observed clinically and elicit cardiovascular effects consistent with activation of both K+ channels and Ca2+ sensitization, whereas OR-1855 is inactive on endpoints measured in this study.
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Vardhan Janjirala, Seshi. "EFFECT OF LEVOSIMENDAN ON SHORT TERM AND LONG TERM CLINICAL COURSE OF PATIENTS WITH ACUTELY DECOMPENSATED HEART FAILURE IN INDIAN POPULATION." International Journal of Advanced Research 8, no. 9 (September 30, 2020): 1378–79. http://dx.doi.org/10.21474/ijar01/11799.

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We evaluated the efficacy of levosimendan, a positive inodilator, given intravenously to patients with acutely decompensated heart failure (ADHF). Methods: Patients admitted with ADHF received placebo or IV levosimendan for 24 hr in addition to standard treatment. The primary endpoint was a composite that evaluated changes in clinical and laboratory status at 30th day and at 180th day.secondary end point is all cause mortality. Results: In the 125-patient trial, more levosimendan than placebo patients were improved at discharge, whereas fewer levosimendan patients experienced clinical worsening at 6 months. The functional class, cardiac contractility ( FS,EF) were better in simenda group at 3rd month both neumerically and statistically.All-cause mortality at 180 days occurred in 5% patients in the levosimendan group and 28%patients in the placebo group. The levosimendan group had greater decreases in Brain Natriuretric peptide level at 24 hours. There were no statistical differences between treatment groups for the other secondary end points (all-cause mortality at 31 days, number of days alive and out of the hospital, patient global assessment, patient assessment of dyspnea at 24 hours, and cardiovascular mortality at 180 days). There was a higher incidence of cardiac failure in the placebo group. There were higher incidences of atrial fibrillation, hypokalemia, and headache in the levosimendan group Conclusions: In patients with ADHF, intravenous levosimendan provided rapid and durable symptomatic relief and levosimendan improved haemodynamic performance more effectively than placebo. 6MHWD, quality of life, worsening of heart failure, cardiac structure and function were statistically and numerically improved in simenda group for first 3monthsHowever the results were not consistent for 180 days.This benefit was accompanied by lower mortality in the levosimendan group than in the placebo group for up to 180 days.
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Rababa'h, Abeer M., Omar F. Khabour, Karem H. Alzoubi, Dua'a Al-momani, and Mera Ababneh. "Assessment of Genotoxicity of Levosimendan in Human Cultured Lymphocytes." Current Molecular Pharmacology 12, no. 2 (April 11, 2019): 160–65. http://dx.doi.org/10.2174/1874467212666190306164926.

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Background and Objective: Levosimendan is a positive inotropic and a vasodilator agent with pleotropic characteristics that include antioxidation, anti-inflammation and smooth muscle vasodilation. Methods: In this study, the effects of levosimendan (0, 0.1, 1, 10, and 20 µg/ml) on oxidative DNA damage and sister-chromatid exchanges (SCEs) were evaluated in human cultured lymphocytes. Results: The results showed that levosimendan increased the frequency of SCEs in all examined concentrations (P<0.01) except for 0.1 µg/ml. On the other hand, levosimendan did not induce oxidative DNA damage as measured by the 8-OHdG biomarker (P > 0.05). In addition, neither mitotic arrest nor proliferation index was affected by levosimendan at all examined doses (P > 0.05). Conclusion: In conclusion, levosimendan might be associated with increases in sister-chromatid exchanges in cultured human lymphocytes. In vivo studies are required to confirm the present findings.
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Babik, Barna, Adam L. Balogh, Roberta Sudy, Orsolya Ivankovitsne-Kiss, Gergely H. Fodor, and Ferenc Petak. "Levosimendan prevents bronchoconstriction and adverse respiratory tissue mechanical changes in rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 5 (November 1, 2017): L950—L956. http://dx.doi.org/10.1152/ajplung.00213.2017.

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Levosimendan has a calcium-sensitizing effect in the myocardium and opens ATP-sensitive potassium channels (KATP) in vascular smooth muscle. Because airway smooth muscle also expresses KATP, we characterized the protective potential of levosimendan against increased airway and respiratory tissue resistances. Animals were administered levosimendan alone ( group L), levosimendan after pretreatment with a KATP channel blocker (glibenclamide, group LG), glibenclamide only ( group G), or solvent alone (dextrose, group C). Airway resistance (Raw), tissue damping, and elastance were determined by forced oscillations under baseline conditions and following provocation tests with intravenous methacholine (MCh). Cardiac output (CO) was assessed by transpulmonary thermodilution. The same sequence of measurements was then repeated during intravenous infusion of levosimendan in groups L and LG or glucose in groups G and C. Sham treatments in groups C and G had no effect on lung responsiveness. However, levosimendan treatment in group L elevated CO and inhibited the MCh-induced airway responses [Raw changes of 87.8 ± 83% (SD) vs. 24.4 ± 16% at 4 μg·kg−1·min−1 MCh, P < 0.001], and in G (35.2 ± 12.7 vs. 25.2 ± 12.9%, P < 0.05). The preventive affect of levosimendan against lung constriction vanished in the LG group. Levosimendan exerts a KATP-mediated potential to prevent bronchoconstriction and may prohibit adverse lung peripheral changes both in the small bronchi and the pulmonary parenchyma. The identification of a further pleiotropic property of levosimendan that is related to the pulmonary system is of particular importance for patients with decreased cardiorespiratory reserves for which simultaneous circulatory support is complemented with prevention of adverse respiratory events.
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Hansen, Mona S., Asger Andersen, Lars P. Tolbod, Nils H. Hansson, Roni Nielsen, Anton Vonk-Noordegraaf, and Jens Erik Nielsen-Kudsk. "Levosimendan improves cardiac function and myocardial efficiency in rats with right ventricular failure." Pulmonary Circulation 8, no. 1 (November 3, 2017): 204589321774312. http://dx.doi.org/10.1177/2045893217743122.

