论文部分内容阅读
目的 :检测冠心病患者血浆中BNP、HCY、CRP水平变化 ,探讨冠心病发病机制及不稳定性心绞痛治疗前后对其影响。方法 :用化学发光和酶联免疫分析 ,对 14 6例冠心病患者和 30例正常对照者血浆BNP、HCY、高敏 -CRP水平变化及相关性进行研究 ,同时对 5 2例UAP经皮冠状动脉成形术 (PTCA)治疗前后对上述三项指标的变化进行分析。结果 :冠心病患者与正常对照组比较BNP水平有显著性差异 (p <0 0 1) ,尤其是AMI和UAP组比SAP组升高更明显 ;CRP水平比正常对照组明显增高 (p <0 0 5 ) ,特别是不稳定心绞痛和急性心肌梗塞组升高明显 (p <0 0 0 1) ;AMI组血浆中HCY水平明显高于正常和其它两组 ,HCY、CRP、BNP三项在UAP组中治疗前后比较差异显著 (p <0 0 5 )。 结论 :BNP、CRP、HCY参与了冠心病的发病过程 ,并可预测心肌梗塞病人远期心功能恢复的情况 ,UAP组经PTCA支架术后三项指标均明显降低 ,可作为疗效观察的一个重要参数 ,HCY参与了冠状动脉粥样硬化的全过程及急性心肌梗塞的发病始末。但其参与的机制有待进一步探讨。
Objective: To detect the changes of plasma BNP, HCY and CRP levels in patients with coronary heart disease (CHD) and to explore the influence of coronary heart disease pathogenesis and unstable angina pectoris before and after treatment. Methods: The levels of plasma BNP, HCY and hypersensitive-CRP in 14 6 CHD patients and 30 normal controls were studied by chemiluminescence and enzyme-linked immunosorbent assay (ELISA), and 52 cases of UAP percutaneous coronary The changes of the above three indexes before and after the operation of PTCA were analyzed. Results: BNP levels were significantly different between patients with coronary heart disease and normal controls (p <0.01), especially in the AMI and UAP groups. The level of CRP was significantly higher than that in the normal control group (p <0 Especially in patients with unstable angina pectoris and acute myocardial infarction (p <0.01). The levels of HCY in AMI group were significantly higher than those in normal and other two groups. The levels of HCY, CRP and BNP in UAP There was significant difference before and after treatment in the group (p <0.05). CONCLUSION: BNP, CRP and HCY are involved in the pathogenesis of coronary heart disease, and predict the long-term recovery of cardiac function in patients with myocardial infarction. The three indicators of UAP group after PTCA stenting are significantly reduced, which may be an important observation Parameters, HCY involved in the whole process of coronary atherosclerosis and the onset of acute myocardial infarction. However, the mechanism of its participation needs to be further explored.