Mendelian randomization study of the effect of coronary artery calcification on atherosclerotic cardiovascular diseases
1
Issued Date
2022-12-01
Resource Type
eISSN
20452322
Scopus ID
2-s2.0-85137073207
Pubmed ID
36050433
Journal Title
Scientific Reports
Volume
12
Issue
1
Rights Holder(s)
SCOPUS
Bibliographic Citation
Scientific Reports Vol.12 No.1 (2022)
Suggested Citation
Sae-jie W., Tangcharoen T., Vathesatogkit P., Aekplakorn W., Charoen P. Mendelian randomization study of the effect of coronary artery calcification on atherosclerotic cardiovascular diseases. Scientific Reports Vol.12 No.1 (2022). doi:10.1038/s41598-022-19180-x Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/86396
Title
Mendelian randomization study of the effect of coronary artery calcification on atherosclerotic cardiovascular diseases
Author's Affiliation
Other Contributor(s)
Abstract
Calcium calcification in the wall of arteries (CAC) leads to a higher risk of atherosclerosis related outcomes, especially myocardial infarction (MI). Nevertheless, the causal role of CAC on other related outcomes is unclear. In this study, we used Mendelian randomization (MR) to systematically investigate the causal role of CAC across a broad range of atherosclerotic cardiovascular diseases including coronary heart disease, angina, MI, ischemic heart disease, stroke, and peripheral vascular disease. Publicly available data from the UK biobank and other data sources were used. Using the two-sample Mendelian randomization (MR) approach, we applied 3 MR models including the inverse variance weighted, the weighted-median, and the weighted-mode methods. Eight SNPs associated with CAC were selected as instrumental variables. We observed causal evidence of CAC on MI consistently across all MR models (PIVW = 1.0 × 10−4, PW-Median = 1.1 × 10−4, PW-Mode = 3.8 × 10−2) and this causation is shown in an acute transmural MI of inferior wall (PIVW = 1.5 × 10−4, PW-Median = 4.8 × 10−5, PW-Mode = 3.2 × 10−2) but not consistently observed in an anterior wall. As each site of acute MI was suggested to have relatively specific mechanisms, our finding suggested that the causal role of CAC on MI is in an inferior wall possibly as a consequence of large calcification from a prolonged process, whereas non-calcified artery plaque or other underlying mechanisms may predominantly play role in an anterior infarction during an advanced atherosclerotic process.