新疆地区不同民族心脏瓣膜病流行病学研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的:
     心脏瓣膜病(valvular heart disease,VHD)是新疆地区一种常见的危害健康的心血管疾病。本研究目的在于了解新疆地区成年人心脏瓣膜病的患病率情况及其分布特征,探讨新疆地区老年人群退行性心脏瓣膜病的患病率情况及可能存在的危险因素,探讨新疆地区成年人退行性心脏瓣膜病与动脉粥样硬化的关系,为心脏瓣膜病的防治提供科学依据。
     方法:
     应用四阶段随机整群抽样法,在整个新疆地区抽取首府乌鲁木齐市及其周边的阜康市,北疆地区的克拉玛依市、阿勒泰地区、伊犁地区,东疆地区的的吐鲁番地区,南疆地区的和田地区等地的年龄在35岁以上成年人样本,男女均衡。统计不同民族组、不同年龄组、不同性别组、不同地区组35岁以上成年人群心脏瓣膜病的患病率,分析心脏瓣膜病伴发的心血管基础疾病情况。统计不同年龄组、不同民族组、不同性别组60岁以上老年人群退行性心脏瓣膜病的患病率,分析瓣膜钙化患病率与高血压的关系,应用多因素Logistic逐步回归分析退行性心脏瓣膜病患病的相关危险因素。统计不同民族组、不同性别组、不同年龄组颈动脉粥样硬化患病率,统计不同民族、不同性别、不同年龄颈动脉粥样硬化组瓣膜钙化患病率,不同民族、不同性别、不同年龄瓣膜钙化组颈动脉粥样硬化患病率,探讨颈动脉粥样硬化与退行性心脏瓣膜病的关系.
     结果:
     (1)共抽取35岁以上成年人群14618人,实际完成心脏超声检查的14478人,新疆地区心脏瓣膜病的总体患病率为9.65%,其中男性为9.65%,女性为9.63%,不同民族人群心脏瓣膜病患病率为:汉族13.5%,维吾尔族2.7%,哈萨克族12.3%。经年龄标准化后,汉族、维吾尔族、哈族患病率分别为10.57%、2.36%、12.22%,不同民族心脏瓣膜病患病率比较差异有统计学意义;城镇人群与农牧区人群心脏瓣膜病患病率比较差异有统计学意义;汉族与哈萨克族人群城乡心脏瓣膜病患病率比较无统计学差异,维吾尔族城镇人群与农牧区人群心脏瓣膜病患病率比较差异有统计学意义;心脏瓣膜病患病率随年龄增长逐渐升高。全部心脏瓣膜病患者中合并高血压病者63.2%,糖尿病者7.6%,冠心病者7.5%,心脏瓣膜病者3.2%。
     (2)共抽取60岁以上老年人样本3773人,新疆地区60岁以上老年人群退行性心脏瓣膜病的总体患病率是9.0%,其中男性为10.2%,女性为7.9%,不同性别老年退行性心脏瓣膜病患病率比较差异有统计学意义;维吾尔族患病率为3.7%,汉族为13.2%,哈族为8.5%,不同民族老年退行性心脏瓣膜病患病率比较差异有统计学意义;老年退行性心脏瓣膜病发生风险随年龄增高逐渐升高;在发生钙化的瓣膜中,单纯主动脉瓣钙化占67.4%,单纯二尖瓣钙化占17.9%,二尖瓣+主动脉瓣联合钙化占14.7%;男性与女性瓣膜钙化都是以主动脉瓣钙化为主;汉族与哈萨克族都是以主动脉瓣钙化为主;不同性别、不同民族瓣膜钙化组与无瓣膜钙化组高血压、冠心病等常见心血管疾病患病率比较差异有统计学意义,不同民族、不同性别高血压组与无高血压组瓣膜钙化患病率比较差异有统计学意义;经logistic多因素逐步回归分析显示:年龄、民族、吸烟、高血压、心衰是老年退行性心脏瓣膜病的危险因素,其中年龄是最大的危险因素,高血压、吸烟、心衰的人群患老年退行性心脏瓣膜病的风险分别是无高血压、无吸烟、无心衰人群的1.019、1.612、1.874倍。
     (3)共抽取35岁以上成年人样本14618人,实际完成颈动脉超声检查的13896人,新疆地区成年人群颈动脉粥样硬化患病率为35.5%,其中男性为41.5%,女性为30.2%,不同性别颈动脉粥样硬化患病率比较差异有统计学意义;维吾尔族颈动脉粥样硬化患病率为30.9%,哈萨克族为42.1%,汉族为34,3%,不同民族颈动脉粥样硬化患病率比较差异有统计学意义;颈动脉粥样硬化患病率随年龄增长而逐渐升高;在汉族与维吾尔族检出的颈动脉粥样硬化人群中,不同性别颈动脉粥样硬化患病率比较差异有统计学意义;颈动脉粥样硬化组与无颈动脉粥样硬化组瓣膜钙化患病率比较差异有统计学意义,瓣膜钙化组与无瓣膜钙化组颈动脉粥样硬化患病率比较差异有统计学意义。
     结论:
     (1)新疆地区成年人心脏瓣膜病的患病率高于国内有关研究结果,心脏瓣膜病患病率随年龄升高,并存在民族、城乡差异;汉族与哈萨克族城乡心脏瓣膜病患病率城乡差别不大,维吾尔族人群存在着明显的城乡差异;新疆地区成年人心脏瓣膜病患者合并的主要心血管基础疾病是高血压、糖尿病、冠心病。
     (2)新疆地区60岁以上老年人老年退行性心脏瓣膜病的患病率接近国内相关研究结果,老年退行性心脏瓣膜病患病率随年龄升高,并且存在着民族和性别差异;高血压、冠心病等疾病组更易出现心脏瓣膜钙化,同时心脏瓣膜钙化组也更易出现高血压,提示二者可能具有一定的相关性;年龄、民族、吸烟、高血压、心衰是老年退行性心脏瓣膜病的主要危险因素。
     (3)新疆地区成年人颈动脉粥样硬化患病率接近国内相关研究结果,颈动脉粥样硬化患病率随年龄增高,颈动脉粥样硬化者更容易发生心脏瓣膜钙化,同时退行性心脏瓣膜病钙化组也更容易发生颈动脉粥样硬化,提示颈动脉粥样硬化与退行性心脏瓣膜病这两种疾病可能具有一定相关性。
Objective:
     Valvular Heart Diseases (VHD) is a common disease with high death rate and pooroutcome and it not only endangered people's life but also influenced the quality of life ofpeople and at the same time, it brought heavy burden and pressure to the family andsociety. With improved of diagnosis and treatment technology of cardiovascular disease,the early mortality of cardiovascular disease has greatly reduced, which was high fatalityrate in acute phase of heart disease in the past. However, the incidence and mortality ratesof heart valve disease which still threat seriously to human health has still high.Andtherefore to realize fully the present situation of heart valve disease, to diagnose thisdisease in time and to definite clearly its etiology is the precondition of specific therapy.This study is order to investigate prevalence and distribution of valvular heart diseaseamong adult population in different ethnic groups in Xiniang region, to analyze possiblerisk factors and the correlation between valvular heart disease and carotid atherosclerosis,giving some reliable epidemiological data for the diagnosis and treatment strategies ofvalvular heart disease.
