Abstract
Purpose Genome-wide association studies have identified ADAMTS7 as a risk locus for coronary artery disease (CAD) and myocardial infarction (MI). Functional studies suggest ADAMTS7 may promote cellular processes in atherosclerosis. We studied if risk variant carriers exhibit a greater burden of angiographic CAD. Methods We genotyped ADAMTS7 in the Southampton Atherosclerosis Study (SAS, n = 1359), and replicated in the Emory Genebank (Emory GB, n = 2684). Angiographic CAD was phenotyped as presence of >50% stenosis in epicardial vessel and semi-quantitative scores including the Gensini Score (GS), Sullivan Extent Score (SES) and the Duke Severity Index (DSI); and ex-vivo immunohistochemical analysis of human coronary plaques (n = 48). Results We confirmed an association between ADAMTS7 genotype and presence of CAD under an additive genotype model in SAS (p = 0.05) and Emory GB (p = 0.017), but found no associations with MI in the presence of CAD. ADAMTS genotypes were associated with all of the angiographic severity scores in SAS (GS p = 0.017, SES p = 0.045, DSI p = 0.029), and independently replicated in Emory GB (GS p Conclusions The ADAMTS7 risk variant is associated with multiple angiographic measures of CAD burden and plaque remodelling, further supporting the role of this protease in promoting atherosclerosis.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
