Levosimendan: A promising agent for the treatment of hospitalized patients with decompensated heart failure

Lehtonen, Lasse

doi:10.1007/s11886-000-0074-6

Cited by 14 publications

(8 citation statements)

References 62 publications

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“…Clinical studies suggest long-term survival benefits following short-term drug administration. Therefore, one may expect that Ca 2+ -sensitizers may prove to be beneficial, not only as a short-term, symptomatic treatment for heart failure, but possibly also as long-term therapy aimed at preventing the occurrence and/or worsening of heart failure (16,20,35,63,65,102). In this review we have concentrated on the complex cardiovascular effects of levosimendan that may explain how this drug halts the perpetuation of the vicious cycle of heart failure progression.…”

Section: Congestive Heart Failure and Levosimendanmentioning

confidence: 99%

Pharmacological Mechanisms Contributing to the Clinical Efficacy of Levosimendan

Papp

Csapó

Pollesello

et al. 2005

Cardiovascular Drug Reviews

106

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Acute decompensation of chronic heart failure is a direct life-threatening situation with short-term mortality approaching 30%. A number of maladaptive changes are amplified within the cardiovascular system during the progression of chronic heart failure that makes the decompensation phase difficult to handle. Levosimendan is a new Ca2+-sensitizer for the treatment of acutely decompensated heart failure that has proved to be effective during the decompensation of chronic heart failure and acute myocardial infarction. Levosimendan differs from other cardiotonic agents that are used for acute heart failure in that it utilizes a unique dual mechanism of action: Ca2+-sensitization through binding to troponin C in the myocardium, and the opening of ATP-sensitive K+ channels in vascular smooth muscle. In general, these mechanisms evoke positive inotropy and vasodilation. Clinical studies suggested long-term benefits on mortality following short-term administration. It may, therefore, be inferred that levosimendan has additional effects on the cardiovascular system that are responsible for the prolongation of survival. Results of preclinical and clinical investigations suggest that the combination of levosimendan-induced cardiac and vascular changes has favorable effects on the coronary, pulmonary and peripheral circulations. Redistribution of the circulating blood offers an improved hemodynamic context for the development of a positive inotropic effect through Ca2+-sensitization of the contractile filaments, without a proportionate increase in myocardial oxygen consumption or the development of arrhythmias. Activation of ATP-sensitive K+ channels, both on sarcolemma and mitochondria, may protect against myocardial ischemia, and decreased levels of cytokines may prevent the development of further myocardial remodeling. Collectively, these effects of levosimendan shift the disturbed cardiovascular parameters towards normalization, thereby halting the perpetuation of the vicious cycle of heart failure progression. This may contribute to stabilization of the circulation and improved life expectancy of patients with chronic heart failure.

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Section: Congestive Heart Failure and Levosimendanmentioning

confidence: 99%

Pharmacological Mechanisms Contributing to the Clinical Efficacy of Levosimendan

Papp

Csapó

Pollesello

et al. 2005

Cardiovascular Drug Reviews

106

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“…We therefore report on the safety and feasibility of therapy with levosimendan, a noncatecholaminergic inodilator, whose mechanism of action includes calcium sensitization of contractile proteins, the opening of ATP‐dependent potassium channels and inhibition of phosphodiesterase‐3 in TTC patients with severe LV dysfunction and at least one Mayo Clinic risk marker .…”

Section: Introductionmentioning

confidence: 99%

Safety and Feasibility of Levosimendan Administration in Takotsubo Cardiomyopathy: A Case Series

Santoro

Ieva

Ferraretti

et al. 2013

Cardiovascular Therapeutics

120

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SUMMARYBackground: Levosimendan is a noncatecholamine inotrope that does not increase oxygen consumption, utilized for the treatment for acute heart failure with left ventricular (LV) systolic dysfunction. Its use in takotsubo cardiomyopathy (TTC), a disease that contraindicates the use of catecholamine inotropes, is not well known. Methods: We prospectively analyzed 13 consecutive patients with TTC, low ejection fraction (EF) (<35%), and additional Mayo Clinic risk factors who were treated with i.v. infusion of levosimendan. Clinical course of patients, electrocardiogram presentation, LV function, and adverse events at follow-up were recorded. Results: All patients showed an impaired LV function (LVEF at admission 28 AE 5%), which significantly improved at discharge (51 AE 8%, P < 0.001). Mean hospital stay was 10 AE 4 days. Troponin levels at admission were directly related to length of hospitalization (r = 0.6, P < 0.001). Male gender (relative risk (RR) 1.85, P < 0.05), physical stress (RR 1.90, P < 0.05), ST elevation at ECG (RR 1.87, P < 0.05), and absence of chest pain (RR 2.23, P < 0.01) were found to be the predictors of longer hospital stay. Only 15% of subjects had adverse events during hospital stay; two patients incurred noncardiovascular death at follow-up. Age was the only predictor of adverse event at follow-up (RR 2.13, P < 0.05). Conclusions: The use of levosimendan may be safe and feasible in patients with TTC. Randomized studies are warranted to further confirm these preliminary results.

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“…There is a scarcity of scientific data defining the role of inotropic and other therapy in the treatment of CS. Levosimendan is a novel inotropic drug with vasodilator effects that is used in the treatment of CS 4. In 2003, Sweden was one of the first countries to approve levosimendan (Simdax ® ) for an indication in acute heart failure (AHF).…”

Section: Introductionmentioning

confidence: 99%

Levosimendan neither improves nor worsens mortality in patients with cardiogenic shock due to ST-elevation myocardial infarction

Ömerovic

Råmunddal²,

Albertsson³

et al. 2010

VHRM

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Background:The aim of this study was to evaluate the effect of levosimendan on mortality in cardiogenic shock (CS) after ST elevation myocardial infarction (STEMI).Methods and results:Data were obtained prospectively from the SCAAR (Swedish Coronary Angiography and Angioplasty Register) and the RIKS-HIA (Register of Information and Knowledge about Swedish Heart Intensive Care Admissions) about 94 consecutive patients with CS due to STEMI. Patients were classified into levosimendan-mandatory and levosimendan-contraindicated cohorts. Inotropic support with levosimendan was mandatory in all patients between January 2004 and December 2005 (n = 46). After the SURVIVE and REVIVE II studies were presented, levosimendan was considered contraindicated and was not used in consecutive patients between December 2005 and December 2006 (n = 48). The cohorts were similar with respect to pre-treatment characteristics and concomitant medications. There was no difference in the incidence of new-onset atrial fibrillation, in-hospital cardiac arrest and length of stay at the coronary care unit. There was no difference in adjusted mortality at 30 days and at one year.Conclusion:The use of levosimendan neither improves nor worsens mortality in patients with CS due to STEMI. Well-designed randomized clinical trials are needed to define the role of inotropic therapy in the treatment of CS.

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Levosimendan: A promising agent for the treatment of hospitalized patients with decompensated heart failure

Cited by 14 publications

References 62 publications

Pharmacological Mechanisms Contributing to the Clinical Efficacy of Levosimendan

Pharmacological Mechanisms Contributing to the Clinical Efficacy of Levosimendan

Safety and Feasibility of Levosimendan Administration in Takotsubo Cardiomyopathy: A Case Series

Levosimendan neither improves nor worsens mortality in patients with cardiogenic shock due to ST-elevation myocardial infarction

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