頸動(dòng)脈粥樣硬化危險(xiǎn)因素及意義的研究進(jìn)展

楊　欣(綜述)，丁　毅(審校)

(桂林市人民醫(yī)院 a.重癥科，b.內(nèi)分泌科，廣西 桂林 541002)

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頸動(dòng)脈粥樣硬化危險(xiǎn)因素及意義的研究進(jìn)展

楊欣a(綜述)，丁毅b※(審校)

(桂林市人民醫(yī)院 a.重癥科，b.內(nèi)分泌科，廣西 桂林 541002)

摘要：頸動(dòng)脈粥樣硬化是指在頸動(dòng)脈任一部位存在動(dòng)脈粥樣斑塊，高血壓、糖尿病、肥胖、血脂異常、年齡、性別、吸煙、飲酒、尿酸、同型半胱氨酸都是導(dǎo)致頸動(dòng)脈粥樣硬化的獨(dú)立危險(xiǎn)因素。頸動(dòng)脈粥樣硬化可通過(guò)多普勒超聲檢測(cè)。頸動(dòng)脈粥樣硬化能預(yù)測(cè)腦卒中及冠狀動(dòng)脈粥樣硬化性心臟病的發(fā)病風(fēng)險(xiǎn)，因而研究頸動(dòng)脈粥樣硬化具有非常深遠(yuǎn)的意義。

關(guān)鍵詞：頸動(dòng)脈粥樣硬化；危險(xiǎn)因素；冠狀動(dòng)脈粥樣硬化性心臟??；腦卒中；

Research Progress on the Risk Factors and Clinical Significance of Carotid Atherosclerosis

YANGXina,DINGYib.(a.IntensiveCareUnit,b.DepartmentofEndocrinology,GuilinPeople′sHospital,Guilin541002,China)

Abstrac：Carotid atherosclerosis refers to the carotid artery plaque existed at any area of carotid artery.Independent risk factors of carotid atherosclerosis include high blood pressure,diabetes,obesity,dyslipidemia,age,gender,smoking,alcohol consumption,uric acid,homocysteine.Carotid atherosclerosis can be detected by doppler ultrasound and can predict the risk of stroke and coronary heart disease,therefore,research on carotid atherosclerosis has great significance.

Key words：Carotid atherosclerosis； Risk factor； Coronary heart disease； Stroke

頸動(dòng)脈粥樣硬化反映了總體動(dòng)脈硬化負(fù)荷，其是卒中形成的最主要因素[1-3]。頸動(dòng)脈粥樣硬化可通過(guò)多普勒超聲檢查，方法無(wú)創(chuàng)、簡(jiǎn)單，可觀察到動(dòng)脈粥樣斑塊、硬化及狹窄等。頸動(dòng)脈粥樣硬化能預(yù)測(cè)心、腦等重要器官的梗死，但其發(fā)病機(jī)制未明，其形成、發(fā)生、發(fā)展與多種危險(xiǎn)因素相關(guān)。現(xiàn)對(duì)導(dǎo)致頸動(dòng)脈粥樣硬化的危險(xiǎn)因素及其研究意義進(jìn)行綜述。

1導(dǎo)致頸動(dòng)脈粥樣硬化的危險(xiǎn)因素

1.1糖尿病糖尿病的發(fā)生、發(fā)展與頸動(dòng)脈粥樣硬化密切相關(guān)。1994年，社區(qū)動(dòng)脈粥樣硬化風(fēng)險(xiǎn)大型試驗(yàn)提示，肥胖、糖耐量異常與頸動(dòng)脈內(nèi)膜中層厚度呈正相關(guān)，糖尿病組患者的頸動(dòng)脈壁厚度較對(duì)照組增加0.07 mm，空腹糖耐量受損患者頸動(dòng)脈壁厚度較對(duì)照組增加 0.02 mm[4]。2003年，Wagenknecht等[5]就糖尿病與頸動(dòng)脈粥樣硬化的關(guān)系進(jìn)行研究發(fā)現(xiàn)，未經(jīng)診斷治療的糖尿病患者的內(nèi)膜-中層厚度(intima-media thickness,IMT)指數(shù)是已確診并治療的糖尿病和糖耐量減退患者的2倍。未經(jīng)診斷治療的糖尿病患者其頸動(dòng)脈粥樣硬化進(jìn)展快。Simsek等[6]對(duì)糖尿病患者頸動(dòng)脈和降主動(dòng)脈傳速進(jìn)行研究發(fā)現(xiàn)，糖尿病頸動(dòng)脈IMT顯著高于對(duì)照組，主動(dòng)脈傳播速度顯著低于對(duì)照組。因此，為預(yù)防動(dòng)脈粥樣硬化的發(fā)生和發(fā)展就必須對(duì)糖尿病患者進(jìn)行嚴(yán)格治療。

