单纯疱疹病毒感染与急性心肌梗死关系的研究

Relation between herpes simplex virus infection and acute myocardial infarction

目的探讨单纯疱疹病毒(HSV)感染与急性心肌梗死之间的关系。方法采用ELISA方法检测72例急性心肌梗死患者与79例正常对照组血清中HSV-1及HSV-2抗体水平,同时检测两组的IL-6(pg/ml)、TNF-α(pg/ml)、sV-CAM-1(nmol/L)、hsCRP(mg/L)水平;并进行冠心病危险因素调查。结果急性心肌梗死组HSV-1 IgG抗体阳性率(73.61%)、HSV-2 IgG抗体阳性率(58.33%)显著高于对照组(39.24%,36.71%;P<0.01,P<0.05)。急性心肌梗死组IL-6(69.08±108.29)、TNF-α(36.79±5.78)s、VCAM-1(30.03±25.86)、hsCRP(23.80±33.44)水平与对照组(22.91±17.37,2.11±3.32,5.53±5.37,2.10±1.79)比较差异有统计学意义(P<0.01)。调整冠心病危险因素前后,HSV-1和HSV-2 IgG抗体阳性率均与急性心肌梗死有相关性(分别:HSV-1:OR1=4.4,P=0.01;OR2=4.8,P=0.001;OR3=3.5,P=0.012。HSV-2:OR1=2.2,P=0.001;OR2=3.5,P=0.006;OR3=3.3,P=0.009)。结论HSV感染可能通过激发和加重冠状动脉内炎症反应,参与动脉粥样硬化、急性心肌梗死的病理过程。

Objective To study the correlation between herpes simplex virus infection and acute myocardial infarction（AMI）. Methods HSV-1 and HSV-2 IgG antibodies of 72 patients with AMI and 79 normal controls were measured by ELISA.The levels of interleukin-6 （IL-6）, tumor necrosis factor a（TNF-α）, soluble vascular cell adhesion molecule-1 （sVCAM-1） and hypersensitive C-re- active protein （hsCRP） were also determined. Meanwhile,the risk factors of coronary heart disease were investigated.Results The positive rates of HSV-1 and HSV-2 IgG antibody（73.61%, 58.33 % ）in AMI .group were significantly higher than those in control （39.24%, 36.71% ; P 〈 0.01, P 〈 0.05）. Before and after the adjustment of cardiovascular risk factors, IgG antibodies to HSV-1 and HSV-2 were both correlated with AMI （ HSV- 1 ： OR1 = 4.4, P = 0.01 ; OR2 = 4.8, P = 0.001 ; OR3 = 3.5, P = 0.012. HSV-2： OR1 = 2.2, P = 0.001 ; OR2 = 2.9, P = 0.006; OR3 = 3.3, P = 0.009, respectively ）. The concentrations of IL-6 （69 08 ±108.29 ）, TNF-α（36.79± 5.78） ,sVCAM-1 （30.03±25.86） and hsCRP（23.80±33.44） in the AMI group were all higher than those （22.91 ± 17.37,2.11 ±3.32,5.53±5.37,2.10± 1.79）in the control group （all P 〈0.01）. Conclusion There is significant correlation between herpes simplex virus infection and AMI. Herpes simplex virus infection may be involved in the pathogenesis of atherosclerosis and myocardial infarction by inducing and accelerating coronary artery inflammation.