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Levosimendan is an inotropic and vasodilator drug, which is known to improve cardiac function in animal models of right ventricular (RV) failure. The effects of levosimendan on oxygen consumption and myocardial efficiency in the failing RV is unknown. We investigated the effects of levosimendan on RV function, myocardial oxygen consumption, myocardial external efficiency (MEE), and myocardial metabolism in rats with RV hypertrophy and failure. RV hypertrophy and failure were induced by pulmonary trunk banding in rats. Rats were randomized to seven weeks of treatment with vehicle (n = 16) or levosimendan (3 mg/kg/day) (n = 13). Control animals without pulmonary banding received vehicle treatment (n = 11). RV MEE and RV metabolism were evaluated by echocardiography, 11C-acetate positron emission tomography (PET), 18F-FDG PET, and invasive pressure measurements. We found that levosimendan improved RV MEE (26 ± 3 vs. 14 ± 1%, P < 0.01) by increasing RV external work (0.62 ± 0.06 vs. 0.30 ± 0.03 mmHgċmL, P < 0.001) without affecting RV myocardial oxygen consumption ( P = 0.64). The improvement in RV MEE was not associated with a change in RV myocardial glucose uptake (1.3 ± 0.1 vs. 1.0 ± 0.1 µmol/g/min, P = 0.44). In conclusion, in the hypertrophic and failing RV of the rat, levosimendan improves RV function without increasing myocardial oxygen consumption leading to improved MEE. The improvement in RV MEE was not associated with a change in myocardial glucose uptake. This study emphasizes the potential therapeutic value of chronic levosimendan treatment RV failure. It extends previous observations on the effect profile of levosimendan and motivates clinical testing of levosimendan in RV failure.
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Ramaswamykanive, H., D. Bihari, and T. R. Solano. "Myocardial Depression Associated with Pneumococcal Septic Shock Reversed by Levosimendan." Anaesthesia and Intensive Care 35, no. 3 (June 2007): 409–13. http://dx.doi.org/10.1177/0310057x0703500316.

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Levosimendan is a myocardial calcium sensitiser and potassium-ATP channel opener. Levosimendan has been used in critically ill patients in various conditions to support myocardial function as an inotrope, lusitrope and vasodilator. We report the use of levosimendan in a patient with invasive streptococcal septic shock.
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Rognoni, Andrea, Alessandro Lupi, Chiara Cavallino, Alessia Veia, Sara Bacchini, Roberta Rosso, Gioel Gabrio Secco, and Angelo Sante Bongo. "Levosimendan Preoperative." Current Pharmaceutical Design 19, no. 22 (May 1, 2013): 3974–78. http://dx.doi.org/10.2174/1381612811319220005.

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Juguet, William, Damien Fard, Laureline Faivre, Athanasios Koutsoukis, Camille Deguillard, Nicolas Mongardon, Armand Mekontso-Dessap, Raphaelle Huguet, and Pascal Lim. "Levosimendan Plus Dobutamine in Acute Decompensated Heart Failure Refractory to Dobutamine." Journal of Clinical Medicine 9, no. 11 (November 9, 2020): 3605. http://dx.doi.org/10.3390/jcm9113605.