1.2高血壓高血壓可促進(jìn)動(dòng)脈粥樣硬化的發(fā)展。2001年一項(xiàng)臺(tái)灣社區(qū)的研究顯示，患有高血壓、左心室肥厚、年齡>65歲的患者患頸動(dòng)脈粥樣硬化風(fēng)險(xiǎn)更大，其中高血壓和吸煙是頸動(dòng)脈狹窄≥50%的重要影響因素[7]。Casalnuovo等[8]對(duì)6209例患有高血壓而無(wú)冠狀動(dòng)脈粥樣硬化性心臟病(冠心病)的患者進(jìn)行調(diào)查發(fā)現(xiàn)，平均動(dòng)脈壓高及心輸出量過(guò)高是頸動(dòng)脈硬化的獨(dú)立因素。預(yù)防動(dòng)脈粥樣硬化性疾病必須嚴(yán)格控制血壓，尤其是平均動(dòng)脈壓。

1.3血脂異常以往觀點(diǎn)認(rèn)為，高脂血癥通常是指低密度脂蛋白(low-density lipoprotein，LDL)的增高。低密度脂蛋白膽固醇(low density lipoprotein-cholesterol，LDL-C)是主要的膽固醇載脂蛋白[9]，其不僅作用于外周器官而且還作用于動(dòng)脈血管壁[10]。2011年，Khera等[10]提出，高密度脂蛋白(high densitv lipoprotein，HDL)能從巨噬細(xì)胞中搬運(yùn)膽固醇，HDL-C與IMT呈負(fù)相關(guān)。2011年歐洲血脂異常治療指南提出，LDL-C仍是血脂干預(yù)的首要目標(biāo)，是最主要的干預(yù)靶點(diǎn)，HDL-C水平升高可預(yù)測(cè)動(dòng)脈粥樣硬化斑塊的消退，其與動(dòng)脈斑塊硬化呈負(fù)相關(guān)[11]。因此，預(yù)防和延緩頸動(dòng)脈斑塊的血脂異常應(yīng)以LDL-C作為重中之重。

1.4肥胖肥胖是頸動(dòng)脈粥樣硬化疾病的一個(gè)獨(dú)立危險(xiǎn)因素。Urbina等[12]將肥胖年輕人以及伴有肥胖相關(guān)的2型糖尿病患者與體型較瘦的研究對(duì)象進(jìn)行比較發(fā)現(xiàn)，兩者頸動(dòng)脈硬化指數(shù)與IMT均大于體型較瘦者。Herouvi等[13]的最新報(bào)道指出，兒童型肥胖患者動(dòng)脈血管的結(jié)構(gòu)和功能會(huì)在兒童時(shí)期就開(kāi)始改變，具體機(jī)制不明確。因此，對(duì)于肥胖人群動(dòng)脈病變的監(jiān)測(cè)和預(yù)防不容忽視。

1.5年齡年齡與頸動(dòng)脈粥樣硬化的相關(guān)性已受到關(guān)注，年齡>65歲的老年人危險(xiǎn)因素較多，常合并心腦血管及其他血栓形成等疾病造成的靶器官損害[14-16]。防治頸動(dòng)脈粥樣硬化應(yīng)把老年人作為重點(diǎn)對(duì)象。同時(shí)，合并危險(xiǎn)因素的青年患者發(fā)病率也不容忽視。2009年，Urbina等[12]對(duì)10~24歲的青年人進(jìn)行調(diào)查發(fā)現(xiàn)，合并有肥胖、肥胖相關(guān)性2型糖尿病的青年人頸動(dòng)脈硬化指數(shù)高于體型瘦弱組。在有這些危險(xiǎn)因素的青年人群中，心腦血管事件及心肌梗死的發(fā)病率增加。

