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Deletion polymorphism at the angiotensin-converting enzyme gene in Turkish patients with coronary artery disease

N Akar1, O Aras, K Omürlü

  • 1Department of Pediatric Molecular Genetics, Ankara University, Turkey. mol-pat@yahoo.com

Scandinavian Journal of Clinical and Laboratory Investigation
|December 1, 1998
PubMed

Insights

The angiotensin-converting enzyme (ACE) gene

Area of Science:

  • Genetics
  • Cardiovascular Medicine
  • Molecular Biology

Background:

  • Coronary artery disease (CAD) is a complex condition influenced by genetic and environmental factors, varying across populations.
  • The angiotensin-converting enzyme (ACE) gene's insertion/deletion (I/D) polymorphism is implicated in cardiovascular diseases.
  • Limited data exists on the ACE I/D polymorphism's role in CAD within the Turkish population.

Purpose of the Study:

  • To investigate the association between the ACE gene I/D polymorphism and coronary artery disease (CAD) in Turkish patients.
  • To determine if the ACE I/D polymorphism is a risk factor for myocardial infarction (MI) and hypertension in this population.

Main Methods:

  • Genotyping of the ACE gene I/D polymorphism using polymerase chain reaction (PCR).
  • Comparison of allele and genotype frequencies between 218 CAD patients and 107 healthy controls.
  • Analysis of specific subgroups including patients with myocardial infarction and hypertension.

Main Results:

  • A significantly higher frequency of the DD genotype and D allele was observed in CAD patients compared to controls (p=0.002).
  • The D allele was significantly more prevalent in patients with myocardial infarction (p=0.03) and hypertension (p=0.01).
  • Inferior myocardial infarction showed a significant association with the D allele (p=0.002), unlike anterior MI.

Conclusions:

  • The D allele of the ACE gene I/D polymorphism is associated with an increased risk of coronary artery disease in the Turkish population.
  • This polymorphism may serve as a genetic marker for myocardial infarction and hypertension in this demographic.
  • Further research is warranted to elucidate the specific mechanisms linking ACE I/D polymorphism to CAD pathogenesis.

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