Trial reportClinical drug investigation2014
Anti-oxidative stress effect of loading-dose rosuvastatin prior to percutaneous coronary intervention in patients with acute coronary syndrome: a prospective randomized controlled clinical trial.
Trial report in Clinical drug investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.
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
6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 11 citations in OpenAlex.
- Effect of Statins on Superoxide Dismutase Level: A Systematic Review.Current medicinal chemistry · 2025Pooled it
- Efficacy of high-dose rosuvastatin preloading in patients undergoing percutaneous coronary intervention: a meta-analysis of fourteen randomized controlled trials.Lipids in health and disease · 2015Pooled it
- Article
- Effects of Catheterization on Artery Function and Health: When Should Patients Start Exercising Following Their Coronary Intervention?Sports medicine (Auckland, N.Z.) · 2019Review
- Reply to "Generic Statins and Angiotensin Receptor Blockers: Are They Really Useful in Ebola?".mBio · 2016Article
- Prognosis of patients with coronary artery disease treated in different therapy units at department of cardiology: a retrospective cohort study.International journal of clinical and experimental medicine · 2015Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesAdministration of a loading dose of a statin (HMG-CoA reductase inhibitor) prior to percutaneous coronary intervention (PCI) contributes to protection from myocardial ischemic-reperfusion injury. This trial was designed to investigate the effect and mechanism of loading-dose rosuvastatin therapy before PCI in patients with acute coronary syndrome.
methodsOne hundred and forty-three patients with acute coronary syndrome were randomized to either the loading-dose (rosuvastatin 40 mg given 4 h before PCI) or conventional-dose (rosuvastatin 10 mg given 4 h before PCI) group. Blood samples were collected before and 0, 24, and 72 h post-PCI for measurement of serum cardiac troponin-I (cTn I), creatine kinase-MB (CK-MB), superoxide dismutase (SOD), reactive oxygen species (ROS), and malondialdehyde (MDA). Echocardiography and the major adverse cardiac/cerebrovascular events (MACCE) rate were followed up for 6 months post-PCI.
resultsBlood serum CK-MB and cTn I were significantly lower in the loading-dose group than in the conventional-dose group at 24 and 72 h post-PCI [CK-MB: 26.90 ± 3.22 vs. 32.96 ± 2.65 IU/L, P = 0.024; 10.79 ± 4.65 vs. 15.18 ± 5.39 IU/L, P = 0.021. cTn I: 0.046 ± 0.007 vs. 0.055 ± 0.002 ng/mL, P = 0.015; 0.027 ± 0.006 vs. 0.041 ± 0.006 ng/mL, P = 0.026]. Echocardiography at 6 months after PCI revealed significant improvement in cardiac function in the loading-dose group compared with the conventional-dose group (P < 0.05). The MACCE rate at 6 months after PCI in the loading-dose group was lower than in the conventional-dose group (P = 0.0428). The levels of MDA and ROS were decreased and the SOD level was significantly higher in the loading-dose group than in the conventional-dose group at 0, 24, and 72 h post-PCI (P < 0.05).
conclusionAdministration of loading-dose rosuvastatin in patients with acute coronary syndrome prior to PCI exerts myocardial protection by inhibition of oxidative stress.
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