1.6性別2004年，Iemolo等[17]對(duì)性別與頸動(dòng)脈病變進(jìn)行研究時(shí)發(fā)現(xiàn)，在所有年齡段中，女性頸動(dòng)脈狹窄重于男性，但男性的頸動(dòng)脈斑塊多于女性。頸動(dòng)脈粥樣斑塊能預(yù)測(cè)卒中、心肌梗死和猝死，因此男性頸動(dòng)脈病變?cè)斐傻牟l(fā)癥更多。女性頸動(dòng)脈粥樣硬化發(fā)病率相對(duì)男性低，可能與雌激素通過(guò)雌激素受體作用于全身內(nèi)皮細(xì)胞和平滑肌細(xì)胞，舒張血管，并通過(guò)降低LDL-C、增高HDL-C等機(jī)制保護(hù)血管內(nèi)皮細(xì)胞有關(guān)。de Weerd等[18]的試驗(yàn)印證了這一點(diǎn)，在無(wú)癥狀頸動(dòng)脈粥樣硬化中，男性頸動(dòng)脈病變疾病的患病率更高。

1.7吸煙吸煙是動(dòng)脈粥樣硬化的獨(dú)立因素，其與頸動(dòng)脈粥樣硬化呈正相關(guān)。Kallio等[19]報(bào)道，在8~13歲的吸煙人群中，煙齡越長(zhǎng)，頸動(dòng)脈IMT越大；抽煙越頻繁，IMT越大，載脂蛋白B(apolipoprotein-B，apoB)及apoB/apoA明顯增高。Anazawa等[20]發(fā)現(xiàn)，暴露在吸煙環(huán)境下的大鼠，其頸動(dòng)脈IMT增厚，一氧化氮合酶增高，硝酸鹽產(chǎn)生，中層平滑肌細(xì)胞增殖，最后導(dǎo)致IMT增大。

1.8飲酒Kiechl等[21]將40~79歲的飲酒人群作為研究對(duì)象，規(guī)律飲酒與頸動(dòng)脈粥樣硬化存在J曲線。少量飲酒者的患病風(fēng)險(xiǎn)低于大量飲酒者和不飲酒者，每日攝入50 g酒精者有更高的LDL-C，大量飲酒者硬化負(fù)荷明顯增高，飲酒與動(dòng)脈粥樣硬化呈劑量依賴性相關(guān)。Mukamal等[22]的研究證實(shí)，老年人飲酒量越大，IMT越厚。每周28~168 g的飲酒量與動(dòng)脈粥樣硬化呈負(fù)相關(guān)，每周>392 g的飲酒量與動(dòng)脈粥樣硬化呈正相關(guān)。2012年，Xie等[23]調(diào)查了13 037例中國(guó)人發(fā)現(xiàn)，在漢族和哈薩克族人群中，飲酒與頸動(dòng)脈粥樣硬化相關(guān)，而少量飲酒與頸動(dòng)脈粥樣硬化呈負(fù)相關(guān)，但維吾爾族不符合這個(gè)規(guī)律。所以，少量飲酒可以預(yù)防和延緩頸動(dòng)脈粥樣硬化疾病，而酗酒則可促進(jìn)頸動(dòng)脈粥樣硬化的發(fā)生與發(fā)展。

1.9尿酸對(duì)4866例參與者進(jìn)行橫斷面研究發(fā)現(xiàn)，在男性中，隨著尿酸水平的增高，動(dòng)脈粥樣斑塊會(huì)增加，但女性尿酸水平與動(dòng)脈粥樣硬化無(wú)必然聯(lián)系[24]。一些研究猜測(cè)，血清中高尿酸水平可能與內(nèi)皮細(xì)胞[25]以及血小板活動(dòng)[26-27]有關(guān)。尿酸可促進(jìn)平滑肌細(xì)胞增殖及生長(zhǎng)因子的表達(dá)。尿酸可使單核細(xì)胞產(chǎn)生白細(xì)胞介素1β、白細(xì)胞介素6、腫瘤壞死因子α及C反應(yīng)蛋白[28-30]。尿酸是致動(dòng)脈粥樣硬化的一個(gè)獨(dú)立危險(xiǎn)因素。

