一氧化氮合成酶 3 基因多态性及其与急性心肌梗死和慢性稳定型心绞痛的关系:印度北部病例对照研究》。

IF 0.8 Q3 MEDICINE, GENERAL & INTERNAL
Sunil Kumar, Deepak Juyal, Arun Pandey, Preeti Tomar, Vinay Sagar, Rakesh Yadav, Renu Saxena
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引用次数: 0

摘要

背景:冠状动脉疾病(CAD)包括急性心肌梗死(AMI)、慢性稳定型心绞痛(CSA)和不稳定型心绞痛(UA),有许多已知的危险因素。遗传倾向是诱发冠状动脉粥样硬化的主要风险因素,而调控动脉粥样硬化的基因对疾病的预防非常重要。目的:评估三种 NOS3 多态性(-786C/T、894G/T 和 4a4b)在 CAD 患者,尤其是 AMI 和 CSA 患者中的作用,并将其与健康对照组进行比较:纳入 100 名 AMI 和 CSA 组患者及 100 名对照组患者,并通过聚合酶链式反应-限制性片段长度多态性对三种 NOS3 多态性(-786C/T、894G/T 和 4a4b)进行分型。此外,还对血浆中的 NO 代谢物(NOx)进行了评估:结果:在显性模型中,894G/T 多态性与急性心肌梗死有明显相关性(P = 0.052);在显性和隐性模型中,894G/T 多态性与 CSA 有明显相关性(分别为 P = 0.008 和 P = 0.006)。与 AMI 和 CSA 患者(37.05 ± 6.75 和 38.67 ± 5.61)相比,健康对照组的血浆 NO 水平(43.80 ± 6.28)明显更高(P < 0.0001)。在隐性、显性和共显性模型中,均未发现-786C/T和4a4b多态性与AMI和CSA风险有明显关联:我们的研究发现,894G/T 多态性与急性心肌梗死有明显关联,氮氧化物水平与 CAD 有独立关联,这表明北印度人群的 CAD 风险很高。我们的研究结果将有助于确定与 CAD 相关的遗传风险因素,并更好地采取诊断和治疗措施。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nitric Oxide Synthase 3 Gene Polymorphisms and Their Association with Acute Myocardial Infarction and Chronic Stable Angina: A Case-Control Study from Northern India.

Background: Coronary artery disease (CAD) that encompasses acute myocardial infarction (AMI), chronic stable angina (CSA), and unstable angina (UA) has numerous known risk factors. Genetic predispositions contribute as major risk in the development of CAD and the genes regulating atherosclerosis are important for disease prevention. Nitric oxide synthase 3 (NOS3) gene responsible for nitric oxide (NO) production is of special importance.

Aim: To evaluate the role of three NOS3 polymorphisms (-786C/T, 894G/T, and 4a4b) in patients with CAD, particularly in AMI and CSA and their comparison with healthy controls.

Materials and methods: One hundred patients in each AMI and CSA group and 100 controls were included and were typed for three NOS3 polymorphisms (-786C/T, 894G/T, and 4a4b) by polymerase chain reaction-restriction fragment length polymorphism. Plasma NO metabolites (NOx) were also evaluated.

Results: A significant association of 894G/T polymorphism with AMI in dominant model (P = 0.052) and with CSA in dominant and codominant models was detected (P = 0.008 and P = 0.006, respectively). Plasma NO levels were found to be significantly higher (P < 0.0001) in healthy controls (43.80 ± 6.28) compared to AMI and CSA patients (37.05 ± 6.75 and 38.67 ± 5.61). No significant association of -786C/T and 4a4b polymorphism with AMI and CSA risk under recessive, dominant, and codominant models was detected.

Conclusion: Our study revealed a significant association of 894G/T polymorphism with AMI and independent association of NOx levels with CAD, indicating high risk of CAD in the North Indian population. Our findings will be helpful in identifying the genetic risk factors associated with CAD and better management of the diagnostic as well as therapeutic measures.

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