INTRODUCTION: Candidates for coronary artery bypass grafting (CABG) represent a group of patients with well documented, severe coronary artery disease (CAD). Genetic polymorphisms of renin-angiotensin-aldosterone system (RAAS) components have been associated with CAD. We examined the association of polymorphisms of angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT(1) receptor) with severe CAD in CABG patients. MATERIALS AND METHODS: One hundred and fifty-four CABG patients and 155 non-CAD controls were included in the study. Established PCR methods were used for genotyping of AGT M235T, AGT T174M, AT(1) receptor A1166C, and ACE I/D polymorphisms. Cumulative effect of analysed polymorphisms was assessed by calculation of each individual's RAAS gene score (addition of 0.5 points for each variant allele and then calculating the sum for all four polymorphisms). RESULTS: No association between AGT M235T, AGT T174M, ACE I/D and AT(1) receptor A1166C polymorphisms and CAD was observed. Within CABG patients, the frequency of homozygous AGT 235TT genotype was higher in hypertensive compared to normotensive CABG patients (21.7% vs. 6.3%, p=0.03). RAAS gene score did not differ between CABG patients and non-CAD controls. CONCLUSIONS: There is no association of the analysed RAAS polymorphisms with severe CAD in CABG patients. However, within these patients, an association was found between AGT 235TT genotype and hypertension.
INTRODUCTION: Candidates for coronary artery bypass grafting (CABG) represent a group of patients with well documented, severe coronary artery disease (CAD). Genetic polymorphisms of renin-angiotensin-aldosterone system (RAAS) components have been associated with CAD. We examined the association of polymorphisms of angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT(1) receptor) with severe CAD in CABG patients. MATERIALS AND METHODS: One hundred and fifty-four CABG patients and 155 non-CAD controls were included in the study. Established PCR methods were used for genotyping of AGTM235T, AGTT174M, AT(1) receptor A1166C, and ACE I/D polymorphisms. Cumulative effect of analysed polymorphisms was assessed by calculation of each individual's RAAS gene score (addition of 0.5 points for each variant allele and then calculating the sum for all four polymorphisms). RESULTS: No association between AGTM235T, AGTT174M, ACE I/D and AT(1) receptor A1166C polymorphisms and CAD was observed. Within CABG patients, the frequency of homozygous AGT 235TT genotype was higher in hypertensive compared to normotensive CABG patients (21.7% vs. 6.3%, p=0.03). RAAS gene score did not differ between CABG patients and non-CAD controls. CONCLUSIONS: There is no association of the analysed RAAS polymorphisms with severe CAD in CABG patients. However, within these patients, an association was found between AGT 235TT genotype and hypertension.