Publication details
Atrial Natriuretic Peptide: IS ANP associated with restenosis after Coronary Artery Disease?
| Authors | |
|---|---|
| Year of publication | 2006 |
| Type | Article in Proceedings |
| Conference | New Frontiers in Basic Cardiovascular Research |
| MU Faculty or unit | |
| Citation | |
| Field | Genetics and molecular biology |
| Keywords | Atrial natriuretic peptide; restenosis; PCI |
| Description | 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. |
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