     Materials and methods:
     (1) Study of prevalence and distribution among adult population in different ethnicgroups in Xinjiang: To investigate the prevalence and distributing feature of heartvalvular diseases (VHD) in Xinjiang adult population: Four-stage selected randomsamples from age35and over were used to analyze the prevalence and distributingfeature of heart valvular diseases in different nationality, age, sex and the sampled adultpopulation were collected6locality (Urumqi, Kelamayi, Fukang, the Turfan Basinlocality, Hetian locality, Altay locality, Yili Hazakh autonomous prefecture) from23municipalities,7locality and5autonomous county in Xinjiang. The proportion of male to female accounted for50%.Every subject filled a questionnaire and received Dopplerechocardiographic examination for an observation of the function of valve, opening andclosing activities of valve and evaluating degree of valvular stenosis and valvularregurgitation. Statistic analysis and calculate the prevalence and distribution of valvularheart disease in different sexes, different ethnic groups and different age groups amongadult population in Xinjiang, as well as to analyzed complications of cardiovasculardisease in different populations.
     (2) Epidemiological cross-sectional survey of correlated factors and prevalence ondegenerated valvular heart diseases among older population in different ethnic groups inXinjiang: The same population were enrolled and60years old or above individuals wererandomly selected. And then the sample individuals were divided into different ethnicgroups, different age groups, different sex groups.The sampled population were collected6locality (Urumqi, Ke lamayi, Fu kang, the Turfan Basin locality, He tian locality, Altaylocality, Yi li Hazakh autonomous prefecture) from23municipalities and7locality and5autonomous county in Xin jiang. Each individual filled a questionnaire and receivedDoppler echocardiographic examination for an observation of the function of valve,opening and closing activities of valve and evaluating degree of valvular stenosis andvalvular regurgitation. A logistic regression analysis is also made to identify possible riskfactors with SDVHD and to analyze relationship between hypertension and valvecalcification.
     (3) Study on the correlation between degenerative valvular heart disease and carotidatherosclerosis: The same population were enrolled and each individual received Dopplerultrsonic examination for observation of the heart and carotid artery. To statistic analyzeand calculate of the prevalence of CAS and DVHD and relationship between CAS andDVHD.
     Result:
     (1) The prevalence of valvular heart disease was7.67%(male:7.31%vs female:8.00%). The prevalence of valvular heart disease was10.57%,2.36%, and12.22%inHan, Uygur and Kazakh population, respectively. The prevalence of valvular heartdisease was more lower in Uygur than Hazak and Han people. Among Uygur population,the prevalence of valvular heart disease was more higher in urban areas than inagricultural and pastoral areas.The differences of prevalence of valvular heart diseaseamong Han and Kazakh population between in urban areas and in agricultural and pastoral areas was no statistically significant. Common complications of valvular heartdisease was hypertension (63.2%), diabetes (7.6%), coronary heart disease (7.5%), andfibrillation atrial (3.2%).
     (2) The prevalence of senile degenerative valvular heart disease among older peoplein Xinjiang is9.0%, of which males taked10.2%while females taked14.7%.Amongthem, there are significant difference between different age groups, and there aresignificant difference between different gender, and there are significant differencebetween different nationalities population. In all341cases of calcificated valve, aoticvalvular calcification is67.4%of, mitral valve calcification is17.9%of, mitral valvewith combined aotic valvular calcification is14.7%of. Most common types of valvecalcification among male and female population are aortic valve calcification; there areno significant difference between male and female. Most of valvular calcification in Hanpeople and Kazkh people were aotic valve calcification, and valvular calcification inUygur people were aotic valve calcification and mitral valve with combined aoticvalvular calcification, taked of44.7%, respectively. The prevalence of valve calcificationis higher in hypertension groups in different gender and different ethnic groups, and theprevalence of hypertension is higher in valve calcification groups.Logistic regressionanalysis showed that the risk factors of SDVHD are age, nationality, smoking,hypertension and heart failure.
     (3) The prevalence rates of CAS among adult people in Xinjiang were35.5%androse with increasing age. In non-carotid atherosclerosis group, The prevalence rate ofvalvular calcification in non-carotid atherosclerosis groups is2.5%, and the prevalencerate of valvular calcification in carotid atherosclerosis groups is3.7%, and the differenceof prevalence between the two groups was statistically significant.The prevalence rate ofCAS in non-valvular calcification is35.2%, and the prevalence rate of CAS in valvularcalcification is45.1%, and the difference of prevalence between the two groups wasstatistically significant.
     Conclution:
     (1) The prevalence rates of valvular heart disease increased substantially with age.There was difference between different nationalities and areas. Common complicationsof valvular heart disease was hypertension, diabetes, coronary heart disease andfibrillation atrial.
     (2) The prevalence of SDVHD increased substantially with age.crease of age. The fact that valvular calcification groups had higher prevalence rate of hypertension and thathypertension groups had higher prevalence rate of valvular calcification, suggested thatthe two diseases may be related to each other.SDVHD risk factors include age,nationality, smoking, hypertension, and heart failure.
     (3) The prevalence rates of CAS among the adult population in Xinjiang rose withincreasing age. The fact that carotid atherosclerosis groups had higher prevalence rate ofheart valvular calcification and that heart valvular calcification groups had higherprevalence rate of carotid atherosclerosis, suggested that the two diseases may be relatedto each other.
引文
[1] Kannel WB, Ho K, Thom T. Changing epidemiological features of cardiac failure.Br Heart J,1994,72:S3~S9.
    [2]陆再英,钟南山,主编内科学.第7版.北京:人民卫生出版社,2006.170~179.
    [3]戚文航.心力衰竭的流行病学及治疗进展.现代实用医学,2004,16:6632~6634.
    [4]顾东风,黄广勇,何江,等.中国心脏瓣膜病流行病学调查及其患病率.中华心血管病杂志,2003,31:3~6.
    [5]何秉贤,朱徐,黄定,等.新疆汉维吾尔哈萨克三民族高血压流行病学调查.新疆医学,1992,22:194~201.
    [6] Hiroshi K, Medet J, H iromiM, et al.242hour, blood pressure in Uygur, Kazakh andhan elderly subjects in China. Hypertens Res,2000,23:177~185.
    [7] American Heart Association.2002Heart and Stroke Statistical Up data. Dallas,TX:American Heart Association,2002:19.
    [8]徐新娟,汪师贞,等.新疆地区高血压流行病学调查研究回顾.新疆医科大学学报,2004,27:312~314
    [9]陈国伟.心力衰竭流行病学特点及变迁.2002,18:12
    [10]王长厚,陈树平,彭万忠.1164例心血管住院病人慢性心脏瓣膜病病因分析.中国医刊.2002,31:25~26
    [11] Wolf PAS, Mitchell JB, Baker CS, et al. Impact of atrial fibrillation on mortality,stroke, and medical costs[J]. Arch Intern Med,1998,158:229 234.
