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目的:探讨急性冠状动脉综合征(ACS)患者血清骨保护素(OPG)、可溶性核因子κB受体活化因子配体(sRANKL)与高敏C反应蛋白(hs-CRP)水平及冠状动脉病变程度的关系。方法:随机选择我院住院350例患者分为3组:ACS150例,稳定型心绞痛(SA)100例和对照组100例;采用ELLSA法检测血清OPG、sRANKL,同时测定hs-CRP水平;并对所有患者进行冠状动脉造影,根据造影结果对冠状动脉病变进行Gensini评分,分析3组血清水平与冠状动脉狭窄的数目(1,2,3支血管病变)及冠状动脉病变Gensini评分的相关性。结果:ACS组血清OPG、hs-CRP水平显著高于对照组(P<0.01)及SA组(P<0.01),且随病变血管支数增加而增高(P<0.01);与之相反,血清sRANKL水平显著低于对照组(P<0.01)及SA组(P<0.01),且随病变血管支数增加而减低(P<0.01);冠心病患者OPG水平与Gensini评分、hs-CRP水平呈正相关(P<0.01);sRANKL水平与Gensini评分、hs-CRP水平呈负相关(P<0.01)。结论:ACS患者血清OPG、sRANKL、hs-CRP水平与冠状动脉病变程度有关,提示OPG系统可能通过干预血管炎症反应参与了冠状动脉粥样硬化病变进程。
OBJECTIVE: To investigate the changes of serum osteoprotegerin (OPG), sRANKL, hs-CRP and coronary artery lesions in patients with acute coronary syndrome (ACS) relationship. Methods: A total of 350 hospitalized patients were randomly divided into three groups: ACS150 cases, stable angina pectoris (SA) 100 cases and control group 100 cases. Serum OPG and sRANKL were detected by ELLSA method and hs-CRP levels were measured simultaneously All patients underwent coronary angiography. The Gensini score of coronary artery lesions was determined according to the angiographic results. The correlation between serum levels and the number of coronary artery stenosis (1, 2, and 3 vessel lesions) and coronary artery lesion Gensini score was analyzed. Results: The levels of serum OPG and hs-CRP in ACS group were significantly higher than those in control group (P <0.01) and SA group (P <0.01), and increased with the increase of vessel count (P <0.01) The level of sRANKL in CHD patients was significantly lower than that in control group (P <0.01) and SA group (P <0.01), and decreased with the increase of blood vessel count (P <0.01). The level of OPG in CHD patients was positively correlated with Gensini score and hs- (P <0.01). The level of sRANKL was negatively correlated with Gensini score and hs-CRP level (P <0.01). Conclusion: The serum levels of OPG, sRANKL and hs-CRP in patients with ACS are related to the severity of coronary artery disease, suggesting that OPG may be involved in the pathogenesis of coronary atherosclerosis by interfering with vascular inflammation.