Detailed Information on Publication Record
2006
Atrial Natriuretic Peptide: IS ANP associated with restenosis after Coronary Artery Disease?
SWAMY, Ganesha, Julie BIENERTOVÁ VAŠKŮ, Petr BIENERT, Ota HLINOMAZ, Anna VAŠKŮ et. al.Basic information
Original name
Atrial Natriuretic Peptide: IS ANP associated with restenosis after Coronary Artery Disease?
Name in Czech
Je variabilita v genu pro atriální natriuretický peptid asociována s výskytem restenózy po PCI?
Authors
SWAMY, Ganesha (826 United Kingdom of Great Britain and Northern Ireland), Julie BIENERTOVÁ VAŠKŮ (203 Czech Republic, guarantor), Petr BIENERT (203 Czech Republic), Ota HLINOMAZ (203 Czech Republic) and Anna VAŠKŮ (203 Czech Republic)
Edition
Hungary, New Frontiers in Basic Cardiovascular Research, p. 82-82, 1 pp. 2006
Publisher
INSERM, France
Other information
Language
English
Type of outcome
Stať ve sborníku
Field of Study
Genetics and molecular biology
Country of publisher
Czech Republic
Confidentiality degree
není předmětem státního či obchodního tajemství
RIV identification code
RIV/00216224:14110/06:00017441
Organization unit
Faculty of Medicine
Keywords in English
Atrial natriuretic peptide; restenosis; PCI
Změněno: 2/11/2006 15:10, prof. MUDr. Julie Dobrovolná, Ph.D.
V originále
Background: ANP has shown over recent studies to play an increasingly pivotal role in the regulation of coronary blood flow and atherosclerosis. The gene polymorphism of interest, transition T2238C (ScaI) in the ANP precursor gene, leads to the abolishment of the regular stop codon and instead translation of an additional two arginines. The purpose of the study is to identify the possible influence of ANP ScaI polymorphism on restenotic phenotypes in coronary artery disease (CAD) patients. Method: This study was performed on 96 consecutive caucasians (24 women and 72 men) with clinically significant coronary artery disease confirmed by means of quantitave coronary angiography with minimum one coronary artery with more than 50% lumen stenosis, and all with bare metal stenting in coronary arteries < 3mm. Results: No differences were found in relation to patients with or without restenosis and the genotype distributions as well as allelic frequencies of examined ANP ScaI polymorphism (p = 0.28). However, there is a borderline significant association of ANP genotype distribution with CAD risk factors, such as hypertension and hyperlipidemia (p = 0.05). According to our findings, the allelic frequencies of the ANP ScaI polymorphism in the Czech CAD population do statistically significantly differ from those described in Polish CAD patients (p = 0.01). Conclusion: The ANP ScaI gene polymorphism, based on our data, is not a genetic marker for restenosis after stenting in CAD patients, but the study does suggest that ANP genotypes, specifically A2A2 variants, may be conducive to hypertension. This may be explained by impaired natriuresis in the kidney, perhaps due to reduced affinity or impaired binding of ANP to its receptor, thus leading to sodium retention and increased extracellular volume. Continued research into ANP and its pathophysiological role we believe is imperative to further elucidate how ANP is associated to hypertension.
In Czech
Polymorfismus ScaI v genu pro atriální natriuretický peptid se nezdá být velkým faktorem pro rozvoj restenózy po PCI.
Links
MSM 141100002, plan (intention) |
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