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A polymorphism of angiotensinogen gene codon 174 and coronary artery disease in Japanese subjects

N D Cong1, K Hamaguchi, T Saikawa

  • 1Department of Internal Medicine I, School of Medicine, Oita Medical University, Hasama, Japan.

The American Journal of the Medical Sciences
|November 20, 1998
PubMed

Insights

The angiotensinogen (AGT) T/T genotype at codon 174 may increase coronary artery disease (CAD) risk in Japanese individuals with low BMI, fewer risk factors, or the ACE I/I genotype.

Area of Science:

  • Genetics
  • Cardiology
  • Molecular Biology

Background:

  • Coronary artery disease (CAD) is a significant health concern.
  • Genetic polymorphisms in the renin-angiotensin system, including angiotensinogen (AGT) and angiotensin converting enzyme (ACE), are implicated in cardiovascular disease.
  • Understanding these genetic associations can aid in risk stratification.

Purpose of the Study:

  • To investigate the association between AGT and ACE gene polymorphisms and the prevalence of CAD in a Japanese population.
  • To identify specific genotypes that may confer increased risk for CAD.

Main Methods:

  • A case-control study involving 104 CAD patients and 170 healthy Japanese subjects.
  • Coronary angiography was used to define CAD (luminal diameter stenosis >=50%).
  • Polymerase chain reaction was employed to determine genotypes for AGT (codon 174 and 235) and ACE (I/D polymorphism).

Main Results:

  • AGT codon 174 T/T genotype was significantly more frequent in CAD patients within subgroups characterized by low body mass index (BMI), fewer than three CAD risk factors, or the ACE I/I genotype.
  • AGT codon 235 M/M genotype showed a negative association with CAD.
  • ACE D/D genotype was positively associated with CAD in the overall population.

Conclusions:

  • The AGT codon 174 T/T genotype may represent a specific risk factor for CAD in Japanese individuals with specific genetic and clinical profiles (low BMI, low risk factor burden, or ACE I/I genotype).
  • These findings contribute to understanding the genetic determinants of CAD in diverse populations.

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