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Randomized studies showed that Dobutamine and Levosimendan have similar impact on outcome but their combination has never been assessed in acute decompensated heart failure (ADHF) with low cardiac output. This is a retrospective, single-center study that included 89 patients (61 ± 15 years) admitted for ADHF requiring inotropic support. The first group consisted of patients treated with dobutamine alone (n = 42). In the second group, levosimendan was administered on top of dobutamine, when the superior vena cava oxygen saturation (ScVO2) remained <60% after 3 days of dobutamine treatment (n = 47). The primary outcome was the occurrence of major cardiovascular events (MACE) at 6 months, defined as all cause death, heart transplantation or need for mechanical circulatory support. Baseline clinical characteristics were similar in both groups. At day-3, the ScVO2 target (>60%) was reached in 36% and 32% of patients in the dobutamine and dobutamine-levosimendan group, respectively. After adding levosimendan, 72% of the dobutamine-levosimendan-group reached the ScVO2 target value at dobutamine weaning. At six months, 42 (47%) patients experienced MACE (n = 29 for death). MACE was less frequent in the dobutamine-levosimendan (32%) than in the dobutamine-group (64%, p = 0.003). Independent variables associated with outcome were admission systolic blood pressure and dobutamine-levosimendan strategy (OR = 0.44 (0.23–0.84), p = 0.01). In conclusion, levosimendan added to dobutamine may improve the outcome of ADHF refractory to dobutamine alone.
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du Toit, E., D. Hofmann, J. McCarthy, and C. Pineda. "Effect of levosimendan on myocardial contractility, coronary and peripheral blood flow, and arrhythmias during coronary artery ligation and reperfusion in the in vivo pig model." Heart 86, no. 1 (July 1, 2001): 81–87. http://dx.doi.org/10.1136/hrt.86.1.81.

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OBJECTIVETo determine whether levosimendan, a calcium sensitiser that facilitates the activation of the contractile apparatus by calcium, improves myocardial contractile function during severe ischaemia and reperfusion without exacerbating the incidence of arrhythmias.DESIGNPigs were pretreated orally twice daily for 10 days with 0.08 mg/kg levosimendan or placebo. On day 11 the left main coronary artery was ligated for 30 minutes, followed by 30 minutes of reperfusion. A bolus dose of levosimendan, 11.2 μg/kg intravenously, or placebo was given 30 minutes before coronary ligation, followed by a continuous infusion of 0.2 μg/kg/min levosimendan or placebo for the remainder of the experiment.RESULTSDuring the ischaemic period, cardiac output was higher in the levosimendan group than in the placebo group (mean (SD): 2.6 (0.5) v 2.0 (0.2) l/min, p < 0.05) and systemic vascular resistance was lower (2024 (188) v 2669 (424) dyne.s−1.cm−5, p < 0.005). During reperfusion, cardiac output and contractility (LVmaxdP/dt (pos), 956 (118) v 784 (130) mm Hg/s, p < 0.05) were increased by levosimendan. The incidence of ischaemic ventricular fibrillation and tachycardia was similar in the two groups but there were more arrhythmic events (ventricular tachycardia and ventricular fibrillation) in the levosimendan treated group (8/12 levosimendan v 1/9 control p = 0.05).CONCLUSIONSLevosimendan improved cardiac output and myocardial contractility during coronary artery ligation and reperfusion. However, it increased the number of arrhythmic events during ischaemia in this model of in vivo regional ischaemia.
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Powell, B. P., and D. Simes. "Levosimendan in Acute Pulmonary Embolism." Anaesthesia and Intensive Care 35, no. 5 (October 2007): 771–72. http://dx.doi.org/10.1177/0310057x0703500518.

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Levosimendan has been used successfully in the treatment of ischaemic cardiac failure and myocardial stunning. There is growing evidence from both human and animal experiments that levosimendan has particularly favourable effects on the right ventricle. We describe a case of life-threatening pulmonary embolus supported by the use of levosimendan.
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Yang, Fei, Li Na Zhao, Yi Sun, and Zhuang Chen. "Levosimendan as a new force in the treatment of sepsis-induced cardiomyopathy: mechanism and clinical application." Journal of International Medical Research 47, no. 5 (April 8, 2019): 1817–28. http://dx.doi.org/10.1177/0300060519837103.

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The heart is one of the organs most vulnerable to sepsis. This review describes the general characteristics of sepsis-induced cardiomyopathy and the main pathogenesis of myocardial dysfunction in sepsis. Levosimendan is a novel drug for treatment of sepsis-induced myocardial dysfunction. This review also elaborates on the pathogenesis of levosimendan, including the mechanisms of its anti-inflammatory effects, improvement of myocardial ischaemia, increased synthesis of nitric oxide, vascular endothelial cell protection, increased myocardial contractility, improved diastolic function, and inhibition of hypoxia-inducible factor-1α expression. Many clinical studies have proven that levosimendan effectively prevents myocardial dysfunction in sepsis. In addition to the widespread use of levosimendan in patients with heart failure, the role of levosimendan in the treatment of patients with sepsis-induced cardiomyopathy will be increasingly studied and applied in the future.
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Tawfik, Mona K., Mohamed K. El-Kherbetawy, and Samy Makary. "Cardioprotective and Anti-Aggregatory Effects of Levosimendan on Isoproterenol-Induced Myocardial Injury in High-Fat-Fed Rats Involves Modulation of PI3K/Akt/mTOR Signaling Pathway and Inhibition of Apoptosis." Journal of Cardiovascular Pharmacology and Therapeutics 23, no. 5 (April 23, 2018): 456–71. http://dx.doi.org/10.1177/1074248418763957.

