抗血管紧张素Ⅱ_1受体和α_1肾上腺素受体抗体与高血压患者心脏重构的观察

Clinical observation in patients with hypertension about autoantibodies against α_1 adrenergic receptor and AT1 receptor and cardiac remodeling

目的观察原发性高血压患者血清抗血管紧张素Ⅱ1受体(抗AT1受体)和α1肾上腺素受体自身抗体(抗α1受体抗体)对高血压患者心脏重构的影响。方法采用酶联免疫吸附法(ELISA)对553例原发性高血压患者进行血清抗α1受体和抗AT1受体抗体检测并记录所有患者的超声心动图检查结果。比较不同滴度组血清抗体对心脏重构的影响。结果553例高血压病患者血清抗α1-受体和抗AT1受体抗体阳性率分别为32.3%(179/553),42.3%(234/553)。抗α1受体抗体1∶40(滴度)阳性组左心房扩大比率明显高于阴性组(P=0.021);≥1∶80阳性组左心室扩大比率明显高于阴性组(P=0.006)。抗AT1受体抗体1∶40阳性组右心房扩大比率明显高于阴性组(P=0.011);≥1∶80阳性组左心室扩大比率明显高于阴性组(P=0.004)。双抗阳性组左心室和右心房扩大比率明显高于双抗阴性组(P分别为0.006和0.044)。结论抗α1-受体和AT1受体抗体与高血压病患者心脏扩大有关,可能是导致高血压病患者心脏重构的重要因素之一,且两种抗体可能有相互促进作用。

Objective To investigate the effects of autoantibodies against α1 -adrenergic receptor and AT1 receptor on cardiac remodeling in patients with primary hypertension. Methods The autoantibodies against α1-adrenergic receptor and AT1 receptor in the serum of 553 patients were detected by ELISA and The echocardiography was recorded. Results The positive of the autoantibodies against α1-adrenergie receptor and AT1 receptor were 32, 3 % and 42. 3 %, respectively, Proportion of left atrial enlargement was significantly higher in the autoantibodies against α1-adrenergic receptor positive group with a titer of 1：40 than that in negative group （P〈0. 05）. Proportion of right atrial enlargement was significantly higher in the autoantibodies against AT1 receptor positive group with a titer of 1 ： 40 than that in negative group （P〈0. 05）. There was significant difference between the autoantibodies against al -adrenergic receptor positive group with a titer of 1：≤ 80 and negative group on the rate of left ventricular enlargement （P〈0.01）. Proportion of right atrial and left ventricular enlargement in group of double positive of autoantibodies against α1 -adrenergic receptor and AT1 receptor were higher than that in the group of double negative. Conclusions The autoantibodies against α1 -adrenergic receptor and AT1 receptor have some relationship with cardiac enlargement and may be an important factor in resulting in cardiac remodeling of primary hypertension.