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急性冠脉综合征

Abstract

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Improved outcomes in patients with ST-elevation myocardial infarction during the last 20 years are related to implementation of evidence-based treatments: experiences from the SWEDEHEART registry 1995-2014 Association of the PHACTR1/EDN1 Genetic Locus With Spontaneous Coronary Artery Dissection Refractory Angina: From Pathophysiology to New Therapeutic Nonpharmacological Technologies Cardiovascular Mortality After Type 1 and Type 2 Myocardial Infarction in Young Adults Implications of Alternative Definitions of Peri-Procedural Myocardial Infarction After Coronary Revascularization Incidence and prognostic implication of unrecognized myocardial scar characterized by cardiac magnetic resonance in diabetic patients without clinical evidence of myocardial infarction Early Natural History of Spontaneous Coronary Artery Dissection Prognostic value of fibrinogen in patients with coronary artery disease and prediabetes or diabetes following percutaneous coronary intervention: 5-year findings from a large cohort study
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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.

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