Literature DB >> 30621952

Association of the PHACTR1/EDN1 Genetic Locus With Spontaneous Coronary Artery Dissection.

David Adlam1, Timothy M Olson2, Nicolas Combaret3, Jason C Kovacic4, Siiri E Iismaa5, Abtehale Al-Hussaini6, Megan M O'Byrne7, Sara Bouajila3, Adrien Georges8, Ketan Mishra5, Peter S Braund6, Valentina d'Escamard4, Siying Huang8, Marios Margaritis6, Christopher P Nelson6, Mariza de Andrade7, Daniella Kadian-Dodov4, Catherine A Welch6, Stephani Mazurkiewicz8, Xavier Jeunemaitre9, Claire Mei Yi Wong5, Eleni Giannoulatou5, Michael Sweeting6, David Muller5, Alice Wood6, Lucy McGrath-Cadell10, Diane Fatkin5, Sally L Dunwoodie5, Richard Harvey5, Cameron Holloway5, Jean-Philippe Empana8, Xavier Jouven8, Jeffrey W Olin4, Rajiv Gulati2, Marysia S Tweet2, Sharonne N Hayes2, Nilesh J Samani6, Robert M Graham5, Pascal Motreff3, Nabila Bouatia-Naji11.   

Abstract

BACKGROUND: Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndromes (ACS) afflicting predominantly younger to middle-aged women. Observational studies have reported a high prevalence of extracoronary vascular anomalies, especially fibromuscular dysplasia (FMD) and a low prevalence of coincidental cases of atherosclerosis. PHACTR1/EDN1 is a genetic risk locus for several vascular diseases, including FMD and coronary artery disease, with the putative causal noncoding variant at the rs9349379 locus acting as a potential enhancer for the endothelin-1 (EDN1) gene.
OBJECTIVES: This study sought to test the association between the rs9349379 genotype and SCAD.
METHODS: Results from case control studies from France, United Kingdom, United States, and Australia were analyzed to test the association with SCAD risk, including age at first event, pregnancy-associated SCAD (P-SCAD), and recurrent SCAD.
RESULTS: The previously reported risk allele for FMD (rs9349379-A) was associated with a higher risk of SCAD in all studies. In a meta-analysis of 1,055 SCAD patients and 7,190 controls, the odds ratio (OR) was 1.67 (95% confidence interval [CI]: 1.50 to 1.86) per copy of rs9349379-A. In a subset of 491 SCAD patients, the OR estimate was found to be higher for the association with SCAD in patients without FMD (OR: 1.89; 95% CI: 1.53 to 2.33) than in SCAD cases with FMD (OR: 1.60; 95% CI: 1.28 to 1.99). There was no effect of genotype on age at first event, P-SCAD, or recurrence.
CONCLUSIONS: The first genetic risk factor for SCAD was identified in the largest study conducted to date for this condition. This genetic link may contribute to the clinical overlap between SCAD and FMD.
Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  cardiovascular disease in women; fibromuscular dysplasia; genetic association; myocardial infarction

Mesh:

Substances:

Year:  2019        PMID: 30621952     DOI: 10.1016/j.jacc.2018.09.085

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  32 in total

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7.  A Study of Associations Between rs9349379 (PHACTR1), rs2891168 (CDKN2B-AS), rs11838776 (COL4A2) and rs4880 (SOD2) Polymorphic Variants and Coronary Artery Disease in Iranian Population.

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Review 8.  Spontaneous Coronary Artery Dissection and Fibromuscular Dysplasia: Vasculopathies With a Predilection for Women.

Authors:  Siiri E Iismaa; Stephanie Hesselson; Lucy McGrath-Cadell; David W Muller; Diane Fatkin; Eleni Giannoulatou; Jason Kovacic; Robert M Graham
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