中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2008年
6期
535-537
,共3页
吴玉付%李醒三%何显菁%曾晓聪
吳玉付%李醒三%何顯菁%曾曉聰
오옥부%리성삼%하현정%증효총
风湿性心脏病%二尖瓣狭窄%左心房结构重构%肾素%血管紧张素%醛固酮
風濕性心髒病%二尖瓣狹窄%左心房結構重構%腎素%血管緊張素%醛固酮
풍습성심장병%이첨판협착%좌심방결구중구%신소%혈관긴장소%철고동
Rheumatic heart disease%Mitral stenosis%Left atrial structure remodeling%Renin%Angiotonin%Aldosterone
目的 研究风湿性心脏病(风心病)二尖瓣狭窄(MS)患者血浆肾素血管紧张素醛固酮系统的变化,并探讨其与左心房重构的关系.方法 MS组患者55例,按有无心房颤动分为2组:窦性心律组(SR组)25例,心房颤动组(AF组)30例.正常对照组(NC组)17例.应用放射免疫方法(RIA)测定清晨空腹卧位循环血浆肾素活性(PRA)、血管紧张素Ⅱ(Ang Ⅱ)、醛固酮(Ald)水平.结果 AF组左心房内径与SR组、NC组相比显著增大,分别增大16.9%[(57.71±8.07)mm和(48.48±5.05)mm,P＜0.01)]与87.8%[(57.71±8.07)mm与(30.18±2.86)mm,P＜0.01],且SR组与NC组相比左心房内径亦明显增大,增大60.6%[(48.48±5.05)mm与(30.18±2.86)mm,P＜0.01)].AF、SR组患者循环PRA、AngⅡ、Ald浓度与NC组相比均显著增高(P＜0.01),AF组与SR组相比循环PRA、AngⅡ、Ald浓度亦均明显增高(P＜0.01,P＜0.05).应用Pearson相关分析显示MS患者左心房内径大小与循环PRA、AngⅡ、Ald浓度呈正相关系(r分别为0.277、0.485、0.431,P值分别为＜0.05,＜0.01,＜0.01).经多元线性逐步回归分析表明:循环AngⅡ和Ald与左心房内径呈直线相关(Bate值分别为0.362、0.261,P＜0.01、P＜0.05).结论 MS患者存在循环肾素血管紧张素醛固酮系统(RAAS)的激活,循环AngⅡ和Ald可能与左心房重构有关.
目的 研究風濕性心髒病(風心病)二尖瓣狹窄(MS)患者血漿腎素血管緊張素醛固酮繫統的變化,併探討其與左心房重構的關繫.方法 MS組患者55例,按有無心房顫動分為2組:竇性心律組(SR組)25例,心房顫動組(AF組)30例.正常對照組(NC組)17例.應用放射免疫方法(RIA)測定清晨空腹臥位循環血漿腎素活性(PRA)、血管緊張素Ⅱ(Ang Ⅱ)、醛固酮(Ald)水平.結果 AF組左心房內徑與SR組、NC組相比顯著增大,分彆增大16.9%[(57.71±8.07)mm和(48.48±5.05)mm,P＜0.01)]與87.8%[(57.71±8.07)mm與(30.18±2.86)mm,P＜0.01],且SR組與NC組相比左心房內徑亦明顯增大,增大60.6%[(48.48±5.05)mm與(30.18±2.86)mm,P＜0.01)].AF、SR組患者循環PRA、AngⅡ、Ald濃度與NC組相比均顯著增高(P＜0.01),AF組與SR組相比循環PRA、AngⅡ、Ald濃度亦均明顯增高(P＜0.01,P＜0.05).應用Pearson相關分析顯示MS患者左心房內徑大小與循環PRA、AngⅡ、Ald濃度呈正相關繫(r分彆為0.277、0.485、0.431,P值分彆為＜0.05,＜0.01,＜0.01).經多元線性逐步迴歸分析錶明:循環AngⅡ和Ald與左心房內徑呈直線相關(Bate值分彆為0.362、0.261,P＜0.01、P＜0.05).結論 MS患者存在循環腎素血管緊張素醛固酮繫統(RAAS)的激活,循環AngⅡ和Ald可能與左心房重構有關.
