The CC genotype of the angiotensin II type I receptor gene independently associates with acute myocardial infarction in a Tunisian population

Author:

Mehri Sounira12,Mahjoub Sinda2,Finsterer Josef3,Zaroui Amira4,Mechmeche Rachid4,Baudin Bruno5,Hammami Mohamed1

Affiliation:

1. Laboratoire de Biochimie, UR Human Nutrition and Metabolic Disorders, Faculté de Médecine de Monastir, Tunisie.

2. Unité de Recherche, Epidémiologie Génétique et Moléculaire, Faculté de Médecine de Tunis, Tunisie.

3. Krankenanstalt Rudolfstiftung Vienne et Université de Danube Krems, Autriche.

4. Service des Explorations Fonctionnelles Cardiologiques, Hôpital La Rabta de Tunis, Tunisie.

5. Service de Biochimie A, Hôpital Saint-Antoine, Paris, France.

Abstract

Acute myocardial infarction (AMI) is a multifactorial disease influenced by environmental and genetic factors. The aim of this study was to assess the association of angiotensin II type 1 receptor (ATR1) gene polymorphisms with AMI as well as to evaluate the role of serum angiotensin-converting enzyme (ACE) activity and that of cardiac troponin I (cTnI) in Tunisian AMI patients. One hundred and eighteen AMI patients were compared to 150 healthy controls. ATR1 genotypes were determined by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The ATR1 A1166C polymorphism was significantly associated with AMI ( p = 0.024). CC genotype and C allele frequencies were associated with increased AMI risk [CC vs. AC and AA: OR = 2.06; p = 0.045; 95 % CI (1.02–4.18); C vs. A: OR = 1.68; p = 0.004; 95 % CI (1.17–2.41)]. By multivariate logistic regression analysis, CC genotype, hypertension, diabetes, serum ACE activity and peak-cTnI were significant independent predictors of AMI. Increased serum ACE activity and cTnI peak levels were associated with the CC genotype in AMI patients. In conclusion, the ATR1 A1166C polymorphism is associated with AMI and the CC genotype associated with increased ACE activity and cTnI levels appear to predispose for AMI risk.

Publisher

Hindawi Limited

Subject

Endocrinology,Internal Medicine

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