天津医科大学学报
天津醫科大學學報
천진의과대학학보
JOURNAL OF TIANJIN MEDICAL UNIVERSITY
2015年
3期
196-198,202
,共4页
心房颤动%左心房内径%脂蛋白相关性磷脂酶A2%高敏C反应蛋白%炎症
心房顫動%左心房內徑%脂蛋白相關性燐脂酶A2%高敏C反應蛋白%炎癥
심방전동%좌심방내경%지단백상관성린지매A2%고민C반응단백%염증
atrial fibrillation%left atrial diameter%Lp-PLA2%hs-CRP%inflammation
目的:观察不同类型心房颤动(房颤)患者左心房内径(LAD)与脂蛋白相关性磷脂酶A2(Lp-PLA2)及高敏C-反应蛋白(hs-CRP)水平之间的关系,探讨炎症诱发房颤的机制。方法:将122例房颤患者分为阵发性房颤组38例,持续性房颤组40例,永久性房颤组44例,随机选取41例窦性心律患者为对照组,记录患者临床资料及检测指标。结果:Lp-PLA2水平在持续性房颤组及永久性房颤组明显高于阵发性房颤组及对照组(P<0.05)。hs-CRP水平在持续性房颤组及永久性房颤组高于阵发性房颤组及对照组,阵发性房颤组高于对照组(P<0.05)。 LAD在永久性房颤组及持续性房颤组大于阵发性房颤组和对照组(P<0.05)。阵发性房颤组中hs-CRP与LAD成正相关,持续性房颤组及永久性房颤组中Lp-PLA2、hs-CRP与LAD均呈正相关。结论:炎症在房颤的发生、发展和维持中发挥着重要作用,作用机制之一可能与炎症导致心房重构有关。
目的:觀察不同類型心房顫動(房顫)患者左心房內徑(LAD)與脂蛋白相關性燐脂酶A2(Lp-PLA2)及高敏C-反應蛋白(hs-CRP)水平之間的關繫,探討炎癥誘髮房顫的機製。方法:將122例房顫患者分為陣髮性房顫組38例,持續性房顫組40例,永久性房顫組44例,隨機選取41例竇性心律患者為對照組,記錄患者臨床資料及檢測指標。結果:Lp-PLA2水平在持續性房顫組及永久性房顫組明顯高于陣髮性房顫組及對照組(P<0.05)。hs-CRP水平在持續性房顫組及永久性房顫組高于陣髮性房顫組及對照組,陣髮性房顫組高于對照組(P<0.05)。 LAD在永久性房顫組及持續性房顫組大于陣髮性房顫組和對照組(P<0.05)。陣髮性房顫組中hs-CRP與LAD成正相關,持續性房顫組及永久性房顫組中Lp-PLA2、hs-CRP與LAD均呈正相關。結論:炎癥在房顫的髮生、髮展和維持中髮揮著重要作用,作用機製之一可能與炎癥導緻心房重構有關。
목적:관찰불동류형심방전동(방전)환자좌심방내경(LAD)여지단백상관성린지매A2(Lp-PLA2)급고민C-반응단백(hs-CRP)수평지간적관계,탐토염증유발방전적궤제。방법:장122례방전환자분위진발성방전조38례,지속성방전조40례,영구성방전조44례,수궤선취41례두성심률환자위대조조,기록환자림상자료급검측지표。결과:Lp-PLA2수평재지속성방전조급영구성방전조명현고우진발성방전조급대조조(P<0.05)。hs-CRP수평재지속성방전조급영구성방전조고우진발성방전조급대조조,진발성방전조고우대조조(P<0.05)。 LAD재영구성방전조급지속성방전조대우진발성방전조화대조조(P<0.05)。진발성방전조중hs-CRP여LAD성정상관,지속성방전조급영구성방전조중Lp-PLA2、hs-CRP여LAD균정정상관。결론:염증재방전적발생、발전화유지중발휘착중요작용,작용궤제지일가능여염증도치심방중구유관。
Objective:To observe the relationship between plasma levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) , high sensitivity C reactive protein (hs-CRP) and left atrial diameter (LAD) in patients with different types of atrial fibrillation(AF) and to explore the mechanism of inflammation-induced AF. Methods:One hundred and twenty two AF patients were divided into three groups:paroxysmal AF group (A, n=38), persistent AF group (B, n=40) and permanent AF group (C, n=44).Furthermore, forty-one sinus rhythm patients was randomly selected as control group (D, n=41). Basic clinical data and testing indexes of all groups were recorded. Results:Lp-PLA2 level in persistent and permanent AF group were significantly higher that in than paroxysmal AF and control groups(P<0.05). Hs-CRP levels in persistent and permanent groups were higher than those in paroxysmal and control groups. Paroxysmal group was also higher than control group (P<0.05). LAD in permanent and persistent groups were greater than paroxysmal and control groups (P<0.05). Hs-CRP was positively correlated with LAD in paroxysmal group. Hs-CRP and Lp-PLA2 were positively correlated with LAD both in persistent and permanent groups. Conclusion:Inflammation is an important factor for genesis, developing and sustaining AF. One mechanism may be related to inflammation induced atrial remolding.