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Investigating potential mediator between statin and coronary artery calcification

Authors
Lee, DonghunJoo, Hyung JoonJung, Ho-WonLim, Do-Sun
Issue Date
18-9월-2018
Publisher
PUBLIC LIBRARY SCIENCE
Keywords
Statin; coronary artery calcification; HDL-cholesterol; causal mediation analysis
Citation
PLOS ONE, v.13, no.9
Indexed
SCIE
SCOPUS
Journal Title
PLOS ONE
Volume
13
Number
9
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/73085
DOI
10.1371/journal.pone.0203702
ISSN
1932-6203
Abstract
Statins are mainstay anti-lipidaemic treatments for preventing cardiovascular diseases but also known to increase coronary artery calcification (CAC). However, underlying relationship between statin and CAC is still unclear. This study explored the mediating role of five statin-related biochemical factors [i.e., low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, triglyceride, glucose, and high sensitivity C-reactive protein levels]. Seoul Metabolic Syndrome cohort study includes 1370 participants suspected of metabolic syndrome. For causal mediation analysis, the dataset for 2016 including 847 participants with coronary computed tomography without any missing value were analysed using the Mediation package in R software. This study identified a causal mediation mechanism of HDL-cholesterol among the five biochemical factors. It implied that statin treatment increases the HDL-cholesterol level, leading to decreasing the probability of CAC score > 0. Estimated values of interest in HDL-cholesterol mediation were (1) average causal mediation effect, -0.011 with 95% CI [-0.025, -0.003], (2) average direct effect, 0.143 with 95% CI [0.074, 0.219], and total effect, 0.132 with 95% CI [0.063, 0.209]. Its mediation effect was maintained regardless of statin intensity. Sensitivity analysis also provided a robustness of the results under potential existence of a confounder between HDL-cholesterol and CAC. This study suggests a potential causal pathway between statin and CAC (the positive association of statin on CAC) through HDL-cholesterol as an inhibitor.
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College of Medicine > Department of Medical Science > 1. Journal Articles
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