The influence of Angiotensin converting enzyme and angiotensinogen gene polymorphisms on hypertrophic cardiomyopathy.

The influence of Angiotensin converting enzyme and angiotensinogen gene polymorphisms on hypertrophic cardiomyopathy.
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血管紧张素转换酶和血管紧张素原基因多态性对肥厚型心肌病的影响

DOI:
10.1371/journal.pone.0077030
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Wu X
Wu X
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Luo R;Li X;Wang Y;Li Y;Deng Y;Wan Y;Jiang Z;Hua W;Wu X

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已有研究报道血管紧张素转换酶(ACE)和血管紧张素原(AGT)基因与肥厚型心肌病(HCM)相关。然而,不同的研究之间存在着不一致的结果。为了阐明血管紧张素转换酶和血管紧张素转换酶对肥厚性心肌病的影响,对病例对照研究进行了系统回顾和荟萃分析。计算机检索PubMed数据库、Embase数据库、Cochrane对照试验数据库、中国国家知识信息数据库和中国科技期刊数据库,以确定相关研究。检索词“肥厚型心肌病”、“血管紧张素转换酶”或“血管紧张素转换酶”和“基因多态或突变”。为了研究血管紧张素转换酶基因M235T多态与肥厚性心肌梗死的关系,将血管紧张素转换酶或血管紧张素转换酶替换为血管紧张素原。共有17项研究纳入我们的综述。对于ACE I/D多态与HCM的关联,11篇文献进入了外显性与基因关联的Meta分析。同样,AGT M235T的荟萃分析包括6项病例对照研究。对于ACE I/D多态,在Meta分析中比较DI/II和DD两种基因型。排除偏离Hardy-Weinberg平衡的OR值为0.73(95%CI:0.527,0.998,P = 0.049,POWER = 94%,α = 0.05),提示ACE I/D基因多态性可能与肥厚性心肌梗死有关。AGT M235T基因多态性对肥厚性心肌梗死的危险性无显著影响。此外,ACE I/D基因多态性对肥厚心肌病患者的室间隔厚度无显著影响。结论:ACE基因I/D多态可能与肥厚性心肌梗死的发病风险相关。
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.
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