angiotensinogen and Coronary-Stenosis

Previous studies have reported controversial results regarding the risk of restenosis with polymorphisms of endothelial nitric oxide synthase (eNOS), matrix metalloproteinase 3 (MMP-3), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT1R) after percutaneous coronary intervention (PCI). This study aimed to summarize the association between these polymorphisms and risk of restenosis after PCI.. We searched the electronic databases of PubMed, Embase, Cochrane's Library, and ClinicalTrials.gov for studies on the association of eNOS, MMP-3, AGT, and AT1R polymorphisms with restenosis.. A total of 17 studies (7781 patients) were analyzed, including 5 studies on eNOS G298A (n = 912), 5 studies on MMP3 5A/6A (n = 4519), 6 studies on AGT M235T (n = 1801), and 7 studies on AT1R A1166C (n = 2477). For the G298A variant of the eNOS gene, the allele odds ratio (OR) was 1.685 (95% CI, 1.269-2.338; P < 0.001), the heterozygote OR was 2.144 (95% CI, 1.490-3.085; P < 0.001), the dominant OR was 2.078 (95% CI, 1.462-2.954; P < 0.001), and the overdominant OR was 0.496 (95% CI, 0.348-0.706; P < 0.001). For the 5A/6A variant of the MMP3 gene, the heterozygote OR was 0.839 (95% CI, 0.722-0.975; P = 0.022), the dominant OR was 0.846 (95% CI, 0.733-0.976; P = 0.022), and the overdominant OR was 1.141 (95% CI, 1.001-1.301; P = 0.049). For the M235T variant of the AGT gene, the heterozygote OR was 1.594 (95% CI, 1.179-2.155; P = 0.002), the dominant OR was 1.437 (95% CI, 1.077-1.918; P = 0.014), and the overdominant OR was 0.694 (95% CI, 0.555-0.869; P = 0.001). Positive results were observed in the AT1R gene A1166C polymorphism under 3 models (homozygote OR = 2.009; 95% CI, 1.433-2.816; P < 0.001; recessive OR 1.874; 95% CI, 1.353-2.595; P < 0.001; and dominant OR = 1.350; 95% CI, 1.105-1.649; P = 0.003).. The G298A variant of eNOS, the 5A/6A variant of MMP3, the M235T variant of AGT, and the A1166C variant of A1TR may increase the risk of restenosis after PCI.

Topics: Angiotensinogen; Coronary Stenosis; Genetic Predisposition to Disease; Humans; Matrix Metalloproteinase 3; Nitric Oxide Synthase Type III; Percutaneous Coronary Intervention; Polymorphism, Single Nucleotide; Postoperative Complications; Receptor, Angiotensin, Type 1; Recurrence

The objective of the study was to explore the role of a genetic variant of angiotensinogen (AGT), M235T, as an independent risk factor for acute myocardial infarction (AMI) and to investigate the possible association with the severity of coronary artery disease (CAD), estimated on the basis of the number of coronary stenoses and critical arterial occlusions.. 123 AMI patients were compared to 144 healthy controls. AGT genotypes were determined by PCR.. A significant association was found between AGT M235T polymorphism and AMI (p = .021). By logistic regression, the TT genotype appeared to confer 1.9-fold increased risk for AMI in both the univariate and the multivariate model. The frequencies of the TT genotype and T allele increased with the number of stenoses in coronary vessels. Moreover, the TT genotype and the T allele were more frequent in the subgroup of patients with stenoses in at least four coronary vessels than in other patients, including subjects with one- to three-vessel disease. Furthermore, the TT genotype and the T allele were significantly more frequent in patients with critical arterial occlusions (> 90%) than in subjects without critical stenoses.. The AGT M235T polymorphism associates with AMI risk and influences CAD severity.

Topics: Alleles; Angiotensinogen; Coronary Occlusion; Coronary Stenosis; Female; Gene Frequency; Genetic Predisposition to Disease; Humans; Male; Middle Aged; Myocardial Infarction; Polymorphism, Single Nucleotide

The present study was designed to prospectively test the hypothesis that gene polymorphisms of the renin-angiotensin system are associated with recurrent restenosis after repeated percutaneous transluminal coronary angioplasty. Five hundred and eleven patients after first successful angioplasty were characterized with respect to the angiotensinogen M235T, angiotensin-converting enzyme insertion/deletion and angiotensin II type 1 receptor A1166C gene polymorphisms. In 164 of these patients repeated angioplasty on a restenotic lesion was performed. After repeated angioplasty, 46 patients had recurrent restenosis as defined by a greater than 50% progression of residual stenosis. In the recurrent restenosis group there was a statistically significant higher percentage of patients receiving cholesterol-lowering drugs compared with the group of patients without recurrent restenosis. The two groups of patients did not differ with respect to procedural and angiographic parameters. There were significantly more carriers of the angiotensinogen 235T allele in the recurrent restenosis group than in the control group without recurrent restenosis. No differences between the two groups were found with respect to the other gene polymorphisms investigated. According to the results of a multifactorial analysis of variance, only the 235T allele of the angiotensinogen gene and not cholesterol drug therapy independently affected the increase of stenosis at follow-up angiography. In conclusion, the angiotensinogen 235T allele may be an independent predictor for recurrent restenosis after repeated angioplasty.

Topics: Adult; Aged; Angioplasty, Balloon, Coronary; Angiotensinogen; Coronary Angiography; Coronary Stenosis; Female; Follow-Up Studies; Genetic Predisposition to Disease; Genotype; Humans; Male; Middle Aged; Polymorphism, Genetic; Prospective Studies; Recurrence; Renin-Angiotensin System; Risk Factors