Vol 69, No 7 (2011)
Original articles
Published online: 2011-07-18
Combined renin–angiotensin system gene polymorphisms and outcomes in coronary artery disease — a preliminary report
DOI: 10.33963/v.kp.79245
Kardiol Pol 2011;69(7):688-695.
Abstract
Background: Common variants of the renin–angiotensin system (RAS) genes have been linked to a higher risk of coronary
artery disease (CAD) and its complications.
Aim: To determine the prognostic significance of a combination of three common polymorphisms of RAS genes (angiotensin converting enzyme — ACE Ins/Del, angiotensin receptor type 1 — AGT1R A1166C and angiotensinogen — ATG M235T) in patients with CAD.
Methods: The study included 216 patients (mean age 58 ± 9 years, 74% male) prospectively followed for a mean 41 ± 17 months. The end-points were all-cause mortality, myocardial infarction, stroke or the need for coronary revascularisation.
Results: An end-point occurred in 41 (19%) patients. None of the polymorphisms analysed separately was associated with the end-point. Odds ratios were calculated for different combinations of analysed alleles to determine their relation to outcomes. Based on the cut-off points of odds ratios, the study group was divided into three subgroups: 55 patients without ATG 235T allele (T– subgroup); 100 patients with ATG 235T allele alone or ATG 235T allele combined with ACE Del allele or AGT1R 1166C allele (T+ or T+1 subgroup); and 61 patients with all three variants (T+2 subgroup). Multivariate analysis showed that the only independent predictor of the endpoint was an increasing number of variant genes (HR = 2.6, 95% CI 1.4–4.9, p = 0.002).
Conclusions: Co-existing angiotensinogen M235T AGT polymorphism and two other common polymorphisms of the RAS genes are related to adverse events in patients with CAD.
Kardiol Pol 2011; 69, 7: 688–695
Aim: To determine the prognostic significance of a combination of three common polymorphisms of RAS genes (angiotensin converting enzyme — ACE Ins/Del, angiotensin receptor type 1 — AGT1R A1166C and angiotensinogen — ATG M235T) in patients with CAD.
Methods: The study included 216 patients (mean age 58 ± 9 years, 74% male) prospectively followed for a mean 41 ± 17 months. The end-points were all-cause mortality, myocardial infarction, stroke or the need for coronary revascularisation.
Results: An end-point occurred in 41 (19%) patients. None of the polymorphisms analysed separately was associated with the end-point. Odds ratios were calculated for different combinations of analysed alleles to determine their relation to outcomes. Based on the cut-off points of odds ratios, the study group was divided into three subgroups: 55 patients without ATG 235T allele (T– subgroup); 100 patients with ATG 235T allele alone or ATG 235T allele combined with ACE Del allele or AGT1R 1166C allele (T+ or T+1 subgroup); and 61 patients with all three variants (T+2 subgroup). Multivariate analysis showed that the only independent predictor of the endpoint was an increasing number of variant genes (HR = 2.6, 95% CI 1.4–4.9, p = 0.002).
Conclusions: Co-existing angiotensinogen M235T AGT polymorphism and two other common polymorphisms of the RAS genes are related to adverse events in patients with CAD.
Kardiol Pol 2011; 69, 7: 688–695
Keywords: coronary artery diseasepolymorphismsrenin–angiotensin systemoutcomes