1.10同型半胱氨酸(homocysteine，Hcy)血清Hcy在動(dòng)脈粥樣硬化中的作用已經(jīng)被報(bào)道過(guò)[31-32]。Hcy被認(rèn)為是冠心病的一項(xiàng)獨(dú)立危險(xiǎn)因子[33]。在動(dòng)物實(shí)驗(yàn)中，Hcy與血管氧化負(fù)荷增加密切相關(guān)[34]。Hcy誘導(dǎo)還原型煙酰胺腺嘌呤二核苷酸磷酸氧化酶和一氧化氮生成，最后導(dǎo)致血管超氧化物蓄積。另外，細(xì)胞內(nèi)抗氧化歧化酶和谷胱甘肽發(fā)生改變[35]。所以，Hcy對(duì)動(dòng)脈粥樣硬化的作用應(yīng)引起重視。

2頸動(dòng)脈粥樣硬化的研究意義

2.1頸動(dòng)脈粥樣硬化與冠心病的相關(guān)性頸動(dòng)脈粥樣硬化與冠心病密切相關(guān)。Craven等[36]對(duì)有冠心病危險(xiǎn)因素的患者行多普勒超聲檢查發(fā)現(xiàn)，年齡>50歲的患者，冠狀動(dòng)脈病變的嚴(yán)重程度與頸動(dòng)脈病變范圍密切相關(guān)，尤其是女性。Sirimarco等[37]對(duì)23 364例有頸動(dòng)脈粥樣硬化的患者進(jìn)行為期4年的調(diào)查發(fā)現(xiàn)，46%的患者患冠心病的危險(xiǎn)性增加，部分患者發(fā)生了其他血管疾病，總體心血管事件增加了22%。頸動(dòng)脈病變?cè)u(píng)分與冠心病緊密相關(guān)，頸動(dòng)脈粥樣硬化病變可作為冠心病事件的獨(dú)立預(yù)測(cè)因子。

2.2頸動(dòng)脈粥樣硬化與腦卒中的相關(guān)性頸動(dòng)脈粥樣硬化與腦卒中息息相關(guān)，但其發(fā)生、發(fā)展所引起血小板聚集、血管狹窄，最后導(dǎo)致短暫性腦缺血發(fā)作或者卒中事件的機(jī)制是復(fù)雜的。無(wú)癥狀頸動(dòng)脈粥樣硬化引起的卒中目前尚不明確，治療也收效甚微。顱外動(dòng)脈硬化疾病在所有缺血性卒中占15%~20%。北美癥狀性頸動(dòng)脈內(nèi)膜切除術(shù)試驗(yàn)協(xié)作組的實(shí)驗(yàn)證明，頸動(dòng)脈狹窄程度與卒中風(fēng)險(xiǎn)呈顯著的正相關(guān)[37]。無(wú)癥狀的頸動(dòng)脈狹窄與卒中風(fēng)險(xiǎn)不是很明確。18個(gè)月的非再生藥物治療后，頸動(dòng)脈狹窄在70%~79%的卒中發(fā)病率是19%，狹窄在80%~89%的卒中發(fā)病率是28%，狹窄在90%~99%的卒中發(fā)病率是33%。在動(dòng)脈粥樣硬化研究和手術(shù)治療研究中，60%~80%頸動(dòng)脈狹窄無(wú)癥狀患者比其他狹窄患者患卒中的風(fēng)險(xiǎn)更高[38-40]。

3小結(jié)

頸動(dòng)脈粥樣硬化是多種因素所導(dǎo)致的疾病，它反映了全身血管的病變情況，并且能預(yù)知心腦血管事件和其他血管血栓形成疾病的發(fā)生，對(duì)于頸動(dòng)脈粥樣硬化患者，應(yīng)預(yù)防、嚴(yán)格控制上述多種危險(xiǎn)因素，必要時(shí)行干預(yù)治療，防止重要器官發(fā)生血管意外。頸動(dòng)脈粥樣硬化發(fā)生的機(jī)制尚未明確，針對(duì)頸動(dòng)脈粥樣硬化疾病的因素仍待進(jìn)一步發(fā)掘與探索。

參考文獻(xiàn)

[1]Young W,Gofman JW,Tandy R,etal.The quantitation of atherosclerosis.Ⅱ.Quantitative aspects of the relationship of blood pressure and atherosclerosis[J].Am J Cardiol,1960,6:294-299.

[2]Mitchell JR,Schwartz CJ.Relationship between arterial disease in different sites:a study of the aorta and coronary,carotid,and iliac arteries[J].Br Med J,1962,1(5288):1293-1301.