목적 연구풍습성심장병(풍심병)이첨판협착(MS)환자혈장신소혈관긴장소철고동계통적변화,병탐토기여좌심방중구적관계.방법 MS조환자55례,안유무심방전동분위2조:두성심률조(SR조)25례,심방전동조(AF조)30례.정상대조조(NC조)17례.응용방사면역방법(RIA)측정청신공복와위순배혈장신소활성(PRA)、혈관긴장소Ⅱ(Ang Ⅱ)、철고동(Ald)수평.결과 AF조좌심방내경여SR조、NC조상비현저증대,분별증대16.9%[(57.71±8.07)mm화(48.48±5.05)mm,P＜0.01)]여87.8%[(57.71±8.07)mm여(30.18±2.86)mm,P＜0.01],차SR조여NC조상비좌심방내경역명현증대,증대60.6%[(48.48±5.05)mm여(30.18±2.86)mm,P＜0.01)].AF、SR조환자순배PRA、AngⅡ、Ald농도여NC조상비균현저증고(P＜0.01),AF조여SR조상비순배PRA、AngⅡ、Ald농도역균명현증고(P＜0.01,P＜0.05).응용Pearson상관분석현시MS환자좌심방내경대소여순배PRA、AngⅡ、Ald농도정정상관계(r분별위0.277、0.485、0.431,P치분별위＜0.05,＜0.01,＜0.01).경다원선성축보회귀분석표명:순배AngⅡ화Ald여좌심방내경정직선상관(Bate치분별위0.362、0.261,P＜0.01、P＜0.05).결론 MS환자존재순배신소혈관긴장소철고동계통(RAAS)적격활,순배AngⅡ화Ald가능여좌심방중구유관.
Objective To determine the relationship between the rennin-angiotensin-aldosterone systems(RAAS)and left atrial structure remodeling in patients with rheumatic mitral stenosis.Methods The patients with rheumatic mitral stenosis were divided into two groups according to atrial fibrillation:sinus rhythm group(SR group,n=25)and atrial fibrillation group(AF group,n=30).17 normal subjects were selected as normal control group(NC).The plasma concentration of renin,angiotonin Ⅱ(Ang Ⅱ)and aldosterone(Ald)were measured by radioimmunoassay(RIA).Results The average value of the left atrial diameter in AF group was significantly greater than that of both SR group and NC group,increased by 16.9%[(57.71±8.07)mm vs.(48.48±5.05)mm,P＜0.01)]and 87.8%(57.71±8.07 mm vs.30.18±2.85 mm,P＜0.01)respectively.Compared with NC group,the left atrial diameter of SR group was also significantly greater,elevated by 60.6%[(48.48±5.05)mm vs.(30.18±2.85)mm,P＜0.01)].The level of plasma rennin activity(PRA),Ang Ⅱ and Aid in AF and SR patients was significantly higher than those of NC subjects(P＜0.01),and compared with SR patients,the level of those in AF patients was also significantly increased(P＜0.01,P＜0.05).Pearson correlation analysis revealed a positive correlation between the plasma level of PRA,Ang Ⅱ or Ald and the value of the left atrial diameter(r=0.277,0.485,0.431,P＜0.05,P＜0.01,P＜0.01).Multiple liner stepwise regression analysis showed that plasma Ang Ⅱ and Ald were the important risk factors that affected left atrial diameter in patients with rheumatic mitral stenosis(Bate=0.362,0.261,P＜0.01,P＜0.05).Conclusion Patients with rheumatic mitral stenosis are characterized by the activation of circulating RAAS,and the plasma Ang Ⅱ and Ald may contribute to left atrial structure remodeling.
