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Cardiovasc Pathol. 2011 May-Jun;20(3):156-61. doi: 10.1016/j.carpath.2010.04.002. Epub 2010 Jun 7.

Association between AT C573T polymorphism and cardiovascular risk factors in myocardial infarction.

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  • 1Unit of Public Health and Environmental Care, Department of Preventive Medicine and Public Health, University of Valencia, Valencia, Spain. maria.m.morales@uv.es

Abstract

BACKGROUND:

Polymorphisms in the AT1 gene have been associated with various parameters related to the pathogenesis of cardiovascular diseases and to myocardial infarction. This study analyzed the relationship between two polymorphisms of the angiotensin II AT-1 receptor gene (AT1_1166 and AT1_573) and the risk of ischemic heart disease by studying their association with several cardiovascular risk factors.

METHODS:

The sample population comprised 356 subjects: 174 patients who had survived myocardial infarction (61.01 ± 8.15 years), and 182 age- and gender-matched controls (mean age of 60.25 ± 9.43). The polymorphisms of the angiotensin II AT1-receptor gene (C573T and A1166C) were studied by polymerase chain reaction and DNA restriction analysis. We compared the patients' genetic polymorphism with their risk of ischemic heart disease.

RESULTS:

The A1166C polymorphism did not show any significant differences between the groups. However, with respect to C573T, genotypes tended to differ significantly between cases and controls in the CC and TT types, remaining significant when the CC and CT+TT were grouped. Through analysis of the fit of various multivariate models, we found that the CC genotype is a risk factor for myocardial infarction. This risk remains significant after being adjusted for gender, age, homeostasis model assessment, and anthropometric variables.

CONCLUSIONS:

There is a relationship between the C573T polymorphism and the pathogenesis of myocardial infarction that seems to be due to its relationship with some risk factors. However, given the multifactorial nature of this pathology, further studies are needed to confirm the evidence that we report herein.

PMID:
20537563
DOI:
10.1016/j.carpath.2010.04.002
[PubMed - indexed for MEDLINE]
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