ArticleIrish journal of medical science2023
Serum histone deacetylase 4 longitudinal change for estimating major adverse cardiovascular events in acute coronary syndrome patients receiving percutaneous coronary intervention.
Article in Irish journal of medical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Effect of Atorvastatin Combined With Herb-Partitioned Moxibustion on PON-1 in Patients With Atherosclerotic Cerebral Infarction: A Randomized Controlled Trial.Brain and behavior · 2026Trial
- Histone deacetylase 4: A therapeutic target for cardiovascular diseases (Review).International journal of molecular medicine · 2025Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveHistone deacetylase 4 (HDAC4) regulates lipid accumulation, inflammation, endothelial injury, and atherosclerosis to participate in the pathogenesis of cardiovascular diseases. This study aimed to explore the value of serum HDAC4 change before and after percutaneous coronary intervention (PCI) in predicting major adverse cardiovascular events (MACE) risk in acute coronary syndrome (ACS) patients.
methodsHDAC4 from serum was detected by enzyme-linked immunosorbent assay in 340 ACS patients at baseline, day (D)1, D3, and D7 after PCI, and from 30 healthy controls (HCs). MACE was recorded during follow-up.
resultsHDAC4 was decreased in ACS patients versus HCs (P < 0.001). In ACS patients, HDAC4 was negatively related to total cholesterol (P = 0.025), low-density lipoprotein cholesterol (P = 0.007), C-reactive protein (P < 0.001), cardiac troponin I (P < 0.001), and hyperlipidemia history (P = 0.015). Additionally, HDAC4 was lowest in ST-elevation myocardial infarction (STEMI) patients, followed by non-STEMI patients, and highest in unstable angina patients (P = 0.010). After PCI, HDAC4 was decreased from baseline to D1, then increased until D7 (P < 0.001). Furthermore, HDAC4 at baseline (P = 0.002), D1 (P < 0.001), D3 (P < 0.001), and D7 (P < 0.001) were all reduced in patients who experienced MACE versus those who did not. Meanwhile, high HDAC4 at baseline (P = 0.036), D1 (P = 0.010), D3 (P = 0.012), and D7 (P = 0.012) estimated decreased accumulating MACE risk by Kaplan-Meier curve. Multivariate logistic analysis revealed that HDAC4 at D1 was independently linked to lower MACE risk (odds ratio = 0.957, P = 0.039).
conclusionSerum HDAC4 is decreased from baseline to D1, then elevated until D7, and its increased level correlates with lower MACE risk in ACS patients receiving PCI.
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