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Chromosome 1q21.2 and additional loci influence risk of spontaneous coronary artery dissection and myocardial infarction.
- Source :
- Nature Communications; 9/4/2020, Vol. 11 Issue 1, pN.PAG-N.PAG, 1p
- Publication Year :
- 2020
-
Abstract
- Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic cause of myocardial infarction (MI), typically in young women. We undertook a genome-wide association study of SCAD (N<subscript>cases</subscript> = 270/N<subscript>controls</subscript> = 5,263) and identified and replicated an association of rs12740679 at chromosome 1q21.2 (P<subscript>discovery+replication</subscript> = 2.19 × 10<superscript>−12</superscript>, OR = 1.8) influencing ADAMTSL4 expression. Meta-analysis of discovery and replication samples identified associations with P < 5 × 10<superscript>−8</superscript> at chromosome 6p24.1 in PHACTR1, chromosome 12q13.3 in LRP1, and in females-only, at chromosome 21q22.11 near LINC00310. A polygenic risk score for SCAD was associated with (1) higher risk of SCAD in individuals with fibromuscular dysplasia (P = 0.021, OR = 1.82 [95% CI: 1.09–3.02]) and (2) lower risk of atherosclerotic coronary artery disease and MI in the UK Biobank (P = 1.28 × 10<superscript>−17</superscript>, HR = 0.91 [95% CI :0.89–0.93], for MI) and Million Veteran Program (P = 9.33 × 10<superscript>−36</superscript>, OR = 0.95 [95% CI: 0.94–0.96], for CAD; P = 3.35 × 10<superscript>−6</superscript>, OR = 0.96 [95% CI: 0.95–0.98] for MI). Here we report that SCAD-related MI and atherosclerotic MI exist at opposite ends of a genetic risk spectrum, inciting MI with disparate underlying vascular biology. Spontaneous coronary artery dissection (SCAD) is a cause of myocardial infarction Here, the authors present a genome-wide association study of SCAD, finding an association at 1q21.2 which potentially affects expression of ADAMTSL4. [ABSTRACT FROM AUTHOR]
- Subjects :
- CORONARY arteries
CHROMOSOMES
CORONARY disease
YOUNG women
Subjects
Details
- Language :
- English
- ISSN :
- 20411723
- Volume :
- 11
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Nature Communications
- Publication Type :
- Academic Journal
- Accession number :
- 145492613
- Full Text :
- https://doi.org/10.1038/s41467-020-17558-x