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Hyperlipidemia and hypercoagulability states are linked with the increased risks of myocardial infarction (MI). Levosimendan has vasorelaxant and anti-aggregatory properties. The present study evaluated the anti-aggregatory and cardioprotective effects of levosimendan versus cilostazol in high-fat diet (HFD)-fed rats subjected to isoproterenol-induced MI. Rats were assigned to normal, HFD, HFD + isoproterenol, HFD + isoproterenol + cilostazol, and HFD + isoproterenol + levosimendan. The present study investigated the anti-aggregatory effect of both levosimendan and cilostazol and revealed that both drugs attenuated the severity of platelet aggregation. Moreover, both levosimendan and cilostazol revealed effectiveness in attenuating the severity of HFD/isoproterenol-induced myocardial injury as revealed by electrocardiogram signs, apoptotic markers, and histopathological score via counteracting the oxidative stress burden, increments in the expression of inflammatory mediators, and modulating nuclear factor kappa-B (NF-κB) and phosphatidylinositide 3-kinases (PI3K)/protein kinase B (Akt)/ mechanistic target of rapamycin (mTOR) pathway. It was obvious that levosimendan offered more cardioprotective properties than cilostazol. The study showed the relations between hyperlipedemia, hyperaggregability state, and myocardial injury with the modulation of NF-κB and PI3K/Akt/mTOR pathway.
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Krychtiuk, Konstantin A., Lukas Watzke, Christoph Kaun, Elisabeth Buchberger, Renate Hofer-Warbinek, Svitlana Demyanets, Julia Pisoni, et al. "Levosimendan exerts anti-inflammatory effects on cardiac myocytes and endothelial cells in vitro." Thrombosis and Haemostasis 113, no. 02 (March 2015): 350–62. http://dx.doi.org/10.1160/th14-06-0549.

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SummaryLevosimendan is a positive inotropic drug for the treatment of acute decompensated heart failure (HF). Clinical trials showed that levosimendan was particularly effective in HF due to myocardial infarction. Myocardial necrosis induces a strong inflammatory response, involving chemoattractants guiding polymorphonuclear neutrophils (PMN) into the infarcted myocardial tissue. Our aim was to examine whether levosimendan exhibits anti-inflammatory effects on human adult cardiac myocytes (HACM) and human heart microvascular endothelial cells (HHMEC). Cardiac myocytes and endothelial cells were stimulated with interleukin-1β (IL)-1β (200 U/ml) and treated with levosimendan (0.1–10 μM) for 2–48 hours. IL-1β strongly induced expression of IL-6 and IL-8 in HACM and E-selectin and intercellular adhesion molecule-1 (ICAM-1) in HHMEC and human umbilical vein endothelial cells (HUVEC). Treatment with levosimendan strongly attenuated IL-1β-induced expression of IL-6 and IL-8 in HACM as well as E-selectin and ICAM-1 in ECs. Levosimendan treatment further reduced adhesion of PMN to activated endothelial cells under both static and flow conditions by approximately 50 %. Incubation with 5-hydroxydecanoic acid, a selective blocker of mitochondrial ATP-dependent potassium channels, partly abolished the above seen anti-inflammatory effects. Additionally, levosimendan strongly diminished IL-1β-induced reactive oxygen species and nuclear factor-κB (NF-κB) activity through inhibition of S536 phosphorylation. In conclusion, levosimendan exhibits anti-inflammatory effects on cardiac myocytes and endothelial cells in vitro. These findings could explain, at least in part, the beneficial effects of levosimendan after myocardial infarction.
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Ellermann, Christian, Anja Kohnke, Dirk G. Dechering, Simon Kochhäuser, Florian Reinke, Michael Fehr, Lars Eckardt, and Gerrit Frommeyer. "Ranolazine Prevents Levosimendan-Induced Atrial Fibrillation." Pharmacology 102, no. 3-4 (2018): 138–41. http://dx.doi.org/10.1159/000490572.

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Objectives: Levosimendan is a calcium sensitizer that is used as positive inotropic drug in acute decompensated heart failure. An increased incidence of atrial fibrillation after levosimendan-treatment was observed in clinical and experimental studies. Due to the limited range of antiarrhythmic drugs, the aim of the present study was to assess potential antiarrhythmic effects of ranolazine in levosimendan-pretreated isolated rabbit hearts. Methods: Twelve rabbit hearts were excised and retrogradely perfused employing the Langendorff setup. Left and right atrial catheters were used to record monophasic action potentials and to obtain cycle length-dependent atrial action potential durations (aAPD90) and effective refractory periods (aERP). After obtaining baseline data, 0.5 µmol/L levosimendan was infused. Subsequently, 10 µmol/L ranolazine was administered. Results: Infusion of levosimendan led to a reduction of aAPD90 (–9 ms, p < 0.05) and aERP (–13 ms, p < 0.05). Additional treatment with ranolazine prolonged aAPD90 (+23 ms, p < 0.01) and aERP (+30 ms, p < 0.05). Under baseline conditions, a predefined pacing protocol induced 77 episodes of atrial fibrillation. Infusion of levosimendan enhanced the vulnerability to atrial fibrillation (132 episodes, p = 0.14). Further treatment with ranolazine had a significant antiarrhythmic effect (61 episodes, p < 0.05). Conclusions: In this study, ranolazine seems to prevent atrial fibrillation in levosimendan-pretreated hearts. Underlying mechanism is a prolongation of atrial repolarization and aERP.
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39

