Trial reportHeart and vessels2017
Soluble TNF-related apoptosis induced ligand (sTRAIL) is augmented by Post-Conditioning and correlates to infarct size and left ventricle dysfunction in STEMI patients: a substudy from a randomized clinical trial.
Trial report in Heart and vessels, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- The Dual Role of the TRAIL-DR5 Signaling Axis in Cardiovascular Disease: From Molecular Mechanisms to Targeted Therapies.Biologics : targets & therapy · 2025Review
- Effect of butylphthalide injection combined with gastrodin to improve sTRAIL and inflammatory factors in elderly patients with cerebral infarction.American journal of translational research · 2023Article
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- TRAIL and Cardiovascular Disease-A Risk Factor or Risk Marker: A Systematic Review.Journal of clinical medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low levels of Soluble TNF-related apoptosis induced ligand (sTRAIL) seem to be related to worse prognosis after an acute coronary syndrome. PostConditioning (PostCond) may protect the heart from reperfusion injury. We sought to evaluate the impact of PostCond on sTRAIL in relationship to infarct size (area under the curve of Troponin T, AUCTnT) and left ventricle ejection fraction (LVEF) in a series of patients undergoing primary coronary intervention for ST-segment elevation myocardial infarction (STEMI). In a substudy of a randomized trial that tested the effects of PostCond in STEMI-patients, sTRAIL was measured 24 h after reperfusion (PostCond n = 39, Control n = 39). Correlations between sTRAIL and both AUCTnT and LVEF were studied for each study arm. At 24 h, sTRAIL was higher for PostCond vs Controls (46.4 ± 30.6 vs 32.9 ± 23.4, p = 0.031), was negatively related to AUCTnT [B = -0.09, 95 % CI (-0.15 to -0.30), p = 0.005] and was positively related to both in-hospital [B = 0.10, 95 % CI (0.02-0.17), p = 0.018], and follow-up LVEF [B = 0.21, 95 % (0.10-0.32), p = 0.001]. No significant relationship was found for Controls. On multivariate analysis, PostCond was an independent predictor for sTRAIL [B = 12.13 95 % CI (0.40-23.87), p = 0.043]. In conclusion, PostCond positively influenced sTRAIL, which was related to reduced infarct size and better LVEF. Further studies are needed to understand potential mechanisms elicited by PostCond in infarct size reduction.
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