摘要
目的探讨血管紧张素转换酶(ACE)和血管紧张素Ⅱ1型受体(AT1R)基因多态性与早发冠心病(CAD)的关系。方法用PCR法检测41例早发CAD和64例迟发CAD患者体细胞ACE基因插入/缺失(I/D)多态性和AT1R-A1166C基因多态性,并与50例健康者对照。结果105例CAD患者ACE的DD基因频率分布与对照组比较差异有显著性(P<0.05);早发和迟发CAD患者与对照组比较,D等位基因和DD基因频率显著高于对照组(P<0.05)。早发CAD组AT1R的CC基因型和C等位基因频率与对照组相比差异有显著性(P=0.036,P=0.008)。联合基因多态分析,早发CAD合并ACE-DD+AT1R-CC基因型频率显著高于对照组(P=0.036);迟发CAD合并ACE-DD+AT1R-CC基因型频率与对照组比较差异无显著性(P=0.206)。结论早发CAD组与ACE的DD基因频率和AT1R的A1166C基因频率分布相关,ACE-DD基因频率与AT1R-CC基因频率在早发CAD的发病中具有协同作用。
Objective To investigate the association between anglotensin converting enzyme(ACE)and anglotensin Ⅱ receptor Ⅰ polymorphisms ( AT1R ) with the premature coronary artery disease ( CAD). Methods By using PCR analysis method,insertion/deletion polymorphisms of angiotensin-converting enzyme ( ACE-I/D ) gene and A1166C polymorphisms of angiotensin II receptor I(AT1R-A1166C ) gene were analyzed in 41 patients in premature CAD and 64 patients in mature CAD group as well as 50 healthy subjects in control group. Results ACE-DD genotype was more frequent in premature and mature CAD groups than those of control group( P 〈0.05 ) ;ACE-DD genotype and D alleles were more frequent in premature and mature CAD groups than those of control group ( P 〈 0.05 ) ; AT, R-CC genotype and C alleles were more frequent in premature CAD groups than those of control group (P = 0.036,P = 0. 008 ) ;The combining analysis indicated that ACE-DD and AT1R-CC genotype frequency was significantly higher in premature CAD group than those in control group( P =0. 036 ) ;ACE-DD and AT1R-CC frequency was not significantly different in mature CAD group than those of control group ( P = 0.206 ). Conclusion The distribution of ACE-DD genotype and AT1 R-A1166C genotype are associated with premature CAD, and the frequency of ACE-DD and AT, R-CC genotype has a synergistic effect on the risk of premature CAD.
出处
《中国综合临床》
北大核心
2006年第11期971-974,共4页
Clinical Medicine of China
基金
广东省珠海市科技局项目(200301031)
关键词
冠心病
血管紧张素转换酶
血管紧张素Ⅱ1型受体
基因多态性
Coronary artery disease
Angiotensin-converting enzyme
Angiotensin type Ⅰ receptor
Gene polymorphism