Evidence map›Paper›PMID 31428804›Full record

Trial reportIntensive care medicine2019

Levosimendan in septic shock in patients with biochemical evidence of cardiac dysfunction: a subgroup analysis of the LeoPARDS randomised trial.

David B Antcliffe, Shalini Santhakumaran, Robert M L Orme, Josie K Ward, Farah Al-Beidh, Kieran O'Dea, Gavin D Perkins, Mervyn Singer, Daniel F McAuley, Alexina J Mason and 3 more

Open access · greenAbstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Intensive care medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  7. Current standard of care for septic shock.Intensive care medicine · 2026
    Review
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  16. Observational
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 7 institutions in 1 country.

David B AntcliffeSection of Anaesthetics, Pain Medicine and Intensive Care Medicine, Department of Surgery and Cancer, Imperial College London and Imperial College Healthcare NHS Trust, London, UK.
Shalini SanthakumaranImperial Clinical Trials Unit, Imperial College London, London, UK.
Robert M L OrmeDepartment of Critical Care, Cheltenham General Hospital, Cheltenham, UK.
Josie K WardSection of Anaesthetics, Pain Medicine and Intensive Care Medicine, Department of Surgery and Cancer, Imperial College London and Imperial College Healthcare NHS Trust, London, UK.
Farah Al-BeidhSection of Anaesthetics, Pain Medicine and Intensive Care Medicine, Department of Surgery and Cancer, Imperial College London and Imperial College Healthcare NHS Trust, London, UK.
Kieran O'DeaSection of Anaesthetics, Pain Medicine and Intensive Care Medicine, Department of Surgery and Cancer, Imperial College London and Imperial College Healthcare NHS Trust, London, UK.
Gavin D PerkinsWarwick Clinical Trials Unit, Warwick Medical School, University of Warwick, Warwick, UK.
Mervyn SingerBloomsbury Institute of Intensive Care Medicine, University College London, London, UK.
Daniel F McAuleyWellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, UK.
Alexina J MasonDepartment of Health Services Research and Policy, London School of Hygiene and Tropical Medicine, London, UK.
Mary CrossImperial Clinical Trials Unit, Imperial College London, London, UK.
Deborah AshbyImperial Clinical Trials Unit, Imperial College London, London, UK.
Anthony C GordonSection of Anaesthetics, Pain Medicine and Intensive Care Medicine, Department of Surgery and Cancer, Imperial College London and Imperial College Healthcare NHS Trust, London, UK. anthony.gordon@imperial.ac.uk.ORCID 0000-0002-0419-547X
Imperial College Healthcare NHS Trust · GBImperial College London · GBBury College · GBCheltenham General Hospital · GBLondon School of Hygiene & Tropical Medicine · GBQueen's University Belfast · GBUniversity of Warwick · GB

Funding

RESEARCH IN COLLABORATIVE DECISION MAKING IN NURSINGF06TW001408 · FIC · UNIVERSITY OF RHODE ISLAND · PI KIM, HESOOK S · 1988 to 1988
–
Department of Health NIHR/CS/009/007Department of Health RP-2015-06-018Efficacy and Mechanism Evaluation Programme 11-14-08Medical Research Council MC_PC_13093National Institute for Health Research RP-2015-06-018
6 · The paper itself

Abstract

purposeMyocardial dysfunction is common in sepsis but optimal treatment strategies are unclear. The inodilator, levosimendan was suggested as a possible therapy; however, the levosimendan to prevent acute organ dysfunction in Sepsis (LeoPARDS) trial found it to have no benefit in reducing organ dysfunction in septic shock. In this study we evaluated the effects of levosimendan in patients with and without biochemical cardiac dysfunction and examined its non-inotropic effects.

methodsTwo cardiac biomarkers, troponin I (cTnI) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and five inflammatory mediators were measured in plasma from patients recruited to the LeoPARDS trial at baseline and over the first 6 days. Mean total Sequential Organ Failure Assessment (SOFA) score and 28-day mortality were compared between patients with normal and raised cTnI and NT-proBNP values, and between patients above and below median values.

resultsLevosimendan produced no benefit in SOFA score or 28-day mortality in patients with cardiac dysfunction. There was a statistically significant treatment by subgroup interaction (p = 0.04) in patients with NT-proBNP above or below the median value. Those with NT-proBNP values above the median receiving levosimendan had higher SOFA scores than those receiving placebo (mean daily total SOFA score 7.64 (4.41) vs 6.09 (3.88), mean difference 1.55, 95% CI 0.43-2.68). Levosimendan had no effect on the rate of decline of inflammatory biomarkers.

conclusionAdding levosimendan to standard care in septic shock was not associated with less severe organ dysfunction nor lower mortality in patients with biochemical evidence of cardiac dysfunction.

Indexed as

AgedBiomarkersChemokine CCL2Double-Blind MethodFemaleHeart DiseasesHSP90 Heat-Shock ProteinsHumansIntensive Care UnitsInterleukin-10Interleukin-6Interleukin-8MaleMiddle AgedNatriuretic Peptide, BrainOrgan Dysfunction ScoresBiomarkersCCL2 protein, humanChemokine CCL2HSP90 Heat-Shock ProteinsIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6Interleukin-8Natriuretic Peptide, BrainPeptide Fragmentspro-brain natriuretic peptide (1-76)SimendanTRAP1 protein, humanTroponin IcTnIInflammationLevosimendanN-terminal prohormone of brain natriuretic peptideSeptic shockTroponin

Identifiers

PMID31428804
OpenAlexW2968386157

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.