冠心病合并非酒精性脂肪肝患者冠状动脉病变特点分析

Characteristics of coronary lesion in patients with coronary heart disease combined with nonalcoholic fatty liver

目的：观察冠心病（CHD）患者非酒精性脂肪肝（NAFLD）的发病率及冠状动脉病变特点。方法纳入2011年6月~2012年12月苏北人民医院经冠状动脉造影（CAG）确诊为CHD的患者158例作为冠心病组，另纳入CAG检查结果阴性者142例作为对照组，通过肝脏彩超结果及饮酒情况比较两组NAFLD发病率。将所有患者按照是否合并NAFLD分为NAFLD组（n=158）及非NAFLD组（n=142），观察NAFLD组及非NAFLD组间病变血管数以及血管狭窄程度有无差异，同时采用放射免疫法测定一氧化氮（NO）和硝酸还原酶法测定内皮素（ET）水平，比较两组NO和ET的水平差异。结果冠心病组NAFLD发病率明显高于正常组（58.2% vs.36.6%），NAFLD患者冠脉多支病变（41.8% vs.31.1%）和重度狭窄（24.7%vs.10.6%）及完全闭塞（19.0%vs.6.3%）的比例明显高于不合并NAFLD患者（P＜0.05）；与非NAFLD组相比，NAFLD组NO明显下降、ET明显升高（P＜0.05）。结论NAFLD对冠心病的诊断及病变程度有预测价值，其机制可能与影响内皮功能有关。

Objective To discuss the incidence of nonalcoholic fatty liver （NAFLD）, characteristics of coronary lesion and possible mechanism in patients with coronary heart disease （CHD）. Methods The patients （n=158） with CHD diagnosed by CAG were chosen as CHD group from the Subei People’s Hospital from Jun. 2011 to Dec. 2012. Other 142 patients with negative CAG results were chosen as control group. The incidence of NAFLD was compared according to color Doppler ultrasound and drinking status between two groups. CHD group was further divided into NAFLD sub-group （n=158） and non-NAFLD sub-group （n=142）. The number of lesion vessels and degree of vascular stenosis were observed and compared between two sub-groups. The levels of nitric oxide （NO） and endothelin （ET） were detected and compared respectively by using radioimmunoassay and nitrate reductase method in two sub-groups. Results The incidence of NAFLD was significantly higher in CHD group than that in control group （58.2%vs. 36.6%）. The percentages of multiple coronary vessel lesion （41.8%vs. 31.1%）, severe stenosis （24.7%vs. 10.6%） and complete occlusion （19.0%vs. 6.3%） were significantly higher in NAFLD sub-group than those in non-NAFLD sub-group （P〈0.05）. The level of NO decreased significantly and level of ET increased significantly （P〈0.05） in NAFLD sub-group compared with non-NAFLD sub-group. Conclusion Nonalcoholic fatty liver has predictive value to diagnosis and severity of CHD, and the mechanism may be related to endothelial function effected by NAFLD.