    [12] Furberg CD, Manolio TA, Gardin JM, et al. Rautaharju PM. Prevalence of atrialfibrillation in elderly subjects(the cardiovasular health study)[J]. Am J Cardiol,1994,74:236 241.
    [13] Kannel WB, Savage DD, Mcnamara PM, et al. Coronary heart disease and atrialfibrillation:the Framingham study[J]. Am Heart J,1983,106:389 396.
    [14] Friberg J, Scharling H, Gadsboll N, et al. Sex specific increase in the prevalenceof atrial fibrillation(The Copenhagen City Heart Study)[J]. Am J Cardiol,2003,92(12):1419 1423.
    [15] Levy S, Coumel P. Charaterization of different subsets of atrial fibrillation ingeneral practice in France:the ALFA study[J]. Circulation,1999,99:3028 3035.
    [16] Murgatroyd FD, Baiyan X. Double blind placebocontrolled trial of digoxin insymptomatic paroxysmal artrial fibrillation[J]. Circulation,1999,99:2765 2770.
    [17] MacIntyre K, Capewell S, Stewart S, et al. Evidence of improving prognosis inheart failure:trends in颈动脉粥样硬化e fatality in66,547patients hospitalizedbetween1986and1995[J]. Circulation,2000,102:1126 1131.
    [18] Palmieri v, Arnett UP, Roman MJ Appetite suppressants and valvular heart diseasein a population~based sample:the HyperGEN study. Am J Med,2002,112:710~715.
    [19] George R, McMahon J, Lytle B, et al. Severe valvular and aortic arch calcificationin a patient with Gaucher's disease homozygous for the D409H mutation. ClinGenet,2001,59:360~363.
    [20]范甲卯,孟方,樊小莉,等.老年退行性心脏瓣膜病患病情况调查分析.中国慢性病预防与控制,2000,8:37~38.
    [21] Branch KR, O' Brien KD, Otto CM. Aortic valve sclerosis is as a marker of activeatherosclerosis. Curr Cardiol Rep,2002,4:111~117.
    [22] Mehrabi MR, Sinzinger H, Ekmekcioglu C, et al. Accumulation of oxidized LDL inhuman semilunar valves correlates with coronary atherosclerosis. Cardiovasc Res,2000,45:874~882.
    [23] Rose AG. Etiology of valvular heart disease. Curr Opin Cardiol,1996,11:98~113.
    [24] Aronne I. J. Modern medical management of obesity:the role of pharmaceuticalintervention. J Am Diet Assoc,1998,98:s23~s26.
    [25] Ferara IA, Mancin M, Celetano M, et al. Early changes of the arterial wall inuncomplicated primary hypertensive patients study by ultrasound high~resolutionB~mode imaging. Arterioscler Thromb,1994,14:1290~1294.
    [26]司全金,李小鹰,曾青云,等.老年原发退行性瓣膜病超声观察及病因分析.中国应用生理学杂志,1998,14:63~65
    [27]宋克勤,聂洁莹.老年SDVHD的临床与超声研究.心血管康复医学杂志,1997,6:24~26.
    [28]王慧芳,林庆民,何还珠.二维彩色多普勒超声心动图评价老年瓣膜钙化.实用老年医学,1999,13:39~40.
    [29]魏松青,黄克明.老年钙化性心脏瓣膜病的超声和临床研究.心血管康复医学杂志,2000,9:41~42
    [30]彭禹.彩色多普勒血流仪诊断老年心脏瓣膜退行性变.中国介人心脏病学杂志,2000,8:147~148.
    [31] Branch KR, O' Brien KD, Otto CM. Aortic valve sclerosis is as a marker of activeatherosclerosis. Curr Cardiol Rep,2002,4:I11~117.
    [32] Mehrabi MR, Sinzinger H, Ekmekcioglu C, et al. Accumulation of oxidized LDL inhuman semilunar valves correlates with coronary atherosclerosis. Cardiovasc Res,2000,45:874~882.
    [33] Rose AG. Etiology of valvular heart disease. Curr Opin Cardiol,1996,11:98~113.
    [34]刘丽,赵玉生,王士雯.老年退行性心脏瓣膜病钙化的发病机制研究进展.中国循环杂志,2004,19:158~160.
    [35] Aronne I. J. Modern medical management of obesity:the role of pharmaceuticalintervention. J Am Diet Assoc,1998,98:s23~s26.
    [36] Ferara IA, Mancin M, Celetano M, et al. Early changes of the arterial wall inuncomplicated primary hypertensive patients study by ultrasound high~resolutionB~mode imaging. Arterioscler Thromb,1994,14:1290~1294.
    [37]卢塞兰,马小波宋雷,等.邵阳地区VHD发病率及病因调查.中国分子生物学杂志,2003,3(1):36~38.
    [38]杨波,王显芝.老年男性心脏瓣膜钙化相关因素分析[J].北京医学,2004,26(6):398400.
    [39] Marijon H, Ou P, Celermajer DS el al. Prevalence of rheumatic heart diseasedetected by echocardiographic screening. N Engl J Med2007;357:470~6.
    [40] Ray S. Changing epidemiology and natural history of valvular heart disease. Clin.Med,2010,10(2):168~171.
    [41] Furberg CD, Manolio TA, Gardin JM, et al. Rautaharju PM. Prevalence of atrialfibrillation in elderly subjects(the cardiovasular health study)[J]. Am J Cardiol,1994,74:236 241.
    [42] Kannel WB, Savage DD, Mcnamara PM, et al. Coronary heart disease and atrialfibrillation:the Framingham study[J]. Am Heart J,1983,106:389 396.
    [43] Friberg J, Scharling H, Gadsboll N, et al. Sex specific increase in the prevalenceof atrial fibrillation(The Copenhagen City Heart Study)[J]. Am J Cardiol,2003,92(12):1419 1423.
    [44] Levy S, Coumel P. Charaterization of different subsets of atrial fibrillation ingeneral practice in France:the ALFA study[J]. Circulation,1999,99:3028 3035.
    [45] Murgatroyd FD, Baiyan X. Double blind placebocontrolled trial of digoxin insymptomatic paroxysmal artrial fibrillation[J]. Circulation,1999,99:2765 2770.
    [46] MacIntyre K, Capewell S, Stewart S, et al. Evidence of improving prognosis inheart failure:trends in carotid atherosclerosis fatality in66,547patientshospitalized between1986and1995[J]. Circulation,2000,102:1126 1131.
    [47] Nkomo VT, Gardin|M, Skelton TN et al. Burden of valvular heart disease:apopulation~based study. Lancet2006;368:1005~11.
    [48] Nkomo VT. Epidemiology and prevention of valvular heart disease and infectiveendo~carditis in Africa. Heart2007;93:1510~9.
    [49] Bloor CM. The senile heart valvular disease. J Am Geriatrics,1982,30:469.
