中国实用医刊
中國實用醫刊
중국실용의간
CENTRAL PLAINS MEDICAL JOURNAL
2013年
6期
9-12
,共4页
林荣海%李振光%于成勇%张道强
林榮海%李振光%于成勇%張道彊
림영해%리진광%우성용%장도강
心房颤动%脂蛋白相关性磷脂酶A2%缺血性卒中%炎症
心房顫動%脂蛋白相關性燐脂酶A2%缺血性卒中%炎癥
심방전동%지단백상관성린지매A2%결혈성졸중%염증
Atrial fibrillation%Lipoprotein-associated phospholipase A2%Ischemic stroke%Inflammation
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24 h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24 h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个月三组间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.LP-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.
目的 觀察非瓣膜性心房顫動(NVAF)患者血漿脂蛋白相關性燐脂酶A2 (Lp-PLA2)含量變化的特點,探索心房顫動相關性卒中的病理生理學機製,為臨床進行抗栓治療提供依據.方法 選取經臨床和輔助檢查確診的235例未接受抗栓治療的NVAF患者、119例NVAF閤併急性腦梗死患者以及120例無NVAF的急性腦梗死患者納入本研究.測定其血漿Lp-PLA2的含量變化,年齡匹配的健康體檢者作為對照組.同時觀察不同年齡組的NVAF患者血漿Lp-PLA2含量的差異.結果 各年齡組的NVAF患者血漿Lp-PLA2含量均顯著增高,與對照組相比差異有統計學意義(P均<0.01).其中≥76歲年齡組Lp-PLA2升高更顯著,與≤60歲年齡組相比差異有統計學意義(P<0.01).髮病24 h時NVAF閤併急性腦梗死組患者血漿Lp-PLA2含量顯著高于NVAF組(P<0.01)及對照組(P<0.01).髮病24 h時NVAF閤併急性腦梗死組血漿Lp-PLA2含量顯著高于無NVAF的急性腦梗死組(P<0.01).無NVAF的急性腦梗死組血漿Lp-PLA2含量顯著高于對照組(P<0.01).至髮病後1週,NVAF閤併急性腦梗死組患者血漿Lp-PLA2含量仍高于無NVAF的急性腦梗死組及對照組(P<0.05).髮病後2週、1箇月三組間Lp-PLA2含量比較差異無統計學意義.結論 NVAF患者血漿Lp-PLA2含量顯著升高,提示其體內存在Lp-PLA2相關性炎性反應,NVAF相關性腦梗死患者炎性反應持續時間較長.LP-PLA2可作為一種理想的分子標記物用于判斷NVAF患者體內炎性反應狀態.
목적 관찰비판막성심방전동(NVAF)환자혈장지단백상관성린지매A2 (Lp-PLA2)함량변화적특점,탐색심방전동상관성졸중적병리생이학궤제,위림상진행항전치료제공의거.방법 선취경림상화보조검사학진적235례미접수항전치료적NVAF환자、119례NVAF합병급성뇌경사환자이급120례무NVAF적급성뇌경사환자납입본연구.측정기혈장Lp-PLA2적함량변화,년령필배적건강체검자작위대조조.동시관찰불동년령조적NVAF환자혈장Lp-PLA2함량적차이.결과 각년령조적NVAF환자혈장Lp-PLA2함량균현저증고,여대조조상비차이유통계학의의(P균<0.01).기중≥76세년령조Lp-PLA2승고경현저,여≤60세년령조상비차이유통계학의의(P<0.01).발병24 h시NVAF합병급성뇌경사조환자혈장Lp-PLA2함량현저고우NVAF조(P<0.01)급대조조(P<0.01).발병24 h시NVAF합병급성뇌경사조혈장Lp-PLA2함량현저고우무NVAF적급성뇌경사조(P<0.01).무NVAF적급성뇌경사조혈장Lp-PLA2함량현저고우대조조(P<0.01).지발병후1주,NVAF합병급성뇌경사조환자혈장Lp-PLA2함량잉고우무NVAF적급성뇌경사조급대조조(P<0.05).발병후2주、1개월삼조간Lp-PLA2함량비교차이무통계학의의.결론 NVAF환자혈장Lp-PLA2함량현저승고,제시기체내존재Lp-PLA2상관성염성반응,NVAF상관성뇌경사환자염성반응지속시간교장.LP-PLA2가작위일충이상적분자표기물용우판단NVAF환자체내염성반응상태.
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 examined 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 LpPLA2 was assayed by ELISA.Meanwhile,the Lp-PLA2 levels during different time point after stroke onset 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≥76 years group P <0.001).In age≥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 ischemic 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 prothrombotic states.The time window for an tithrombotic therapy to NVAF-associated ischemic stroke would be longer.