Highlights
- •The association of gene variants with ultrasonographic determined atherosclerosis was explored.
- •The PON2 (rs7493) gene variant associates with a worse ultrasonographic profile.
- •The Cys311Cys homozygosity was found to be associated with an increased risk of stroke.
Abstract
Objective
Common variants of the Paraoxonase (PON), 5-Methyl-Tetrahydrofolate-Reductase (MTHFR)
and Angiotensin-II receptor 1 (AT1R) genes have been associated with ischemic stroke
(IS) risk. Moreover, carotid atherosclerosis is a common cause of IS. The aim of this
study is to explore whether variants in these genes associate with the severity of
ultrasonographic determined atherosclerosis assessed in carotid arteries.
Patients and methods
Etiologic subtype of cerebral ischemia was determined according to the TOAST classification.
Genotypes were detected by PCR and restriction analysis. An ultrasonographic supra-aortic
trunks study was performed to all patients to assess their atherosclerotic involvement
based on predefined criteria.
Results
In IS patients, none of the analyzed gene distributions differed concerning the stenosis
degree. Nevertheless, a trend was observed for the rs662 and rs7493 variants of the
PON1 and PON2 genes respectively. When evaluated the results based on different inheritance
models, a significant contribution of rs7493 variant according to a dominant (OR = 2.397, 95% CI (1.001–5.376); p = 0.045) and log-additive inheritance forms (OR = 1.85, 95% CI (1.07–3.2); p = 0.03) was observed. Only rs7493 reached statistical significance (p = 0.013), when genotype distribution was analyzed according to carotid intima-media
thickness (cIMT) and remain significant in multivariate logistic regression analysis
(OR = 2.66, 95% CI (1.1 to 6.4); p = 0.03).
Conclusion
In IS patients of the north area of the Gran Canaria island the PON2 (rs7493) gene
variant associates with a worse ultrasonographic profile. Conversely, the Cys311Cys
homozygosis of the rs7493 variant was also related to a better ultrasonographic profile
in our study.
Keywords
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Article info
Publication history
Published online: May 06, 2017
Accepted:
May 5,
2017
Received in revised form:
May 3,
2017
Received:
February 6,
2017
Identification
Copyright
© 2017 Elsevier B.V. All rights reserved.