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Completed

NCT Number: NCT04917497

Levosimendan Infusion in Critically Ill Patients With Cardiogenic Shock

To determine whether Levosimendan infusion in patients with cardiogenic shock and cardiorenal syndrome refractory to standard inotropic therapy, improves hemodynamics and renal function, whilst being safe.

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Key information

Conditions

Cardiogenic Shock Acute Kidney Failure Acute Kidney Injury Cardio-Renal Syndrome Cardiorenal Syndrome Cardiovascular Diseases Female Urogenital Diseases Female Urogenital Diseases and Pregnancy Complications Heart Diseases Heart Failure Infarction Ischemia Kidney Diseases Male Urogenital Diseases Myocardial Infarction Myocardial Ischemia Necrosis Pathologic Processes Pathological Conditions, Signs and Symptoms Renal Insufficiency Shock Shock, Cardiogenic Urogenital Diseases Urologic Diseases Vascular Diseases

Age range

18 year and older

Sex eligibility

All sexes

Study type

Observational

About this study

Cardiogenic Shock or the state of systemic hypoxia albeit initially preserved intra-vascular volume and intact vascular function, is solely the result of insufficient cardiac output [1-2]. The ensuing centralization and redistribution of blood-volume, is induced by a stimulation of the renin-angiotensin system, as well as vasopressin and endogenous catecholamine liberation [2-3]. Precipitating Cardiogenic Shock has a direct effect on the kidney, also called the cardiorenal syndrome [4].

The overall consensus for the therapy of cardiogenic shock is the use of inotropes to increase cardiac output and reverse organ hypoxia [2], nevertheless their increase of myocardial and glomerular oxygen consumption make them a double edged sword to use in cardiogenic shock and more prominently in cardiogenic shock coupled with pronounced cardiorenal syndrome.

Levosimendan is an inotropic agent that was developed for the treatment of severely decompensated heart failure. It exerts its inotropic effects primarily through sensitizing Troponin C to calcium and thereby increasing contraction of cardiac myofilaments during systole [5]. Unlike other inotropic agents, Levosimendan acts independently of the beta adrenergic receptor [5]. Additionally, the effect of Levosimendan could be beneficial for the kidneys function by decreasing pre-glomerular arteriolar vasotonus whilst keeping post-glomerular arteriolar vasotonus constant [6].

In light of the scarce but promising literature the question arises if Levosimendan can safely ameliorate cardiac and renal function concomitantly in patients presenting the combination of cardiogenic shock and cardiorenal syndrome.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Levosimendan
  • Cardiogenic Shock
  • Continuous monitoring of cardiac output at the start of and during treatment with Levosimendan

Exclusion criteria

  • Extracorporal hemodynamic support or an implanted ventricular assist device
  • Previous therapy with Levosimendan during the index hospitalization
  • Refusal of participation in the study

Treatment and study plan

Levosimendan

Drug

Levosimendan was administered according to a standardized treatment protocol. A total dose of 12.5mg or 25mg (corresponding to one or two ampoules) was given at an infusion rate of 0.05 μg/kg/min to 0.2μg/kg/min with or without a loading dose (6 μg/kg or 3 μg/kg over 10 minutes). The decision about total dose, infusion rate and loading dose was at the discretion of the treating physician.

Primary outcomes

  1. Change in Cardiac Index

    Time frame: Mixed Model Assessment at 0, 1, 2, 4, 6, 12, 24, 48, 72, 96 and 120 hours post Levosimendan Infusion

    Temporal development of Cardiac Index post Levosimendan Infusion up until 120 hours

  2. Change in Cardiac Preload Pressures

    Time frame: Mixed Model Assessment at 0, 1, 2, 4, 6, 12, 24, 48, 72, 96 and 120 hours post Levosimendan Infusion

    Temporal development of Wedge Pressure/ Central Venous Pressure post Levosimendan Infusion up until 120 hours

  3. Change in Mean Arterial Pressure

    Time frame: Mixed Model Assessment at 0, 1, 2, 4, 6, 12, 24, 48, 72, 96 and 120 hours post Levosimendan Infusion

    Temporal development of Mean Arterial Pressure post Levosimendan Infusion up until 120 hours

  4. Change in Vasoactive/ Inotropic Dosage

    Time frame: Mixed Model Assessment at 0, 1, 2, 4, 6, 12, 24, 48, 72, 96 and 120 hours post Levosimendan Infusion

    Temporal development of Norepinephrine/ Dobuatmine Dosage post Levosimendan Infusion up until 120 hours

  5. Change in Renal Function

    Time frame: Mixed Model Assessment at 0, 1, 2, 4, 6, 12, 24, 48, 72, 96 and 120 hours post Levosimendan Infusion

    Temporal development of eGFR (Creatinin estimated) post Levosimendan Infusion up until 120 hours

  6. Change in Fluid Balance

    Time frame: Mixed Model Assessment at 0, 1, 2, 4, 6, 12, 24, 48, 72, 96 and 120 hours post Levosimendan Infusion

    Temporal development of Fluid Balance post Levosimendan Infusion up until 120 hours

Sponsors and collaborators

Lead sponsor

University of Zurich

Other

Registry information

Important dates

Study start
2011
Primary completion
2014
Study completion
2014
First posted
Jun 8, 2021
Registry last updated
Jun 8, 2021

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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