    [50] Branch KR, O' Brien KD, Otto CM. Aortic valve sclerosis is as a marker of activeatherosclerosis. Curr Cardiol Rep,2002,4:I11~117.
    [51] Mehrabi MR, Sinzinger H, Ekmekcioglu C, et al. Accumulation of oxidized LDL inhuman semilunar valves correlates with coronary atherosclerosis. Cardiovasc Res,2000,45:874~882.
    [52] Rose AG. Etiology of valvular heart disease. Curr Opin Cardiol,1996,11:98~113.
    [53] Aronne I. J. Modern medical management of obesity:the role of pharmaceuticalintervention. J Am Diet Assoc,1998,98:s23~s26.
    [54] Ferara IA, Mancin M, Celetano M, et al. Early changes of the arterial wall inuncomplicated primary hypertensive patients study by ultrasound high~resolutionB~mode imaging. Arterioscler Thromb,1994,14:1290~1294.
    [55] Palmieri v, Arnett UP, Roman MJ Appetite suppressants and valvular heart diseasein a population~based sample:the HyperGEN study. Am J Med,2002,112:710~715.
    [56] George R, McMahon J, Lytle B, et al. Severe valvular and aortic arch calcificationin a patient with Gaucher's disease homozygous for the D409H mutation. ClinGenet,2001,59:360~363.
    [57] Raggi P, Boulay A, Chasan~Taber S, et al. Cardiac calcification in adulthemodialysis patients. A link between end~stage renal disease and cardiovasculardisease? J Am Coll Cardio1,2002,39:695~701.
    [58] Bloor CM. The senile heart valvular disease. J Am Geriatrics,1982,30:469.
    [59] Branch KR, O' Brien KD, Otto CM. Aortic valve sclerosis is as a marker of activeatherosclerosis. Curr Cardiol Rep,2002,4:I11~117.
    [60] Mehrabi MR, Sinzinger H, Ekmekcioglu C, et al. Accumulation of oxidized LDL inhuman semilunar valves correlates with coronary atherosclerosis. Cardiovasc Res,2000,45:874~882.
    [61] Rose AG. Etiology of valvular heart disease. Curr Opin Cardiol,1996,11:98~113.
    [62] Aronne I. J. Modern medical management of obesity:the role of pharmaceuticalintervention. J Am Diet Assoc,1998,98:s23~s26.
    [63] Ferara IA, Mancin M, Celetano M, et al. Early changes of the arterial wall inuncomplicated primary hypertensive patients study by ultrasound high~resolutionB~mode imaging. Arterioscler Thromb,1994,14:1290~1294.
    [64] He J, Gu D, Wu X, et al. Major causes of death among men and w om en in China[J]. N Engl J Med,2005,353(11):1124~1134.
    [65] Tuttle KR, Short RA, Johnson RJ. Sex differences in uricacid and risk factors forcoronary art ery disease[J]. Am J Cardiol,2001,87(12):1411~1414.
    [66] Jacobs A K. Coronary intervention in2009:are women no different than men[J].Circ Cardiovasc Interv,2009,2(1):69~78.
    [67]李岩,赵冬.中国女性心血管疾病流行趋势与治疗概况[J].中华老年多器官疾病杂志,2009,8(3):213~215.
    [68] Elsaesser A, Hamm CW. Acute coronary syndrome:the risk of being female[J].Circulation,2004,109(5):565~567.
    [69] Pohjola Sintonen S, Rissanen A, Li skola P, et al. Family history as a risk factor ofcoronary heart disease inpatients under60years of age[J]. Eur H eart J,1998,19(2):235~239.
    [70] Gertler MM, Gran SM, Levine SA. Serum uricacid in relation to age and physiquein health and in coronary heart disease.[J]. Ann Intern Med,1951,34(6):1421~1431.
    [71] Fang J, Alderman MH. Serum uricacid and cardiovascular mortality:the NHANESIepidemiologic follow up study,1971~1992[J]. JAMA,2000,283(18):2404~2410.
    [72] Chen JH, Chuang SY, Chen HJ, et al. Serum uricacid level as an independent riskfactor for all cause cardiovascular, and ischemic stroke mortality:a Chinese cohortstudy[J]. Arthritis Rheum,2009,61(2):225~232.
    [73]孙志宏,李淼,高爱玲,等.血清尿酸水平与冠心病相关性研究[J].中华实用诊断与治疗杂志,2010,24(9):873~874.
    [74] Kanellis J, Watanabe S, Li JH, et al. Uricacid stimulates monocyte chemoat tractantprotein1production in vascular smooth muscle cells via mitogen activated proteinkinase and cyclooxygenase2[J]. Hypertension,2003,41(6):1287~1293.
    [75] Longo Mbenza B, Luila EL, Mbete P, et al. Is hyperuricemia a risk factor of strokeand coronary heart disease among Africans[J]. Int J Cardiol,1999,71(1):17~22.
    [76]刘挺松,吴宗贵,江时森等.2型糖尿病患者血尿酸水平与心功能不全的关系研究[J].中华实用诊断与治疗杂志,2009,23(11):1056.
    [77]郭利平.厄贝沙坦治疗高血压合并高尿酸血症90例疗效观察[J].中华实用诊断与治疗杂志,2009,23(10):1013.
    [78] Descheerder IK, Vande Kraay AM, Lamers JM, et al. Myocardia l malodialdehydeand uricacid release after short lasting coronary occlusions during coronaryangioplasty:potential mechanisms for free redical generation[J]. Am J Cardiol,1991,68(4):392~395.
    [79]党群,王敬,张莹等.高尿酸血症与高血压发生心血管事件的相关性探讨[J].实用诊断与治疗杂志,21(7):505~507.
    [80]周志文,徐亚伟,胡大一.女性冠心病临床特征研究进展[J].中国实用内科杂志,2009,29(8):746~749.
    [81] Yoneda Y, Mori E, Uehara T, et al. Referraland care for acute is chemic stroke in aJapanese tertiary emergency hospital[J]. Eur J Neurol,2001,8(5):483~488.
    [82] Jorgensen HS, Nakayama H, Reith J, et al. Factors delaying hospital admission inacute stroke:the Copenhagen stroke study[J]. Neurology,1996,47:383.
    [83] Brott T, Bogousslavasky J. Treatment of acute ischemic stroke[J]. N Engl J Med,2000,343(10):710~722.
    [84] Mansia G, De Backer G, Dominiczak A, et al.2007ESH~ESC Guidelines for themanagement of arterial hypertension:the task force for the management of arterialhypertension of the European Society of Hypertension(ESH)and of the EuropeanSociety of Cardiology(ESC)[J]. Blood Press,2007,16(3):135~232.
    [85]陆再英,钟南山,谢毅等.内科学[M].第7版.北京:人民卫生出版社,2006:832.
    [86]王陇德.中国居民营养与健康状况调查报告之~2002综合报告[M].北京:人民卫生出版社,2005:115~116.