[3]Craven TE,Ryu JE,Espeland MA,etal.Evaluation of the associations between carotid artery atherosclerosis and coronary artery stenosis:a case-control study[J].Circulation,1990,82(4):1230-1242.

[4]Folsom AR,Eckfeldt JH,Weitzman S,etal.Relation of carotid artery wall thickness to diabetes mellitus,fasting glucose and insulin,body size,and physicalactivity.Atherosclerosis Risk in Communities (ARIC) Study Investigators[J].Stroke,1994,25(1):66-73.

[5]Wagenknecht LE,Zaccaro D,Espeland MA,etal.Diabetes and progression of carotid atherosclerosis: the insulin resistance atherosclerosis study[J].Arterioscler Thromb Vasc Biol,2003,23(6):1035-1041.

[6]Simsek H,Sahin M,Gunes Y,etal.A novel echocardiographic method for the detection of subclinical atherosclerosis in newly diagnosed,untreated type 2 diabetes[J].Echocardiography,2013,30(6):644-648.

[7]Su TC,Jeng JS,Chien KL,etal.Hypertension status is the major determinant of carotid atherosclerosis:a community-based study in Taiwan[J].Stroke,2001,32(10):2265-2271.

[8]Casalnuovo G,Gerdts E,de Simone G,etal.Arterial stiffness is associated with carotid atherosclerosis in hypertensive patients (the Campania Salute Network)[J].Am J Hypertens,2012,25(7):739-745.

[9]Wilson PW.High-density lipoprotein,low-density lipoprotein and coronary artery disease[J].Am J Cardiol,66(6):7A-10A.

[10]Khera AV,Cuchel M,de la Llera-Moya M,etal.Cholesterol efflux capacity,high-density lipoprotein function,and atherosclerosis[J].N Engl J Med,2011,364(2):127-135.

[11]Reiner,Catapano AL,De Backer G,etal.ESC/EAS Guidelines for the management of dyslipidaemias[J].Rev Esp Cardiol,2011,64(12):1168.e1-60.

[12]Urbina EM,Kimball TR,McCoy CE,etal.Youth with obesity and obesity-related type 2 diabetes mellitus demonstrate abnormalities in carotid structure and function[J].Circulation,2009,119(22):2913-2919.

[13]Herouvi D,Karanasios E,Karayianni C,etal.Cardiovascular disease in childhood: the role of obesity[J].Eur J Pediatr,2013,172(6):721-732.

[14]Kragsterman B,Bj?rck M,Lindb?ck J,etal.Long-term survival after carotid endarterectomy for asymptomatic stenosis[J].Stroke,2006,37(12):2886-2891.

[15]Romero JR,Beiser A,Seshadri S,etal.Carotid artery atherosclerosis,MRI indices of brain ischemia,aging,and cognitive impairment:the Framingham study[J].Stroke,2009,40(5):1590-1596.

[16]Calvet D,Mas JL.Carotid stenosis in elderly patients[J].Rev Prat,2012,62(9):1234-1238.

[17]Iemolo F,Martiniuk A,Steinman DA,etal.Sex differences in carotid plaque and stenosis[J].Stroke,2004,35(2):477-481.

[18]de Weerd M,Greving JP,de Jong AW,etal.Prevalence of asymptomatic carotid artery stenosis according to age and sex:systematic review and metaregression analysis[J].Stroke,2009,40(4):1105-1113.

[19]Kallio K,Jokinen E,Saarinen M,etal.Arterial intima-media thickness,endothelial function,and apolipoproteins in adolescents frequently exposed totobacco smoke[J].Circ Cardiovasc Qual Outcomes,2010,3(2):196-203.

[20]Anazawa T,Dimayuga PC,Li H，etal.Effect of exposure to cigarette smoke on carotid artery intimal thickening:the role of inducible NO synthase[J].Arterioscler Thromb Vasc Biol,2004,24(9):1652-1658.

[21]Kiechl S,Willeit J,Rungger G,etal.Alcohol Consumption and Atherosclerosis:What Is the Relation?Prospective Results From the Bruneck Study[J].Stroke,1998,29(5):900-907.

[22]Mukamal KJ,Kronmal RA,Mittleman MA,etal.Alcohol consumption and carotid atherosclerosis in older adults:The Cardiovascular Health Study[J].Arterioscler Thromb Vasc Biol,2003,23(12):2252-2259.

