非瓣膜性心房颤动患者血浆脂蛋白相关性磷脂酶A2含量变化的研究

Changes of plasma lipoprotein-associated phospholipase A2 levels in patients with atrial fibrillation

目的观察非瓣膜性心房颤动（NVAF）患者血浆脂蛋白相关性磷脂酶A2（Lp—PLA2）含量变化的特点，探索心房颤动相关性卒中的病理生理学机制，为临床进行抗栓治疗提供依据。方法选取经临床和辅助检查确诊的235例未接受抗栓治疗的NVAF患者、119例NVAF合并急性脑梗死患者以及120例无NVAF的急性脑梗死患者纳入本研究。测定其血浆Lp．PLA2的含量变化，年龄匹配的健康体检者作为对照组。同时观察不同年龄组的NVAF患者血浆Lp—PLA2含量的差异。结果各年龄组的NVAF患者血浆Lp—PLA2含量均显著增高，与对照组相比差异有统计学意义（P均〈0．01）。其中≥76岁年龄组Lp—PLA2升高更显著，与≤60岁年龄组相比差异有统计学意义（P〈0．01）。发病24h时NVAF合并急性脑梗死组患者血浆Lp—PLA2含量显著高于NVAF组（P〈0．01）及对照组（P〈0．01）。发病24h时NVAF合并急性脑梗死组血浆Lp—PLA2含量显著高于无NVAF的急性脑梗死组（P〈0．01）。无NVAF的急性脑梗死组血浆Lp—PLA2含量显著高于对照组（P〈0．01）。至发病后1周，NVAF合并急性脑梗死组患者血浆Lp—PLA2含量仍高于无NVAF的急性脑梗死组及对照组（P〈0．05）。发病后2周、1个月三组问Lp—PLA2含量比较差异无统计学意义。结论NVAF患者血浆Lp—PLA2含量显著升高，提示其体内存在Lp—PLA2相关性炎性反应，NVAF相关性脑梗死患者炎性反应持续时间较长。IP—PLA2可作为一种理想的分子标记物用于判断NVAF患者体内炎性反应状态。

Objective To investigate the changes of plasma lipoprotein-associated phospholipase A2 （Lp-PLA2） levels in patients with nonvalvular atrial fibrillation （NVAF） or NVAF-associated ischemic stroke and to provide biochemistry evidence to antithrombotic therapy. Methods The present study ex- amined plasma Lp-PLA2 levels using fresh fetched blood in 235 cases of NVAF who were not receiving any antithrombotic therapy, 119 cases of NVAF-associated ischemic stroke and 120 cases of acute cerebral infarction who were not with NVAF enrolled in the Lp-PLA2 and stroke prevention study. Plasma Lp- PLA2 was assayed by ELISA. Meanwhile, the Lp-PLA2 levels during different time point after stroke on- set were observed. Results Lp-PLA2 levels were significantly increased in all NVAF group comparing with controls（age ~〈 60 years group P 〈 0. 01,61-76 years group P 〈 0.01, age I〉 76 years group P 〈 O. 001 ）. In age1〉76 years group, the Lp-PLA2 levels were significantly increased compared with ~〈60 years group（ P 〈0. 01）. Within 24 hours after onset, an elevated Lp-PLA2 levels were seen in NVAF- associated ischemic stroke group （ n = 119 ） comparing with lone NVAF or controls （ P 〈 0. 01, P 〈 0. 001）. Within 24 hours after onset, an elevated Lp-PLA2 levels were seen in NVAF-associated ische- mic stroke group comparing with lone NVAF group or controls. Lp-PLA2 levels in NVAF-associated ischemic stroke group were seen in high lasted one week. Conclusions The plasma Lp-PLA2 levels were significantly elevated in lone NVAF, acute stage of NVAF-associated ischemic stroke or acute cerebral infarction who were not with NVAF. We suggest that Lp-PLA2 associated- inflammation may play an important role in the pathogenesis of thromboembolism in NVAF and the measurement of Lp-PLA2 reflects activation of inflammation in vivo and may be a useful marker for the diagnosis of thrombosis or prothrombotie states. The time window for antithrombotic therapy to NVAF-associated ischemic stroke would be longer.