    [87] Anand SS, Yusuf S, Vuksan V, et al. Differences in risk factors, atherosclerosis andcardiovascular disease between ethnic groups in Canada:the study of healthassessment and risk in ethnic groups(SHARE)[J]. Indian Heart J.2000,52(7):35~43.
    [88] Kastelein JJ, Wiegman A, de Groot E. Surrogate markers of atherosclerosis:impactof statins[J]. Atheroscler Suppl,2003,4(1):31~36.
    [89]张东平,李晋芳,胡长林,等.重庆市中老年钢铁工人颈动脉粥样硬化的流行病学调查[J].中华流行病学杂志,2009,30(4):322~325.
    [90]刘丽,赵玉声,王士雯等.北京地区部分军队老年人群中颈动脉粥样硬化现况调查[J].中华流行病学杂志,2007,28(4):358~361.
    [91]刘力生,龚兰生,方圻等.中国高血压防治指南[J].高血压杂志,2000,8(1):94.
    [92]陈明,徐岩.高血压患者颈动脉内膜中膜厚度与心血管危险因素的相关性[J].中华高血压杂志,2008,16(7):649~650.
    [93]麦垚,寿涛,刘华,等.老年高血压病患者血尿酸水平与颈动脉硬化相关性探讨[J].中华风湿病学杂志,2006,10(10):634~635.
    [94]杨海玉,曾玉杰,黄占军,等.高尿酸血症对血管内皮功能影影响的观察[J].中国实用内科杂志,2004,24(5):289~290.
    [95]宋艳,钱蕴秋,张海滨,等.老年钙化性VHD的超声心动图表现[J].解放军医学杂志,2006,31(5):482~483
    [96]张玉峰,毛莲香.老年性钙化性心瓣膜病的超声诊断[J].中国医学理论与实践,2005,15(5):658
    [97]葛智平.老年SDVHD[J].凝难病杂志,2002,1(1):58~59
    [98]程蕴琳,刘莉.主动脉瓣SD病变的病因和发病机制的研究进展[J].中华老年医学杂志,2004,23(8):123
    [99]初洪钢,金卫国,郭瑞强,等.心脏钙化病变与冠心病关系的研究[J].中华超声影像学杂志,2005,14(11):817~820
    [100] Aminbakhsh A, ManciniGB. Carotid intima~media thickness measurements:Whatdefines an abnormality? A systematic review[J]. Clin InvestMed,1999,22(4):149
    [101]初洪钢,郭瑞强,王世敏,等.主动脉瓣钙化与冠心病之间关系的探讨[J].中华超声影像学杂志,2006,15(8):634~635
    [102]刘江泽,廖丽萍,殷红霞,等.彩色多普勒超声诊断老年性主动脉瓣钙化的临床应用[J].医学信息(西安),2007,20(6):1034~1035
    [103] PeltierM, Iannetta~PeitierMC. Elevatedserum lipoprotiein level isanindependentmarker of severity of thoractic aortic atherosclerosis. Ches, t2002;121:1589~1594.
    [104] YehudsA, Uriel L, AronnorenM, et a1. Relation of non obstructive aortic valvecalcium to carrortid arterial atherosclerosis. AMJ Cardio, l2001;79:1102~1105.
    [105]杨文.颈动脉粥样硬化于老年钙化性心脏瓣膜病的关系.中华老年心脑血管病杂志,2001,3:432
    [106]王肖龙,薛金贵,胡婉英.心脏瓣膜钙化与颈动脉粥样硬化的关系.中国全科医学,2003,6:331~332
    [107]王慧芳,林庆明,何还珠.二维彩色多普勒超声心动图评价老年瓣膜钙化,实用老年医学,1999,13:39~40
    [108] Roberts WC. Morphologic features of the normal angab normal mitral valve. Am JCardio, l1983;51:1005~1028
    [109] AdlerY, LevingerU, KorenA, et al. Relation of non obstructive aortic valve calciumto carotid arterial atherosclerosis, AmJCardio, l2000;86(10):1102
    [110] Roberts WC:The senile cardiac calcification syndrome. Am J Cardio, l1986;58:572~574
    [111] Boon A, Cheriex E, Lodder J, et al. Cardiacvalve calcium:characteristics of patientswith calcification of the mitral annulusor aortic valve. Heart1997;66:967~977
    [112] Akasaka T, Yoshikawa J, YoshidaK, eta. l Age~related val~vular regurgitation:astudy by pulsed Doppler echocardio~graphy[J]. Circulation,1987,76(2):262.
    [113] PrisantLM, Zemel PC, Nichols FT, et a. l Carotid plaque associations amonghypertensive patients[J]. Arch Intern Med,1993,153(4):501.
    [114]冯明.老年钙化性心脏瓣膜病[J].中国老年学杂志,2003,23(7):401.
    [115]吴曼华.老年退行性心脏瓣膜病的临床与超声心动图研究[J].中华心血管病杂志,1994,22(4):289.
    [116]许惠敏,常素华.老年退行性心脏瓣膜病76例临床分析[J].中国心血管病研究杂志,2004,2(7):532.
    [117] Kim KM. Apoptosis and calcification[J]. ScanningMicrosc,1995,9(4):1137.
    [118] MohlerER3rd, Gannon F, Reynolds C, et a. l Bone formation and inflammation incardiac valves[J]. Circulation,2001,103(11):1522.
    [119]钮红音,索珍,李静.老年钙化性心脏瓣膜病与颈动脉粥样硬化关系的探讨[J].实用老年医学,2004,18(6):308.
    [120] PohleK, MAFfertR, RopersD, et a. l Progression of aortic valve calci~fication:association with coronary atherosclerosis and cardiovascular risk factors[J].Circulation,2001,104(16):1927.
    [121]刘军,赵冬,王薇,等.北京大学社区人群基线血脂水平及10年血脂变化与颈动脉粥样硬化的关系[J].中华医学杂志,2006,86(20):120.
    [122]程蕴琳,刘莉.主动脉瓣退行性变病变的病因和发病机制的研究进展[J].中华老年医学杂志,2004,23(8):123.
    [123] Aminbakhsh A, Mancini GB. Carotid intima~media thicknessmeasurements:What defines an abnormality? A systematic review[J]. ClinInvestMed,1999,22(4):149.
    [124] HolajR, Spacil J, Petrasek J, et a. l Relation of the thickness of the intima andmedia of the common carotid artery, atherosclerotic plaque in the carotids andmanifestations of atherosclerosis in the vessels of the lower extremity incomparison to coronary atherosclerosis[J].颈动脉粥样硬化Lek Cesk,1998,137(23):716.
    [125]周永昌,郭万学,徐南图,等主编.超声医学[M].第4版.北京:科学技术文献出版社,2002.796~797.
    [126]王慧芳,林庆民,何还珠,等.二维彩色多普勒超声心动图评价老年瓣膜钙化[J].实用老年医学,1999,13(1):39.
