ArticleCurrent therapeutic research, clinical and experimental2015
Oral Levosimendan Increases Cerebral Blood Flow Velocities in Patients with a History of Stroke or Transient Ischemic Attack: A Pilot Safety Study.
Article in Current therapeutic research, clinical and experimental, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00698763 (Effects of Oral Levosimendan on Ambulatory Electrocardiographic Variables and Cerebrovascular Reactivity in Patients With Recent Stroke or TIA.), which is not on this map. Cited by 7 papers.
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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.
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.
Effects of Oral Levosimendan on Ambulatory Electrocardiographic Variables and Cerebrovascular Reactivity in Patients With Recent Stroke or TIA.
Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Multimodal Monitoring in Eclamptic Intracerebral Hemorrhage Complicated by Reversible Cerebral Vasoconstriction Syndrome (RCVS): A Case Report.Case reports in critical care · 2026Article
- Potentiating Cerebral Perfusion Normalizes Glymphatic Dynamics in Systemic Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Levosimendan inhibits disulfide tau oligomerization and ameliorates tau pathology in TauExperimental & molecular medicine · 2023Article
- Levosimendan in intensive care and emergency medicine: literature update and expert recommendations for optimal efficacy and safety.Journal of anesthesia, analgesia and critical care · 2022Review
- Atrial Cardiomyopathy: An Unexplored Limb of Virchow's Triad for AF Stroke Prophylaxis.Frontiers in cardiovascular medicine · 2020Review
- Use of levosimendan in the treatment of cerebral vascular vasospasm: a case study.Drug design, development and therapy · 2018Article
- Application of 3.0T magnetic resonance arterial spin labeling (ASL) technology in mild and moderate intracranial atherosclerotic stenosis.Experimental and therapeutic medicine · 2016Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntravenous levosimendan is indicated for acute heart failure. The compound has shown promising beneficial effects in ischemic stroke models.
objectiveWe evaluated the efficacy and safety of oral levosimendan in patients with a history of cerebral ischemia.
methodsIn a randomized, double-blind, placebo-controlled, parallel-group study, 16 patients with a history of ischemic stroke/transient ischemic attack received oral levosimendan in 5 escalating doses from 0.125 to 2.0 mg daily for 18-day intervals of each dose; 5 patients received placebo. Twenty-four-hour ambulatory ECG and cerebral blood flow velocities using transcranial Doppler ultrasound were recorded at baseline and at the end of each dosing period. Vasomotor reactivity was assessed via the breath holding index. In addition, plasma levels of N-terminal-pro-B-type natriuretic peptide (NT-pro-BNP) and the metabolites of levosimendan were determined.
resultsLevosimendan induced an increase in cerebral blood flow velocities and a decrease in NT-pro-BNP compared with placebo. There was no significant effect on breath holding index. Doses ≥0.5 mg increased heart rate by 5 to 9 beats/min. The dose level of 2.0 mg exceeded the preset safety margin of ventricular extrasystoles per hour (ie, upper 90% CI of the ratio of levosimendan to placebo above 2) with an estimate of 3.10 (90% CI, 0.95-10.07).
conclusionsOral levosimendan increases cerebral blood flow velocities and diminishes NT-pro-BNP levels in patients with earlier ischemic cerebrovascular event. Daily doses up to 1.0 mg were well tolerated, whereas the 2.0 mg dose level induced an increase in ventricular extrasystoles. ClinicalTrials.gov identifier: NCT00698763.
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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.