The endothelial nitric oxide synthase (eNOS) gene deficiency is known to cause impaired coronary vasodilating capability in animal models. In the general clinical population, the eNOS gene polymorphisms, able to affect eNOS activity, were associated with cardiometabolic risk features and prevalence of coronary artery disease (CAD). To investigate the association of eNOS Glu298Asp gene polymorphism, cardiometabolic profile, obstructive CAD and inducible myocardial ischemia in patients with suspected stable CAD. A total of 506 patients (314 males; mean age 62 ± 9 years) referred for suspected CAD was enrolled. Among these, 325 patients underwent stress ECG or cardiac imaging to assess the presence of inducible myocardial ischemia and 436 patients underwent non-invasive computerized tomography or invasive coronary angiography to assess the presence of obstructive CAD. Clinical characteristics and blood samples were collected for each patient. In the whole population, 49.6% of patients were homozygous for the Glu298 genotype (Glu/Glu), 40.9% heterozygotes (Glu/Asp) and 9.5% homozygous for the 298Asp genotype (Asp/Asp). Obstructive CAD was documented in 178/436 (40.8%) patients undergoing coronary angiography while myocardial ischemia in 160/325 (49.2%) patients undergoing stress testing. Patients with eNOS Asp genotype (Glu/Asp + Asp/Asp) had no significant differences in clinical risk factors and in circulating markers. Independent predictors of obstructive CAD were age, gender, obesity, and low HDL-C. Independent predictors of myocardial ischemia were gender, obesity, low HDL-C and Asp genotype. In the subpopulation in which both stress tests and coronary angiography were performed, the Asp genotype remained associated with increased myocardial ischemia risk after adjustment for obstructive CAD. In this population, low-HDL cholesterol was the only cardiometabolic risk determinant of obstructive CAD. The eNOS Glu298Asp gene polymorphism was significantly associated with inducible myocardial ischemia independently of other risk factors and presence of obstructive CAD.

中文翻译：

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低 HDL 胆固醇和 eNOS Glu298Asp 多态性与疑似稳定性冠状动脉疾病患者的诱导性心肌缺血相关

众所周知，内皮一氧化氮合酶（eNOS）基因缺陷会导致动物模型冠状动脉舒张能力受损。在一般临床人群中，eNOS 基因多态性能够影响 eNOS 活性，与心脏代谢风险特征和冠状动脉疾病 (CAD) 患病率相关。探讨疑似稳定性 CAD 患者的 eNOS Glu298Asp 基因多态性、心脏代谢特征、阻塞性 CAD 和诱导性心肌缺血之间的关系。共有 506 名因疑似 CAD 转诊的患者（314 名男性；平均年龄 62 ± 9 岁）入组。其中，325 名患者接受了负荷心电图或心脏成像以评估是否存在诱导性心肌缺血，436 名患者接受了非侵入性计算机断层扫描或侵入性冠状动脉造影以评估是否存在阻塞性 CAD。收集每位患者的临床特征和血液样本。在整个人群中，49.6% 的患者为 Glu298 基因型（Glu/Glu）纯合子，40.9% 为杂合子（Glu/Asp），9.5% 为 298Asp 基因型（Asp/Asp）纯合子。 178/436 (40.8%) 例接受冠状动脉造影的患者记录有阻塞性 CAD，而 160/325 (49.2%) 例接受压力测试的患者记录有心肌缺血。 eNOS Asp 基因型（Glu/Asp + Asp/Asp）患者的临床危险因素和循环标志物没有显着差异。阻塞性 CAD 的独立预测因素是年龄、性别、肥胖和低 HDL-C。心肌缺血的独立预测因素是性别、肥胖、低 HDL-C 和 Asp 基因型。在同时进行压力测试和冠状动脉造影的亚群中，在对阻塞性 CAD 进行调整后，Asp 基因型仍然与心肌缺血风险增加相关。在这一人群中，低 HDL 胆固醇是阻塞性 CAD 的唯一心脏代谢风险决定因素。 eNOS Glu298Asp 基因多态性与诱导性心肌缺血显着相关，与其他危险因素和阻塞性 CAD 的存在无关。