    [127] Roberts WC. Morphologic features of the normal and abnormal mitral valve[J]. AmJ Cardiol,1983,51(6):1005
    [128] Adler Y, Herz I, Vaturi M, et al. Mitral annular calcium detected by transthoracicechocardiography is a marker for high prevalence and severity of coronary arterydisease in patients undergoing coronary angiography[J]. Am J Cardiol,1998,82(10):1183
    [129] Mohler ER3rd, Chawla MK, Chang AW, et al. Identification and characterizationof calcifying valve cells from human and canine aortic valves[J]. J Heart Valve Dis.1999,8(3):254
    [130] Adler Y, Levinger U, Koren A, et al. Relation of nonobstructive aortic valvecalcium to carotid arterial atherosclerosis[J]. Am J Cardiol,2000,86(10):1102
    [131] Somers P, Knaapen M, Mistiaen W. Histopathology of calcific aortic valvestenosis[J]. Acta Cardiol.2006,61(5):557~562.
    [132]王士雯,钱方毅,主编.老年心脏病学[M].北京:人民卫生出版社,1998.285.
    [133] O'Brien KD. Pathogenesis of Calcific Aortic Valve Disease[J]. Arterioscler ThrombVasc Biol.2006,26(8):1721~1728.
    [134]刘丽,赵玉生,王士雯等.北京地区军队老年人群退行性心脏瓣膜病的流行病学研究[J].中华流行病学杂志.2006,27(10):836~839.
    [135]李惠军.老年退行性瓣膜病的超声心动图研究[J].中国超声诊断杂志.2004,5(5):377~379.
    [136]周永昌,郭万学,主编.超声医学[M].北京:北京科学技术文献出版社,1998.428-432.
    [137]实用内科学编委会,陈灏珠,主编.实用内科学[M].北京:人民卫生出版社,2002.1342~1358.
    [138]卫生部心血管病防治研究中心.中国高血压防治指南[J].中国卒中杂志.2006,1(8):575~582.
    [139]邹艳秋,戈晓华.颈部动脉超声多普勒实用手册[M].北京:学苑出版社,1998.8~12.
    [140]中国成人血脂异常防治指南制定联合委员会.中国成人血脂异常防治指南[J].中华心血管病杂志.2007,35(5):390~409.
    [141] Stewart BF, Siscovick D, Lind BK, et a1. Clinical factors associated with calcificartic valve disease. Cardiovascular Health Study[J]. J Am Coll Cardiol.1997,29(3):630~634.
    [142]王采荣,张蕾.老年人群钙化性VHD的超声所见与常见病相关因素分析[J].中国超声医学杂志.2003,19(8):631~632.
    [143]王士雯,王琳,余颂涛.老年钙化性心瓣膜病的病理学研究[J].实用老年医学.2000,14(6):283~286.
    [144] O’Brien KD, Reichenbach DD, Marcovina SM, et al. Apolipoproteins B,(a), and Eaccumulate in the morphologically early lesion of 'degenerative' valvular aorticstenosis[J]. Arterioscler Thromb Vasc Biol.1996,16(4):523–532.
    [145] Pohle K, M ffert R, Ropers D, et al. Progression of aortic valvecalcification:association with coronary atherosclerosis and cardiovascular riskfactors[J]. Circulation,2001,104(16):1927~1932.
    [146] Boon A, Cheriex E, Lodder J, et al. Cardiac valve calcification:characteristics ofpatients with calcification of the mitral annulus or aortic valve[J]. Heart.1997,78(5):472~474.
    [147] Stewart BF, Siscovick D, Lind BK, et al. Clinical factors associated with calcificaortic valve disease:Cardiovascular Health Study. J Am Coll Cardiol.1997,29(3):630–634.
    [148] Gerber Y, Goldbourt U, Feinberg MS, et al. Are triglyceride~rich lipoproteinsassociated with aortic valve sclerosis? A preliminary report[J]. Atherosclerosis,2003,170(2):301~305.
    [149] Olsson M, Thyberg J, Nilsson J. Presence of oxidized low density lipoprotein innonrheumatic aortic valves[J]. Arterioscler Thromb Vasc Biol.1999,19(5):1218~1222.
    [150] Rajamannan NM, Subramaniam M, Springett M, et al. Atorvastatin inhibitshypercholesterolemia~induced cellular proliferation and bone matrix productionin the rabbit aortic valve[J]. Circulation.2002,105(22):2660~2665.
    [151] Chui MC, Newby DE, Panarelli M, et al. Association between calcific aorticstenosis and hypercholesterolemia:is there a need for a randomized controlled trialof cholesterol~lowering therapy?[J]. Clin Cardiol,2001,24(1);52~55.2524
    [152] Bellamy MF, Pellikka PA, Klarich KW, et al. Association of cholesterol levels,hydroxymethylglutaryl coenzyme~A reductase inhibitor treatment, andprogression of aortic stenosis in the community[J]. J Am Coll Cardiol.2002,40(10):1723~1730.
    [153] Antonini~Canterin F, Popescu BA, Huang G, et al. Progression of aortic valvesclerosis and aortic valve stenosis:what is the role of statin treatment?[J]. Ital HeartJ.2005,6(2):119~124.
    [154] Moura LM, Ramos SF, Zamorano JL, et al. Rosuvastatin Affecting Aortic ValveEndothelium to Slow the Progression of Aortic Stenosis[J]. J Am Coll Cardiol.2007,49(5):554~561.
    [155] Cowell SJ, Newby DE, Prescott RJ, et al. A Randomized Trial of Intensive Lipid~Lowering Therapy in Calcific Aortic Stenosis[J]. N Engl J Med.2005,352(23):2389~2397.
    [156] Cacciola RR, Guarino F, Polosa R, et al. Relevance of endothelial~haemostaticdysfunction in cigarette smoking[J]. Curr Med Chem.2007,14(17):1887~92.
    [157] O'Brien KD, Chait A. The biology of the artery wall in atherogenesis[J]. Med ClinNorth Am.1994,78(1),41–67.
    [158]王新房,李治安.彩色多普勒诊断学[M].北京:人民卫生出版社,1991.
    [159] Otto CM, Lind BK, Kitzman DW, et al. Association of aortic~valve sclerosis withcardiovascular mortality and morbidity in the elderly[J]. N Engl J Med.1999,341(3):142–147.
    [160]孟迅吾,邢小平.原发性甲状旁腺功能亢进症的诊断(附134例分析)[J].中国医学科学院学报.1994,16(1):13~19.
    [161]万里凯.老年前期及老年期钙化性心瓣膜病超声心动图特点分析[J].广西医科大学学报.2002,19(3):375~376.
    [162] Wong M, Tei C, Shah PM.. Degenerative calcific valvular disease and systolicmurmurs in the elderly[J]. J Am Geriatric Soc.1983,31(3):156~163.
    [163]张玉珍,王士雯,韦立新.老年钙化性心脏瓣膜病的病理[J].中华心血管病杂志.1991,19(6):372~374.
    [164]齐欣,王瑞萍,钱贻简等.老年人钙化性主动脉瓣狭窄并发心肌梗死临床和病理特点[J].中华内科杂志.2000,39(2):88~90.
