title: The influence of Angiotensin converting enzyme and angiotensinogen gene polymorphisms on hypertrophic cardiomyopathy.
abstract: Some studies have reported that angiotensin converting enzyme (ACE) and angiotensinogen (AGT) genes have been associated with hypertrophic cardiomyopathy (HCM). However, there have been inconsonant results among different studies. To clarify the influence of ACE and AGT on HCM, a systemic review and meta-analysis of case-control studies were performed. The following databases were searched to indentify related studies: PubMed database, the Embase database, the Cochrane Central Register of Controlled Trials database, China National Knowledge Information database, and Chinese Scientific and Technological Journal database. Search terms included "hypertrophic cardiomyopathy", "angiotensin converting enzyme" (ACE) or "ACE" and "polymorphism or mutation". For the association of AGT M235T polymorphism and HCM, "angiotensin converting enzyme" or "ACE" was replaced with "angiotensinogen". A total of seventeen studies were included in our review. For the association of ACE I/D polymorphism and HCM, eleven literatures were included in the meta-analysis on association of penetrance and genotype. Similarly, six case-control studies were included in the meta-analysis for AGT M235T. For ACE I/D polymorphism, the comparison of DI/II genotype vs DD genotype was performed in the present meta-analysis. The OR was 0.73 (95% CI: 0.527, 0.998, P = 0.049, power = 94%, alpha = 0.05) after the study which deviated from Hardy-Weinberg Equilibrium was excluded, indicating that the ACE I/D gene polymorphism might be associated with HCM. The AGT M235T polymorphism did not significantly affect the risk of HCM. In addition, ACE I/D gene polymorphism did not significantly influence the interventricular septal thickness in HCM patients. In conclusion, the ACE I/D polymorphism might be associated with the risk of HCM.
authors.affiliation: The Center for Heart Development, Key Laboratory of MOE for Developmental Biology and Protein Chemistry, College of Life Sciences, Hunan Normal University, Changsha, Hunan, P.R. China ; Medical Science Research Center, Guangxi Medical University, Nanning, Guangxi, P.R China.
authors.forename: Rong
authors.initials: R
authors.lastname: Luo
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Li
authors.forename: Yuequn
authors.initials: Y
authors.lastname: Wang
authors.forename: Yongqing
authors.initials: Y
authors.lastname: Li
authors.forename: Yun
authors.initials: Y
authors.lastname: Deng
authors.forename: Yongqi
authors.initials: Y
authors.lastname: Wan
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Jiang
authors.forename: Wei
authors.initials: W
authors.lastname: Hua
authors.forename: Xiushan
authors.initials: X
authors.lastname: Wu
mesh_terms: D000808:Angiotensinogen / Q000235:genetics*; D002312:Cardiomyopathy, Hypertrophic / Q000235:genetics*; D016022:Case-Control Studies; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A