Chang, Wei, Jian-Feng Xie, Jing-Yuan Xu, and Yi Yang. "Effect of levosimendan on mortality in severe sepsis and septic shock: a meta-analysis of randomised trials." BMJ Open 8, no. 3 (March 2018): e019338. http://dx.doi.org/10.1136/bmjopen-2017-019338.

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ObjectiveWe aim to synthesise up-to-date randomised trials to investigate the effects of levosimendan on mortality and clinical outcomes in severe sepsis and septic shock.MethodsA collection of databases including PubMed, EMBASE, Cochrane Central Register and Web of Science were searched updated to August 2017. Randomised trials were included when they pertain to the use of levosimendan in severe sepsis or septic shock compared with any category of inotropes, or as an adjunct to standard therapy with mortality reported. The primary outcome was mortality, and the secondary outcomes were clinical performances including serum lactate, cardiac function, vasopressor requirement and fluid infusion.ResultsA total of 10 studies with 1036 patients were included in this meta-analysis. The results revealed that levosimendan could not reduce mortality significantly in severe sepsis and septic shock (OR 0.89, 95% CI 0.69 to 1.16, P=0.39). Levosimendan use could reduce serum lactate more effectively, and enhance cardiac contractibility with increased cardiac index and left ventricular ejection fraction. However, its use could also increase fluid infusion but not reduce norepinephrine dose. No significant benefit in mortality could be observed of levosimendan versus dobutamine use, or in patients with proven cardiac dysfunction.ConclusionsCurrent evidence is not sufficient to support levosimendan as superior to dobutamine or as an optimal adjunct in severe sepsis and septic shock. More large-scale randomised trials are necessary to validate levosimendan use in sepsis.
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Kocabeyoglu, Sinan Sabit, Umit Kervan, Dogan Emre Sert, Mehmet Karahan, Emre Aygun, Osman Fehmi Beyazal, Ertekin Utku Unal, Yesim Akin, Burcu Demirkan, and Mustafa Pac. "Optimization with levosimendan improves outcomes after left ventricular assist device implantation." European Journal of Cardio-Thoracic Surgery 57, no. 1 (June 1, 2019): 176–82. http://dx.doi.org/10.1093/ejcts/ezz159.

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Abstract OBJECTIVES The aim of this study was to examine the haemodynamic effects of preoperative levosimendan infusion in patients who underwent left ventricular assist device implantation and evaluate the prognoses. METHODS Between May 2013 and October 2018, 85 adult patients who underwent left ventricular assist device implantation were included; 44 and 41 patients suffered from dilated cardiomyopathy and ischaemic cardiomyopathy, respectively. Patients were divided into 2 groups: group A (58 patients) included those who received levosimendan infusion in addition to other inotropes and group B (27 patients) included those who received inotropic agents other than levosimendan. Levosimendan infusion was started at a dose of 0.1 µg⋅kg−1⋅min−1 for a maximum of 48 h without a bolus. The primary outcome was early right ventricular failure (RVF). The secondary outcomes were in-hospital mortality, need for right ventricular assist device, late RVF and recovery of end-organ functions. The safety end points of levosimendan included hypotension, atrial fibrillation, ventricular tachycardia or fibrillation and resuscitated cardiac arrest. RESULTS Patient characteristics were similar in both groups. No significant differences between groups were observed in the rates of early mortality, RVF, need for right ventricular assist device, cardiopulmonary bypass time and intensive care unit stay. Survival rates at 30 days, 1 year and 3 years and freedom from late RVF were similar between the groups. Administration of levosimendan was safe, generally well-tolerated and not interrupted because of side effects. CONCLUSIONS Levosimendan therapy was well-tolerated in patients who received permanent left ventricular assist devices. Combined preoperative therapy with inotropes and levosimendan significantly improves end-organ functions.
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Pan, Kevin C., Sai Shankar, Johnny Millar, Roberto Chiletti, Warwick Butt, Yves d’Udekem, and Siva P. Namachivayam. "Role of levosimendan in weaning children requiring veno-arterial extracorporeal membrane oxygenation after cardiac surgery." European Journal of Cardio-Thoracic Surgery 59, no. 1 (September 10, 2020): 262–68. http://dx.doi.org/10.1093/ejcts/ezaa275.

