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Objective: To study the effect of the angiotensinogen gene M235T polymorphism on coronary artery disease and its severity in patients with and without acute myocardial infarction., Methods: A cross sectional study was carried out with 305 Caucasians who were divided into two groups. One group with 201 patients with coronary artery disease proven by coronary angiography (obstructive lesion > 50%) was further divided into two subgroups; 110 patients with acute myocardial infarction and 91 without it. The control group consisted of 104 individuals with normal coronary arteries. Three angiographic criteria were evaluated to determine severity of the coronary artery disease: number of diseased vessels, morphology of the atherosclerosis plaque and jeopardy score. Risk factors were also analyzed. Gene polymorphism was evaluated by the polymerase chain reaction followed by restriction endonuclease digestion., Results: The angiotensinogen gene TT, MT and MM genotypic frequencies were neither statistically different between coronary artery disease patients and controls (chi-square = 0.123; p = 0.939) nor between the acute myocardial infarction subgroup (chi-square = 2.171; p = 0.338). The coronary artery disease and acute myocardial infarction risk analyzed between TT vs. MM, MT vs. MM and TT+MT vs. MM genotypes were not significant. The severity of atherosclerotic disease analysis within the group of patients with coronary artery disease showed no correlation with the genotypes. Similar results were found between groups with and without acute myocardial infarction., Conclusions: No association was found between the angiotensinogen gene M235T polymorphism and coronary artery disease, neither with its severity nor with acute myocardial infarction.

Objective: To assess the association of the A1166C polymorphism of the angiotensin II type-1 receptor (AT1R) gene with acute myocardial infarction and also with the severity of coronary artery disease., Methods: A prospective, cross-sectional study was carried out with 110 patients with acute myocardial infarction, who, on coronary angiography, had significant lesions (> 50%) assessed according to 3 criteria of severity: number of vessels affected, morphology of the atherosclerotic plaque, and coronary risk score. The control group comprised 104 individuals with no coronary lesions. The A1166C polymorphism of AT1R gene was determined by polymerase chain reaction in the DNA of leukocytes in peripheral blood. The classic coronary risk factors were analyzed in all individuals., Results: When stratifying the genotypes in regard to risk factors, only smoking predominated in the AC heterozygous patients (P = 0.02). The genotypic frequency in the infarcted patients was as follows: AA = 54.5%; AC = 35.5%; and CC = 10%, which was similar and nonsignificant in regard to that in the control group (P = 0.83). No risk increase occurred for acute myocardial infarction when comparing the genotypes as follows: CC vs AA (OR = 1.35; 95% CI = 0.50 - 3.59); AC vs AA (OR = 1.03; 95% CI = 0.58 - 1.84); and AA+AC vs AA (OR = 1.33; 95% CI = 0.51 - 3.45). None of the severity criteria showed a significant correlation with the genotypes., Conclusion: According to our results, no correlation exists between the A1166C polymorphism of the angiotensin II type-1 receptor (AT1R) gene and acute myocardial infarction or the severity of coronary artery disease.