    [165] Kallikazaros I, Tsioufis C, Sideris S, et al. Carotid artery disease as a marker for thepresence of severe coronary artery disease in patients evluated for chest pain[J].Stroke.1999,30(5):1002~1007.
    [166] Graven TE, Ryu JE, Espeland MA, et al. Evaluation of the associations betweencarotid artery atherosclerosis and coronary artery stenosis[J]. Circulation.1990,82(4):1230~1242.
    [167]刘丽,赵玉生,王士雯.北京军队干休所老年人群颈动脉粥样硬化与老年退行性心脏瓣膜病的关系[J].中华老年多器官疾病杂志.2007,6(1):38~41.
    [168] Adler Y, Koren A, Fink N, et al. Association Between Mitral Annulus Calcificationand Carotid Atherosclerotic Disease[J]. Stroke.1998;29(9):1833~1837.
    [169] Mazzone A, Epistolato MC, Gianetti J. Biological features(inflammation andneoangiogenesis)and atherosclerotic risk factors in carotid plaques and calcifiedaortic valve stenosis:two different sites of the same disease[J]? Am J Clin Pathol.2006,126(4):494~502.
    [170] Sgorbini L, Scuteri A, Leggio M, et al. Association of mitral annulus calcification,aortic valve calcification with carotid intima media thickness[J]. CardiovascUltrasound.2004,8(2):19.
    [171] Adler Y, Levinger U, Koren A, et al. Association between mitral annuluscalcification and peripheral arterial atherosclerotic disease[J]. Angiology.2000,51(8):639~646.
    [172]郭春艳,王佩显.老年钙化性心脏瓣膜病与钙磷代谢[J].中国老年学杂志.2004,12(24):1127~1128.
    [173] Carotid plaques increase the risk of stroke and subtypes of cerebral infarction inasymptomatic elderly:the Rotterdam study[J]. Hollander M, Bots ML, Del Sol AI,et al. Circulation.2002,105(24):2872~2877.24
    [174] Hollander M, Hak AE, Koudstaal PJ, et al. Comparison between measures ofatherosclerosis and risk of stroke:the Rotterdam Study[J]. Stroke.2003,34(10):2367~2372.
    [175] Wernig F, Xu Q. Mechanical stress~induced apoptosis in the cardiovascularsystem[J].. Prog Biophys Mol Biol.2002,78(2~3):105~37.
    [176] Mohler ER III. Are atherosclerotic processes involved in aortic~valvealcification[J]?The Lancet.2000,356(9229):524~525.
    [177] Freeman RV and Otto CM. Spectrum of Calcific Aortic Valve Disease:athogenesis,Disease Progression, and Treatment Strategies[J]. Circulation.2005,11(24):3316~3326.
    [1] Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez~Sarano M.Burden of valvular heart diseases:a population~based study. Lancet.2006;368:1005~1011.
    [2] d’Arcy JL, Prendergast BD, Chambers JB, Ray SG, Bridgewater B. Valvular heartdisease:the next cardiac epidemic[published correction appears in Heart.2011;97:1112]. Heart.2011;97:91~93.
    [3] Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL, Lehman B, BenjaminEJ. Prevalence and clinical determinants of mitral, tricuspid, and aorticregurgitation(the Framingham Heart Study)[published correction appears in Am JCardiol.1999;84:1143]. Am J Cardiol.1999;83:897~902.
    [4] Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE, KitzmanDW, Otto CM;for the Cardiovascular Health Study. Clinical factors associated withcalcific aortic valve disease. J Am Coll Cardiol.1997;29:630~634.
    [5] Iung B, Vahanian A. Epidemiology of valvular heart disease in the adult. Nat RevCardiol.2011;8:162~172.
    [6] Roberts WC, Ko JM. Frequency by decades of unicuspid, bicuspid, and tricuspidaortic valves in adults having isolated aortic valve replacement for aortic stenosis,with or without associated aortic regurgitation. Circulation.2005;111:920~925.
    [7] Owens DS, Katz R, Takasu J, Kronmal R, Budoff MJ, O’Brien KD. Incidence andprogression of aortic valve calcium in the Multi~Ethnic Study ofAtherosclerosis(MESA). Am J Cardiol.2010;105:701~708.
    [8] Lung B, Baron G, Butchart EG, Delahaye F, Gohlke~Ba¨rwolf C, Levang OW,Tornos P, Vanoverschelde JL, Vermeer F, Boersma E, Ravaud P, Vahanian A. Aprospective survey of patients with valvular heart disease in Europe:the Euro HeartSurvey on Valvular Heart Disease. Eur Heart J.2003;24:1231~1243.
    [9] Otto CM, Lind BK, Kitzman DW, Gersh BJ, Siscovick DS. Association of aortic~valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl JMed.1999;341:142~147.
    [10]Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, delNido P, Fasules JW, Graham TP Jr, Hijazi ZM, Hunt SA, King ME, Landzberg MJ,Miner PD, Radford MJ, Walsh EP, Webb GD. ACC/AHA2008guidelines for themanagement of adults with congenital heart disease:a report of the American Collegeof Cardiology/American Heart Association Task Force on PracticeGuidelines(writing committee to develop guidelines on the management of adultswith congenital heart disease). Circulation.2008;118:e714~e833.
    [11]Rowe JC, Bland EF, Sprague HB, White PD. The course of mitral stenosis withoutsurgery:ten~and twenty~year perspectives. Ann Intern Med.1960;52:741~749.
    [12]Freed LA, Levy D, Levine RA, Larson MG, Evans JC, Fuller DL, Lehman B,Benjamin EJ. Prevalence and clinical outcome of mitral~valve prolapse. N Engl JMed.1999;341:1~7.
    [13]Lee GM, Wessels MR. Changing epidemiology of acute rheumatic fever in theUnited States. Clin Infect Dis.2006;42:448~450.
    [14]Miyake CY, Gauvreau K, Tani LY, Sundel RP, Newburger JW. Characteristics ofchildren discharged from hospitals in the United States in2000with the diagnosis ofacute rheumatic fever. Pediatrics.2007;120:503~508.
    [15]Gerber MA, Baltimore RS, Eaton CB, Gewitz M, Rowley AH, Shulman ST, TaubertKA. Prevention of rheumatic fever and diagnosis and treatment of acuteStreptococcal pharyngitis:a scientific statement from the American Heart AssociationRheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council onCardiovascular Disease in the Young, the Interdisciplinary Council on FunctionalGenomics and Translational Biology, and the Interdisciplinary Council on Quality ofCare and Outcomes Research. Circulation.2009;119:1541~1551.
    [16]Thom TJ, Kannel WB, Silbershatz H, D’Agostino RB Sr. Cardiovascular diseases inthe United States and prevention approaches. In:Fuster V, Alexander RW, Schlant RC,O’Rourke RA, Roberts R, Sonnenblick EH, eds. Hurst’s the Heart.10th ed. NewYork, NY:McGraw~Hill;2001:3~18.