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Abstract OBJECTIVES Levosimendan use is associated with more successful decannulation from veno-arterial extracorporeal membrane oxygenation (VA ECMO) in adults. We sought to determine the role of levosimendan in children who required VA ECMO after cardiac surgery. METHODS This observational study compares the outcomes of children who required VA ECMO after cardiac surgery and received levosimendan for weaning with those who did not receive the drug. A doubly robust estimation methodology (inverse probability of treatment weighting with regression adjustment) was used to balance study covariates (age, weight, sex, lactate pre-ECMO, vasoactive-inotropic score pre-ECMO, ECMO indication, ECMO modality, Risk Adjustment for Congenital Heart Surgery-1 category), and the final model was further adjusted for duration of ECMO. RESULTS Between January 2012 and December 2018, 118 eligible children received 145 ECMO runs [failed weaning from cardiopulmonary bypass, 67/145 (46%); low cardiac output state, 30/145 (21%); extracorporeal cardiopulmonary resuscitation, 47/145 (32%); other reasons in 1]. Levosimendan was administered before decannulation in 54/145 (37%) runs. The median time to start levosimendan after ECMO cannulation was 39 h (interquartile range, 14–83 h). The unadjusted rates of weaning failure in the levosimendan vs control group were 7% (4/54) vs 19% (17/91). In the controlled analysis, levosimendan was associated with decreased risk of weaning failure [adjusted relative risk (95% confidence interval), 0.20 (0.07–0.57)] and decreased risk of in-hospital mortality [adjusted relative risk (95% confidence interval), 0.45 (0.26–0.76)]. CONCLUSIONS Levosimendan administration in children requiring VA ECMO after cardiac surgery was associated with decreased risk of weaning failure and decreased in-hospital mortality.
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Al-Chalabi, Ammar, Pamela Shaw, P. Nigel Leigh, Leonard van den Berg, Orla Hardiman, Albert Ludolph, Valtteri V. Aho, Toni Sarapohja, and Mikko Kuoppamäki. "Oral levosimendan in amyotrophic lateral sclerosis: a phase II multicentre, randomised, double-blind, placebo-controlled trial." Journal of Neurology, Neurosurgery & Psychiatry 90, no. 10 (July 17, 2019): 1165–70. http://dx.doi.org/10.1136/jnnp-2018-320288.

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ObjectiveTo evaluate the efficacy and safety of oral levosimendan in patients with amyotrophic lateral sclerosis (ALS). This phase II, randomised, double-blind, placebo-controlled, crossover, three-period study with 6 months open-label follow-up enrolled adults with ALS and sitting slow vital capacity (SVC) 60%–90 % of predicted from 11 sites in four countries.MethodsPatients received levosimendan 1 mg daily, 1 mg two times a day or placebo during three 14-day crossover periods and levosimendan 1–2 mg daily during open-label follow-up. Primary endpoint was sitting SVC; secondary endpoints included supine SVC, ALS Functional Rating Scale-Revised (ALSFRS-R), tolerability and safety.ResultsOf 66 patients randomised, 59 contributed to the double-blind results and 50 entered open-label follow-up. Sitting SVC was not significantly different between the treatments. In post hoc analysis using period-wise baselines, supine SVC favoured levosimendan over placebo, estimated mean differences from baseline being −3.62% on placebo, +0.77% on levosimendan 1 mg daily (p=0.018) and +2.38% on 1 mg two times a day (p=0.001). Headache occurred in 16.7% of patients during levosimendan 1 mg daily (p=0.030), 28.6% during 1 mg two times a day (p=0.002) and 3.3% during placebo. The respective frequencies for increased heart rate were 5.1% (p=0.337), 18.5% (p=0.018) and 1.7%. No significant differences between the treatments were seen for other adverse events.ConclusionsLevosimendan did not achieve the primary endpoint of improving sitting SVC in ALS. Headache and increased heart rate were increased on levosimendan, although it was otherwise well tolerated. A phase III study to evaluate the longer term effects of oral levosimendan in ALS is ongoing.
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Beiras-Fernandez, Andres, Angela Kornberger, Martin Oberhoffer, Felix Kur, Marion Weis, Christian-Friedrich Vahl, and Florian Weis. "Levosimendan as rescue therapy in low output syndrome after cardiac surgery: effects and predictors of outcome." Journal of International Medical Research 47, no. 8 (March 26, 2019): 3502–12. http://dx.doi.org/10.1177/0300060519835087.

