Arca M, Pannitteri G, Campagna F, Candeloro A, Montali A, Cantini R, Seccareccia F, Campa P P, Marino B, Ricci G
Istituto di Terapia Medica Sistematica, Università di Roma La Sapienza, Italy.
Eur J Clin Invest. 1998 Jun;28(6):485-90. doi: 10.1046/j.1365-2362.1998.00313.x.
The deletion (D) allele of the angiotensin-converting enzyme (ACE) gene has been proposed as a genetic marker of the risk of ischaemic heart disease. However, the relationships between ACE genotypes, the development of coronary atherosclerosis and the occurrence of major coronary events are still controversial.
To investigate whether the ACE I/D (insertion/deletion) polymorphism predicts the risk of coronary stenosis and myocardial infarction (MI), ACE genotypes were determined in 394 consecutive patients who underwent coronary angiography. The presence determined in 394 consecutive patients who underwent coronary angiography. The presence of coronary artery disease (CAD) (defined by > 50% stenosis) was detected in 236 patients (CAD+); 85 of these individuals had a history of MI. Patients with coronary stenosis < 10% (n = 158) served as controls (CAD-). ACE genotypes were determined by agarose gel sizing after polymerase chain reaction (PCR) amplification.
The distribution of ACE genotypes in CAD+ patients was not significantly different from that in CAD-patients (chi 2 = 2.63, P < 0.27). After controlling for other coronary risk factors, no significant increase in risk of CAD or MI was found to be associated with the D allele, regardless of whether the D allele was assumed to have a dominant, a codominant or a recessive effect. Similar results were observed in CAD+ patients at lower risk because of low body mass index and apolipoprotein B concentrations. Smoking, apolipoprotein B and history of hypertension were found to be independent predictors of CAD and MI.
Our study did not provide evidence of a significant association between ACE genotypes and the development of coronary atherosclerosis. It also failed to support a role of ACE I/D polymorphism in favouring the conversion of coronary stenosis to MI.
血管紧张素转换酶（ACE）基因的缺失（D）等位基因被认为是缺血性心脏病风险的遗传标志物。然而，ACE基因分型、冠状动脉粥样硬化的发展与主要冠状动脉事件的发生之间的关系仍存在争议。
为了研究ACE I/D（插入/缺失）多态性是否能预测冠状动脉狭窄和心肌梗死（MI）的风险，对394例接受冠状动脉造影的连续患者进行了ACE基因分型。在394例接受冠状动脉造影的连续患者中检测冠状动脉疾病（CAD）（定义为狭窄>50%）的存在情况。236例患者（CAD+）检测到CAD；其中85例有MI病史。冠状动脉狭窄<10%的患者（n = 158）作为对照（CAD-）。通过聚合酶链反应（PCR）扩增后琼脂糖凝胶大小分析确定ACE基因分型。
CAD+患者中ACE基因分型的分布与CAD-患者无显著差异（χ2 = 2.63，P < 0.27）。在控制其他冠状动脉危险因素后，无论假设D等位基因具有显性、共显性还是隐性效应，均未发现D等位基因与CAD或MI风险显著增加相关。在因低体重指数和载脂蛋白B浓度而风险较低的CAD+患者中也观察到类似结果。吸烟、载脂蛋白B和高血压病史是CAD和MI的独立预测因素。
我们的研究没有提供ACE基因分型与冠状动脉粥样硬化发展之间存在显著关联的证据。它也未能支持ACE I/D多态性在促进冠状动脉狭窄转变为MI方面的作用。
