CBS 2019
CBSMD教育中心
中 文

急性冠脉综合征

Abstract

Recommended Article

Chronic Kidney Disease and Coronary Artery Disease Comparative Effectiveness of β-Blocker Use Beyond 3 Years After Myocardial Infarction and Long-Term Outcomes Among Elderly Patients Proportion and Morphological Features of Restenosis Lesions With Acute Coronary Syndrome in Different Timings of Target Lesion Revascularization After Sirolimus-Eluting Stent Implantation Short Duration of DAPT Versus De-Escalation After Percutaneous Coronary Intervention for Acute Coronary Syndromes Association of Plaque Location and Vessel Geometry Determined by Coronary Computed Tomographic Angiography With Future Acute Coronary Syndrome–Causing Culprit Lesions Aggressive lipid-lowering therapy after percutaneous coronary intervention – for whom and how? Positive remodelling of coronary arteries on computed tomography coronary angiogram: an observational study
|<<... 29 30 31 32 33 34 35 36 >>|

Original Research2019 Jan 8;73(1):58-66.

JOURNAL：J Am Coll Cardiol. Article Link

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

Adlam D, Olson TM, Bouatia-Naji N et al. Keywords: cardiovascular disease in women; fibromuscular dysplasia; genetic association; myocardial infarction

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.

>CBS CBS 2019

> CBS 2019 REGISTRATION

> CBS 2019 PROGRAM

> CBS 2019 CALL FOR SCIENCE

> CBS 2019 SPOTLIGHTS

 CBSMD

> CBSMD WEBSITE REGISTRATION

> EDUCATION CENTER

> RECOMMANDED PAPER

> TOP 10 RESEARCH PAPER

> PRE-READING

CBS 2019 CBS 2019 FACULTY Education Resource CBSMD Scientific Library
Copyright ⓒ CBS MD Nanjing China. All rights reserved. 京ICP备16025898号-11
联系我们| Top