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Objectives Calcium sensitizers have been shown to improve outcomes in patients with low cardiac output syndrome (LCOS) after cardiac surgery. We assessed the effects of levosimendan on LCOS in cardiac surgical patients to identify outcome predictors. Methods A total of 106 patients in whom LCOS persisted despite conventional therapy additionally received 0.1 µg/kg/min of levosimendan for 24 hours according to a defined treatment algorithm. Baseline and treatment data as well as hemodynamic and outcome parameters were compared between survivors and nonsurvivors, and a multivariate correlation and regression tree analysis was implemented. Results The ejection fraction significantly increased from 27% ± 4% to 38% ± 8% within 24 hours and to 45% ± 10% within 48 hours of starting levosimendan. These changes were accompanied by a significant increase in cardiac output from 5.2 ± 0.6 to 6.2 ± 0.7 L/min within 24 hours and significant dose reductions in vasopressors and inotropes. In contrast to nonsurvivors, survivors’ need for inotropic support decreased after the addition of levosimendan to the therapy. Conclusion In our patients, all of whom were treated according to the same algorithm, the response to levosimendan in terms of the post-levosimendan need for inotropes and vasopressors predicted survival.
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Kasikcioglu, HA, S. Unal, Z. Tartan, H. Uyarel, E. Okmen, E. Kasikcioglu, and N. Cam. "Effects of Levosimendan on Left Ventricular Functional Remodelling and Exercise Intolerance: A Tissue Doppler Study." Journal of International Medical Research 33, no. 4 (July 2005): 397–405. http://dx.doi.org/10.1177/147323000503300405.

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Levosimendan is a calcium sensitizer that demonstrates enhanced myocardial contractility. There is little information concerning the effect of levosimendan on left ventricular tissue parameters and exercise capacity. We evaluated the effects of a 24-h course of levosimendan therapy on cardiac tissue parameters in 30 patients, aged 48-70 years, admitted to our hospital for the management of decompensated heart failure. All patients underwent echocardiographic examination using tissue Doppler imaging (TDI) and a 6-min walk test. Systolic myocardial velocity of the mitral annulus (Sm) was significantly increased in levosimendantreated patients compared with placebotreated patients. There was a positive correlation between Sm and exercise capacity. Levosimendan might be expected to increase cardiac contractile force, especially Sm velocity, in parallel with exercise tolerance. The study has also shown that the progress of ventricular function after levosimendan treatment in patients with exercise intolerance could be monitored effectively by Sm velocity measurements using TDI.
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Cranley, James, Antonia Hardiman, and Leisa J. Freeman. "Pulsed Levosimendan in advanced heart failure due to congenital heart disease: a case series." European Heart Journal - Case Reports 4, no. 3 (May 1, 2020): 1–6. http://dx.doi.org/10.1093/ehjcr/ytaa080.

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Abstract Background Levosimendan is a non-adrenergic calcium-sensitizing agent with positive inotropic and vasodilatory effects. Its use in acute decompensation of heart failure is established. Good evidence now exists for repetitive infusions of Levosimendan to improve symptoms and reduce hospitalization in advanced heart failure (AdHF) populations. Its use in heart failure resulting from congenital heart disease is not yet commonplace. Case summary We present three cases in which pulsed Levosimendan was used in the management of AdHF secondary to underlying congenital heart disease. There was symptomatic and biomarker evidence of improvement. Discussion Intermittent Levosimendan may represent a valuable therapy to reduce hospitalization and improve quality of life in adults with congenital heart conditions.
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Emelyanchik, V. S., Yu Yu Spichak, P. V. Teplov, K. A. Ilinykh, A. Yu Cheremisina, E. A. Ivanitsky, N. A. Mosyakin, et al. "EXPERIENCE OF LEVOSIMENDAN USING IN YOUNG CHILDREN WITH FUNCTIONAL CLASS IV HEART FAILURE." Pediatria. Journal named after G.N. Speransky 100, no. 1 (February 15, 2021): 201–4. http://dx.doi.org/10.24110/0031-403x-2021-100-1-201-204.

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Objective of the research: to study the results of levosimendan use in young children with heart failure (HF) of functional class IV (FC). Materials and methods: the analysis of observation of patients who received levosimendan: 2 with cardiomyopathies (CMP), 12 with congenital heart defects (CHD). The drug was administered intravenously 0,2 μg/kg/min. Results: in patients with CMP, the ejection fraction doubled after administration of levosimendan, in children with CHD heart contractility increased by 18%, and pulmonary artery pressure decreased by 17 mm Hg. There were no undesirable effects. Conclusion: administration of levosimendan provides an increase in cardiac output and a decrease in pulmonary resistance in children with HF IV FC without undesirable effects.
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Rodríguez-González, Raquel, Piero Pollesello, Aurora Baluja, and Julián Álvarez. "Effects of Levosimendan on Inflammation and Oxidative Stress Pathways in a Lipopolysaccharide-Stimulated Human Endothelial Cell Model." Biological Research For Nursing 21, no. 5 (July 4, 2019): 466–72. http://dx.doi.org/10.1177/1099800419861694.

