Associations of angiotensinogen gene mutations with hypertension and myocardial infarction in a gulf population

Philippe M. Frossard, Susan H. Hill, Yassin I. Elshahat, Eniyoma N. Obineche, Awais M. Bokhari, Gilles G. Lestringant, Anne John, Abdishakur M. Abdulle

Research output: Contribution to journalArticlepeer-review


To date, the human angiotensinogen (AGT) gene and some of its variants represent the best examples of genetic influences that are involved in the determination of essential hypertension (EH) and associated cardiovascular diseases (CVDs). To assess the value of genotyping AGT in a genetically homogeneous population, we carried out a retrospective, case-control study of variants M235T and T174M for putative correlations with CVDs among nationals from the United Arab Emirates (Emirati) - an ethnic group characterized by no alcohol intake and no cigarette smoking. We investigated a sample population of 229 Emirati (119 males and 110 females), comprising groups of controls and patients with clinical diagnoses of EH, left ventricular hypertrophy (LVH), ischaemic heart disease (IHD) and myocardial infarction (MI). M235T and T174M alleles were determined via assays based on the polymerase chain reaction. T174M showed no correlation with any of the four clinical entities included in this study. T235 alleles, however, occurred more frequently in the EH group and less frequently in the group of MI survivors. We also found that T235 allele frequencies decreased with age, indicating that in the Emirati population, T235 alleles are associated with a reduced life span and that this effect could occur through independent mechanisms underlying genetic susceptibilities to both EH and MI.

Original languageEnglish (US)
Pages (from-to)285-293
Number of pages9
JournalClinical Genetics
Issue number4
StatePublished - Oct 1998


  • Angiotensinogen
  • Cardiovascular diseases
  • Genetics
  • Hypertension
  • Left ventricular hypertrophy
  • Myocardial infarction
  • Polymerase chain reaction

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)


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