系统性红斑狼疮合并冠心病与单纯冠心病患者危险因素的对比研究

Comparative Study of Patients with Systemic Lupus Erythematosus Combined with Coronary Heart Disease and Patients with Coronary Heart Disease Alone about Risk Factors

目的总结系统性红斑狼疮(SLE)合并冠心病的临床特点,探讨其危险因素及发病机制。方法选择2008月7月-2012年7月住院的SLE合并冠心病患者48例作为观察组;对照组为50例单纯冠心病患者。记录两组患者的所有传统动脉粥样硬化危险因素,检测血生化指标及血清TNF-α水平,并进行超声心动图检查,记录左室舒张末径、左心室射血分数。结果观察组的吸烟史所占比例、冠心病家族史及高脂血症病史的发生率明显低于对照组(P<0.05)。血LP(a)、CRP的水平明显高于对照组(P<0.05)。观察组患者的左室舒张末内径明显高于对照组(P<0.05),而左心室收缩功能低下比例明显高于对照组(P<0.05)。观察组患者血清TNF-α水平明显高于对照组(P<0.05)。结论传统致动脉粥样硬化的高危因素不足以解释SLE早期发生冠心病,SLE合并冠心病可能是其独特的高危因素。炎症反应参与了SLE合并冠心病的发生发展过程。

Objective To summarize the clinical features of systemic lupus erythematosus （SLE） with coronary heart disease, to explore the risk factors and pathogenesis. Methods Select 48 cases of SLE combined with coronary heart disease in our hospital from July 2008 to July 2012 as the observation group;control group was 50 cases patients with coronary heart disease alone. Two groups of patients with all the traditional artery atherosclerosis risk factors, biochemical indicators of blood and serum TNF-alpha level, echocardiography, record left ventricular end-diastolic diameter and left ventricular ejection fraction were recorded and analyzed. Results The proportion of the smoking history, the incidence of coronary heart disease family history and history of hyperlipidemia of the observation group were significantly lower than those in the control group（ P 〈 0.05 ）. The blood LP（ a）, CRP levels were significantly higher those in the control group（ P 〈 0.05 ）. The left ventricular end diastolic diameter was significantly higher in the observation group（ P 〈 0.05 ）, left ventricular systolic dysfunction ratio was significantly higher（ P 〈 0.05 ）. The serum levels of TNF-α level was significantly higher in the observation group （ P 〈 0.05 ）. Conclusion Traditional risk factors of atherosclerosis had not sufficient to explain the SLE early onset of coronary heart disease, SLE with coronary heart disease may have its own unique risk factors. The inflammatory response may be involved in the development and progression of SLE with coronary heart disease.