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Levosimendan is a myocardial Ca2+sensitizer and opener of ATP-dependent potassium channels with inotropic, vasodilating, and cardioprotective properties. It was originally developed for the treatment of acute decompensated heart failure, but its complex mechanism of action means that it could also play a role in organ protection in response to infection. Using an in vitro approach, we explored whether levosimendan administration influenced cell responses to lipopolysaccharide (LPS). Primary human umbilical vein endothelial cells were stimulated with 1 µg/ml LPS from Escherichia coli ( E. coli). Cells were treated with levosimendan at 0, 0.1, 1, or 10 µM 3 hr later. Samples were taken 24 hr after treatment to measure cell necrosis, apoptosis, pro-inflammatory mediators (interleukin 6 [IL-6] and toll-like receptor 4 [TLR4]), and oxidative stress (total reactive oxygen species/reactive nitrogen species [ROS/RNS]). Levosimendan at 1 and 10 µM protected against LPS-induced endothelial cell death and reduced TLR4 expression ( p < .05). All doses reduced levels of IL-6 and ROS/RNS ( p < .05). Findings suggest that levosimendan may exert protective effects against endothelial cell death in this model via attenuation of inflammation and oxidative stress pathways. Future studies might explore the potential beneficial role of levosimendan in modulating molecular mechanisms triggered by infections.
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48

Visco, Valeria, Cristina Esposito, Paolo Vitillo, Carmine Vecchione, and Michele Ciccarelli. "It is easy to see, but it is better to foresee: a case report on the favourable alliance between CardioMEMS and levosimendan." European Heart Journal - Case Reports 4, no. 4 (June 30, 2020): 1–5. http://dx.doi.org/10.1093/ehjcr/ytaa205.

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Abstract Background In the past years, different devices have been investigated to help in identifying early decompensation events in patients with heart failure (HF) and reduced ejection fraction (EF), reducing hospital admissions. In this report, we present the first patient experience with levosimendan infusion led by CardioMEMS. Case summary A 68-year-old man with HF and reduced EF with more than 20 hospitalizations for exacerbation of HF was enrolled in our HF Clinic from October 2017. Echocardiogram showed a dilated left ventricle with severely reduced EF (29%) and increased pulmonary artery systolic pressure (40 mmHg). From October 2017 to May 2019, the patient went through numerous hospitalizations, despite optimal medical therapy; subsequently, was adopted a strategy of levosimendan infusions guided by CardioMEMS. Levosimendan infusions improved haemodynamic and pressure profiles. The patient was monitored daily by CardioMEMS, and from June to December 2019, he had only two hospitalizations scheduled for levosimendan infusion and none for HF exacerbation. Discussion Our case supports the combination of CardioMEMS and levosimendan for the optimal management of patients with advanced HF. These results further strengthen the development of a randomized clinical trial to demonstrate the clinical usefulness of this device in combination with the levosimendan infusion programme in advanced HF patients.
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49

Janen, Fayçal, Khaoula El Arayedh, Iheb Labbene, Chihebeddine Romdhani, and Mustapha Ferjani. "Use of levosimendan in cardiogenic shock." F1000Research 3 (December 5, 2014): 296. http://dx.doi.org/10.12688/f1000research.5820.1.

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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/m2 and 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.
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50

Deppe, Antje Christin, Thorsten C. W. Wahlers, Carolyn Weber, Matthias Esser, Kaveh Eghbalzadeh, Anton Sabashnikov, Ilija Djordjevic, et al. "Levosimendan Reduces Mortality and Low Cardiac Output Syndrome in Cardiac Surgery." Thoracic and Cardiovascular Surgeon 68, no. 05 (November 26, 2019): 401–9. http://dx.doi.org/10.1055/s-0039-3400496.

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Abstract Background There has been conflicting evidence concerning the effect of levosimendan on clinical outcomes in patients undergoing cardiac surgery. Therefore, we performed a systematic review and conducted this meta-analysis to provide evidence for/against the administration of levosimendan in cardiac surgery patients. Methods We performed a meta-analysis from literature search in PubMed, EMBASE, and Cochrane Library. Only randomized controlled trials comparing the administration of levosimendan in cardiac surgery patients with a control group (other inotrope, standard therapy/placebo, or an intra-aortic balloon pump) were included. In addition, at least one clinical outcome had to be mentioned: mortality, myocardial infarction, low cardiac output syndrome (LCOS), acute kidney injury, renal replacement therapy, atrial fibrillation, prolonged inotropic support, length of intensive care unit, and hospital stay. The pooled treatment effects (odds ratio [OR], 95% confidence intervals [CI]) were assessed using a fixed or random effects model. Results The literature search retrieved 27 randomized, controlled trials involving a total of 3,198 patients. Levosimendan led to a significant reduction in mortality (OR: 0.67; 95% CI: 0.49–0.91; p = 0.0087). Furthermore, the incidence of LCOS (OR: 0.56, 95% CI: 0.42–0.75; p < 0.0001), acute kidney injury (OR: 0.63; 95% CI: 0.46–0.86; p = 0.0039), and renal replacement therapy (OR: 0.70; 95% CI: 0.50–0.98; p = 0.0332) was significantly decreased in the levosimendan group. Conclusion Our meta-analysis suggests beneficial effects for the prophylactic use of levosimendan in patients with severely impaired left ventricular function undergoing cardiac surgery. The administration of levosimendan was associated with a reduced mortality, less LCOS, and restored adequate organ perfusion reflected in less acute kidney injury.
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