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首页> 外文期刊>Clinical chemistry and laboratory medicine: CCLM >Left ventricular size, mass and function in relation to angiotensin-converting enzyme gene and angiotensin-II type 1 receptor gene polymorphisms in patients with coronary artery disease.
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Left ventricular size, mass and function in relation to angiotensin-converting enzyme gene and angiotensin-II type 1 receptor gene polymorphisms in patients with coronary artery disease.

机译:冠心病患者左​​心室大小,质量和功能与血管紧张素转换酶基因和血管紧张素II 1型受体基因多态性的关系。

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The objective of the present study was to analyse the potential synergistic influence of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene (I/D ACE) and the A1166C polymorphism of the angiotensin-II type 1 receptor gene polymorphisms (A1166C AT1R) on the left ventricular size and performance. Three hundred sixty and one consecutive, Caucasian patients with angiographically confirmed coronary artery disease (CAD) were enrolled into the study. Left ventricular diameter, mass and function were evaluated by echocardiography. Screening for the I/D ACE and A1166C AT1R genotypes was performed by polymerase chain reaction of genomic DNA, followed by restriction enzyme digestion and agarose gel electrophoresis. The I/D ACE and A1166C AT1R genotypes separately were not significantly associated with the left ventricular size and function parameters in CAD patients. However, trends towards decreased left ventricular ejection fraction (LVEF) as well as increased left ventricular end-diastolic diameter (LVEDD) and left ventricular mass index (LVMI) were observed when patients with genotype DD+CC/AC and DD+CC were compared to patients homozygous only in one locus (DD or CC). Significant increase in LVEDD and LVMI was observed only in patients with a history of anterior myocardial infarction with combined genotype DD+CC/AC or DD+CC. This study does not support the role of the ACE I/D and AT1R A1166C polymorphisms in the determination of the left ventricular size and performance in patients with significant coronary atherosclerosis. However, it indicates that the influence of polymorphisms may be present in specific patient populations.
机译:本研究的目的是分析血管紧张素转换酶基因(I / D ACE)的插入/缺失多态性与血管紧张素II 1型受体基因多态性(A1166C AT1R)的潜在协同作用在左心室的大小和表现。该研究共纳入361例经血管造影证实为冠状动脉疾病(CAD)的高加索白人患者。超声心动图评估左心室直径,质量和功能。通过基因组DNA的聚合酶链反应,然后进行限制性内切酶消化和琼脂糖凝胶电泳,对I / D ACE和A1166C AT1R基因型进行筛选。 I / D ACE和A1166C AT1R基因型分别与CAD患者的左心室大小和功能参数无关。然而,当比较基因型DD + CC / AC和DD + CC的患者时,观察到左室射血分数(LVEF)降低,左室舒张末期直径(LVEDD)和左室质量指数(LVMI)升高的趋势。仅在一个位点(DD或CC)纯合的患者。仅在具有合并基因型DD + CC / AC或DD + CC的前心肌梗塞病史的患者中观察到LVEDD和LVMI显着增加。这项研究不支持ACE I / D和AT1R A1166C多态性在确定患有严重冠状动脉粥样硬化的患者的左心室大小和性能方面的作用。但是,这表明多态性的影响可能存在于特定的患者人群中。

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