Gardemann A, Nguyen Q D, Humme J, Stricker J, Katz N, Tillmanns H, Hehrlein F W, Rau M, Haberbosch W
Institut für Klinische Chemie und Pathobiochemie, Justus-Liebig-Universität Giessen, Germany.
Eur Heart J. 1998 Nov;19(11):1657-65. doi: 10.1053/euhj.1998.1097.
There is evidence that interaction between angiotensin II type 1 receptor A1166C gene polymorphism and angiotensin I-converting enzyme Insertion/Deletion gene variation might have an effect on the risk of myocardial infarction. The study was carried out in a population of 2244 male Caucasians, whose coronary anatomy was defined by means of coronary angiography. We analysed the relationship, on the risk of ischaemic heart disease, of angiotensin II type 1 receptor A1166C gene variation, not only to myocardial infarction but also to coronary artery disease, and its potential interaction with angiotensin I-converting enzyme Insertion/Deletion gene polymorphism.
No association was detected between angiotensin II type 1 receptor A1166C gene polymorphism and coronary artery disease. Similarly, there was no link to myocardial infarction, either in the total population or in low risk groups. In addition, most importantly, we found no interaction between angiotensin II type 1 receptor A1166C gene variation and angiotensin I-converting Insertion/Deletion polymorphism, either in connection with the risk of coronary artery disease or myocardial infarction.
This angiotensin II type 1 receptor A1166C gene variation is not associated with any detectable increase in risk of ischaemic heart disease. The findings of the present study do not suggest that, as regards risk of coronary artery disease and myocardial infarction, there is interaction between gene polymorphism and angiotensin I-converting enzyme Insertion/Deletion gene variation.
有证据表明,血管紧张素II 1型受体A1166C基因多态性与血管紧张素I转换酶插入/缺失基因变异之间的相互作用可能会影响心肌梗死风险。本研究在2244名男性白种人人群中进行,这些人的冠状动脉解剖结构通过冠状动脉造影确定。我们分析了血管紧张素II 1型受体A1166C基因变异与缺血性心脏病风险之间的关系,不仅涉及心肌梗死,还涉及冠状动脉疾病,以及它与血管紧张素I转换酶插入/缺失基因多态性的潜在相互作用。
未检测到血管紧张素II 1型受体A1166C基因多态性与冠状动脉疾病之间存在关联。同样,在总体人群或低风险组中,也未发现与心肌梗死有联系。此外,最重要的是,我们发现血管紧张素II 1型受体A1166C基因变异与血管紧张素I转换插入/缺失多态性之间,在冠状动脉疾病或心肌梗死风险方面均不存在相互作用。
这种血管紧张素II 1型受体A1166C基因变异与缺血性心脏病风险的任何可检测到的增加均无关联。本研究结果并未表明,在冠状动脉疾病和心肌梗死风险方面,基因多态性与血管紧张素I转换酶插入/缺失基因变异之间存在相互作用。