ArticleJournal of interventional medicine2019
Impact of serum levels of lipoprotein lipase, hepatic lipase, and endothelial lipase on the progression of coronary artery disease.
Article in Journal of interventional medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Relationship of intra-pancreatic fat deposition with low-density lipoprotein subfractions and hepatic lipase.Diabetes, obesity & metabolism · 2025Article
- Effect of PCSK9 Inhibitors on Regulators of Lipoprotein Homeostasis, Inflammation and Coagulation.Biomedicines · 2025Article
- Blocking HJournal of molecular medicine (Berlin, Germany) · 2024Article
- Multivessel Coronary Artery Disease Complicated by Diabetes Mellitus Has a Relatively Small Effect on Endothelial and Lipoprotein Lipases Expression in the Human Atrial Myocardium and Coronary Perivascular Adipose Tissue.International journal of molecular sciences · 2023Article
- LIPG endothelial lipase and breast cancer risk by subtypes.Scientific reports · 2021Observational
- Resveratrol Improves Hepatic Redox Status and Lipid Balance of Neonates with Intrauterine Growth Retardation in a Piglet Model.BioMed research international · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe purpose of this study was to investigate the relationship between serum levels of lipoprotein lipase (LPL), hepatic lipase (HL), and endothelial lipase (EL) and the progression of coronary artery disease (CAD). MATERIALS AND
methodsAccording to the inclusion criteria, exclusion criteria, diagnostic criteria, angiography results, and the random matching scheme, the enrolled patients were divided into the following two groups: the progression-free group (n = 47) and the progression group (n = 15). The baseline characteristics and various biochemical parameters were obtained from the medical records and medical history. Serum LPL, HL, and EL levels were detected by ELISA. The correlation between serum LPL, HL, and EL levels and coronary lesions was statistically analyzed with SPSS software.
resultsSignificant differences were observed in serum levels of HL and EL between the progression-free group and the progression group (HL, 75.5 ± 39.2 ng/mL vs. 125.1 ± 42.1 ng/mL, P < 0.05; EL, 139.2 ± 59.6 pg/mL vs. 175.1 ± 40.1 pg/mL, P < 0.05), while the difference in the LPL level was not significant (P > 0.05). Receiver operating characteristic curve (ROC) analysis showed that the area under the curve (AUC) values of LPL, HL, and EL were 0.506 (95% CI: 0.369-0.642, P = 0.9470), 0.792 (95% CI: 0.664-0.888, P < 0.0001), and 0.693 (95% CI: 0.553-0.811, P = 0.0095), respectively. Additionally, logistic regression analysis showed that the serum level of HL was an independent risk factor for coronary artery lesion progression.
conclusionSerum levels of EL and HL, but not the serum level of LPL, were positively correlated with the progression of CAD. The serum level of HL was an independent risk factor for the progression of CAD, while the
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