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Atrial natriuretic peptide gene polymorphism is not associated with hypertrophic cardiomyopathy

Hao Xue1, Hu Wang, Xiao-jian Wang

  • 1Department of Cardiology, Chinese People's Liberation Army General Hospital, and Peking Union Medical College, Beijing 100853, China.

Chinese Medical Journal
|February 9, 2010
PubMed

Insights

Genetic variations in the atrial natriuretic peptide (ANP) gene are not linked to hypertrophic cardiomyopathy (HCM) risk or its varied clinical presentations in patients. These ANP gene polymorphisms do not appear to modify HCM development.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Cardiology
  • Genetic Epidemiology

Background:

  • Hypertrophic cardiomyopathy (HCM) is an inherited heart muscle disease with diverse clinical outcomes, even among individuals with the same mutation.
  • Genetic modifiers may influence HCM's variable phenotypes.
  • Elevated atrial natriuretic peptide (ANP) levels are observed in HCM, and ANP gene promoter polymorphisms have been linked to left ventricular hypertrophy in hypertension.

Purpose of the Study:

  • To investigate the association between two single nucleotide polymorphisms (SNPs) in the ANP gene (-A2843G and A188G) and the risk of developing HCM.
  • To determine if these ANP gene polymorphisms are associated with clinical phenotypes in HCM patients.

Main Methods:

  • Genotyping of -A2843G and A188G polymorphisms in the ANP gene.
  • Comparison of genotype frequencies between 262 HCM patients and 614 healthy controls.
  • Analysis of the association between polymorphisms and clinical phenotypes in HCM patients.

Main Results:

  • No significant difference in genotype frequencies for the -A2843G and A188G polymorphisms was found between HCM patients and controls.
  • The studied ANP gene polymorphisms were not associated with clinical phenotypes within the HCM patient cohort.

Conclusions:

  • Polymorphisms in the ANP gene are not associated with an increased risk of HCM.
  • These ANP gene variations do not appear to act as genetic modifiers for HCM development or its clinical manifestations.
Abstract

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