[23]Xie X,Ma YT,Yang YN,etal.Alcohol consumption and carotid atherosclerosis in China:the Cardiovascular Risk Survey[J].Eur J Prev Cardiol,2012,19(3):314-321.

[24]Neogi T,Ellison RC,Hunt S，etal.Serum uric acid is associated with carotid plaques:the National Heart,Lung,and Blood Institute Family Heart Study[J].J Rheumatol,2009,36(2):378-384.

[25]Kanellis J,Kang DH.Uric acid as a mediator of endothelial dysfunction,inflammation,and vascular disease[J].Semin Nephrol,2005,25(1):39-42.

[26]Lippi G,Montagnana M,Franchini M,etal.The paradoxical relationship between serum uric acid and cardiovascular disease[J].Clin Chim Acta,2008,392(1/2):1-7.

[27]Johnson RJ,Kang DH,Feig D,etal.Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease?[J].Hypertension,2003,41(6):1183-1190.

[28]Ishiro M,Takaya R,Mori Y,etal.Association of Uric Acid with Obesity and Endothelial Dysfunction in Children and Early Adolescents[J].Ann Nutr Metab,2013,62(2):169-176.

[29]Ishizaka N,Ishizaka Y,Toda E,etal.Higher serum uric acid is associated with increased arterial stiffness in Japanese individuals[J].Atherosclerosis,2007,192(1):131-137.

[30]Kawamoto R,Tomita H,Oka Y,etal.Relationship between serum uric acid concentration,metabolic syndrome and carotid atherosclerosis[J].Intern Med,2006,45(9):605-614.

[31]Akalin A,Alatas O,Colak O.Relation of plasma homocysteine levels to atherosclerotic vascular disease and inflammation markers in type 2 diabetic patients[J].Eur J Endocrinol,2008,158(1):47-52.

[32]Zhou J,M?ller J,Danielsen CC,etal.Dietary supplementation with methionine and homocysteine promotes early atherosclerosis but not plaquerupture in ApoE-deficient mice[J].Arterioscler Thromb Vasc Biol,2001,21(9):1470-1476.

[33]Christen WG,Ajani UA,Glynn RJ,etal.Blood levels of homocysteine and increased risks of cardiovascular disease: causal or casual?[J].Arch Intern Med,2000,160(4):422-434.

[34]Wang H,Jiang X,Yang F,etal.Hyperhomocysteinemia accelerates atherosclerosis in cystathionine beta-synthase and apolipoprotein E doubleknock-out mice with and without dietary perturbation[J].Blood,2003,101(10):3901-3907.

[35]Ungvari Z,Csiszar A,Edwards JG,etal.Increased superoxide production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha,NAD(P)H oxidase,and inducible nitric oxide synthase[J].Arterioscler Thromb Vasc Biol,2003,23(3):418-424.

[36]Craven TE,Ryu JE,Espeland MA,etal.Evaluation of the associations between carotid artery atherosclerosis and coronary artery stenosis.A case-control study[J].Circulation,1990,82(4):1230-1242.

[37]Sirimarco G,Amarenco P,Labreuche J,etal.Carotid atherosclerosis and risk of subsequent coronary event in outpatients with atherothrombosis[J].Stroke,2013,44(2):373-379.

[38]Clinical alert:benefit of carotid endarterectomy for patients with high-grade stenosis of the internal carotid artery.National Institute of Neurological Disorders and Stroke Stroke and Trauma Division[J].Stroke,1991,22(6):816-817.

[39]Young B,Moore WS,Robertson JT,etal.An analysis of perioperative surgical mortality and morbidity in the asymptomatic Carotid Artheriosclerisis study ACAS Investigators.Asymptomatic Carotid Artheriosclerosis Study[J].Strock,1996,27(12):2216-2224.

[40]Halliday AW,Thomas D,Mansfield A.The Asymptomatic Carotid Surgery Trial (ACST).Rationale and design.Steering Committee[J].Eur J Vasc Surg,1994,8(6):703-710.

收稿日期：2013-10-31修回日期：2014-04-20編輯：辛欣

基金項(xiàng)目：自籌經(jīng)費(fèi)科研項(xiàng)目(2.2013452)

doi：10.3969/j.issn.1006-2084.2015.02.017

中圖分類(lèi)號(hào)R543.4

文獻(xiàn)標(biāo)識(shí)碼：A

文章編號(hào)：1006-2084(2015)02-0239-03