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Aldosterone synthase -344C/T and angiotensin-converting enzyme I/D polymorphisms in Turkish hypertensive patients

Ayhan Olcay1, Yilmaz Nisanci, C Gokhan Ekmekci

  • 1Istanbul University, Istanbul School of Medicine, Department of Cardiology, 34390 Capa, Istanbul, Turkey. aolcay@excite.com

Acta Cardiologica
|February 21, 2006
PubMed

Insights

Genetic variations in the renin-angiotensin-aldosterone system (RAAS) do not predict left ventricular changes in hypertensive patients. Specific gene polymorphisms, including ACE I/D and CYP11B2 -344C/T, were not associated with left ventricular mass, function, or dilatation.

Area of Science:

  • Cardiovascular Genetics
  • Hypertension Research
  • Molecular Cardiology

Background:

  • The renin-angiotensin-aldosterone system (RAAS) is crucial for blood pressure and cardiovascular structure.
  • Hypertension can lead to varied left ventricular (LV) remodeling and heart failure.
  • Understanding genetic influences on LV response in hypertension is clinically significant.

Purpose of the Study:

  • To investigate the association between major RAAS gene polymorphisms and echocardiographic LV parameters.
  • To determine if CYP11B2 -344C/T and ACE I/D genotypes predict LV mass, function, and dilatation in hypertensive patients with normal coronary arteries.

Main Methods:

  • Echocardiography assessed LV dimensions, mass, and function in 88 hypertensive patients.
  • Genotyping performed for aldosterone synthase (CYP11B2) -344C/T polymorphism (n=85) and ACE I/D polymorphism (n=88).
  • Multiple regression analysis adjusted for clinical covariates evaluated genotype associations with LV indices.

Main Results:

  • No significant association was found between the studied genotypes and LV dilatation.
  • Neither ACE I/D nor CYP11B2 -344C/T polymorphisms predicted LV mass.
  • The investigated RAAS polymorphisms did not correlate with LV function parameters.

Conclusions:

  • ACE I/D and CYP11B2 -344C/T polymorphisms are not predictive of LV mass, function, or dilatation in hypertensive individuals with normal coronary arteries.
  • These specific RAAS genetic variations may not be useful biomarkers for stratifying cardiovascular risk in this patient cohort.
Abstract

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