    [17]Xu J, Kochanek KD, Murphy SL, Tejada~Vera B. Deaths:final data for2007.National Vital Statistics Reports.2010;58:1~135. Hyattsville, MD:National Centerfor Health Statistics;2010.18. Maharaj B, Hammond MG, Appadoo B, Leary WP,Pudifin DJ. HLA~A, B, DR, and DQ antigens in black patients with severe chronicrheumatic heart disease. Circulation.1987;76:259~261.
    [18]安勇,马翔,黄莺等.新疆不同民族心脏瓣膜病流行病学调查.中华流行病学杂志,2011,32(11):1114~1116.
    [19]安勇,黄莺,马翔等.新疆地区不同民族老年人群老年退行性心脏瓣膜病患病率及相关因素的横断面调查.中华流行病学杂志,2011,32(01):99~101.
    [20]卢赛兰,马小波,宋雷等.邵阳地区心脏瓣膜病发病率及病因调查.中国分子心脏病学杂志,2003,3(01)36~38.
    [21]万士荣,吴民,肖大鹊等.退行性钙化性心瓣膜病的超声与临床研究.临床心血管病杂志,2000,16(7):323一323.
    [22]刘丽,赵玉生,王士雯等,北京地区军队老年人群老年退行性心脏瓣膜病流行病学研究.中华流行病学杂志,2006,27(10):836~839.
    [23]王琳.社区老年人群退行性心脏瓣膜病的五年纵向研究[D]:[博士学位论文].中国人民解放军军医进修学院,2011,10~30.
    [24]倪戈敏.我国5~18岁自然人群风湿热和风湿性心脏病流行状况的研究进展.“八·五”国家医学科技攻关通讯.1994,2(14):1.
    [25]徐小玲,王炳焕,金宏义等.浙江省中小学生风湿热与风湿性心脏瓣膜病流行状况.浙江医学,1996,18(6):377~378.
    [26]解玉,王秀英,刘东海等.375例风湿热和风湿性心脏瓣膜病30年临床变迁.实用儿科临床杂志,2003,18(11):875~877.
    [27]刘大鹏,黄亚辉,公兰兰.风湿性心脏病15年调查报告.心血管康复医学杂志,2001,10(3):251~253.
    [1] Bernard Iunga, Gabriel Baronb, Eric G, et al. A prospective survey of patients withvalvular heart disease in Europe:The Euro Heart Survey on Valvular Heart DiseaseEur Heart J.2003;24:1231-1243.
    [2] Rajamannan NM, Evans FJ, Aikawa E, et al. Calcific aortic valve disease:not simplya degenerative process:a review and agenda for research from the national heart andlung and blood institute aortic stenosis work-ing group executive summary:calcificaortic valve disease-2011update. Circulation.2011;124:1783-1791.
    [3] Freeman RV, Otto CM. Spectrum of calcific aortic valve disease:pathogenesis,disease progression, and treatment strategies. Circulation.2005;111:3316-3326.
    [4] Yetkin E, Waltenberger J. Molecular and cellular mechanisms of aortic stenosis. Int JCardiol.2009;135:4-13.
    [5] Kaden JJ, Dempfle CE, Grobholz R, et al. Interleukin-1beta promotes matrixmeta-lloproteinase expression and cell proliferation in calcific aortic valve stenosis.Atherosclerosis.2003;170:205-211.
    [6] Helske S, Kupari M, Lindstedt KA, Kovanen PT. Aortic valve stenosis:an activeatheroinflammatory process. Curr Opin Lipidol.2007;18:483-491.
    [7] Rajamannan NM. Calcific aortic stenosis:lessons learned from ex-perimental andclinical studies. Arterioscler Thromb Vasc Biol.2009;29:162-168.
    [8] Akat K, Borggrefe M, Kaden JJ. Aortic valve calcification:basic science to clinicalpractice. Heart.2009;95:616-623.
    [9] Miller JD, Weiss RM, Heistad DD. Calcific aortic valve stenosis:meth-ods, models,and mechanisms. Circ Res.2011;108:1392-1412.
    [10]Kaden JJ, Kili R, Sariko A, et al. Tumor necrosis factor alpha promotes anosteoblast-like phenotype in human aortic valve myofibroblasts:a potentialregulatory mechanism of valvular calcification. Int J Mol Med.2005;16:869-872.
    [11]Winchester R, Wiesendanger M, O’Brien W, et al. Circulating activated and effectormemory T cells are associated with calcification and clonal expansions in bicuspidand tricuspid valves of calcific aortic stenosis. J Immunol.2011;187:1006-1014.
    [12]Liu AC, Joag VR, Gotlieb AI. The emerging role of valve inter stitial cell phenotypesin regulating heart valve pathobiology. Am J Pathol.2007;171:1407-1418.
    [13]Poggio P, Grau JB, Field BC, et al. Osteopontin controls endothelial cell migration invitro and in excised human valvular tissue from patients with Calcific Aortic Stenosisand controls. J Cell Physiol.2010Dec6.[Epub ahead of print].
    [14]Kaden JJ, Bickelhaupt S, Grobholz R, et al. Expression of bone sialo-protein andbone morphogenetic protein-2in calcific aortic stenosis. J Heart Valve Dis.2004;13:560-566.
    [15]Chen JH, Simmons CA. Cell-matrix inter actions in the pathobiology of calcificaortic valve disease:critical roles for matricellular, matricrine, and matrix mechanicscues. Circ Res.2011;108:1510-1524.
    [16]Yu PJ, Skolnick A, Ferrari G, et al. Correlation between plasma osteo-pontin levelsand aortic valve calcification:potential insights into the patho-genesis of aortic valvecalcification and stenosis. J Thorac Cardiovasc Surg.2009;138:196-199.
    [17]Hofbauer LC, Schoppet M. Clinical implications of the osteoproteger-in/RANKL/RANK system for bone and vascular diseases. JAMA.2004;92:490-495.
    [18]Lee NK, Choi YG, Baik JY, et al. A crucial role for reactive oxygen spe-cies inrankl-induced osteoclast differentiation. Blood.2005;106:852-859.
    [19]Ferrara N, Davis-Smyth T. The bio logy of vascular endothelial growth factor.Endocr Rev.1997;18:4-25.
    [20]Waltenberger J. Modulation of growth factor action:implications for the treatment ofcardiovascular diseases. Circulation.1997;96:4083-4094.
    [21]Chen JH, Chen WL, Sider KL, et al. β-catenin mediates mechanical-ly regulated,transforming growth factor-β1-induced myofibroblast differentiation of aortic valveinter stitial cells. Arterioscler Thromb Vasc Biol.2011;31:590-597.
    [22]Jian B, Narula N, Li QY, et al. Progression of aortic valve stenosis:TGF-beta1ispresent in calcified aortic valve cusps and promotes aortic valve inter stitial cellcalcification via apoptosis. Ann Thorac Surg.2003;75:457-465.
    [23]Soini Y, Salo T, Satta J. Angiogenesis is involved in the pathogenesis ofnonrheumatic aortic valve stenosis. Hum Pathol.2003;34:756-763.
    [24]Satta J, Oiva J, Salo T, et al. Evidence for an altered balance between matrix metalloproteinase-9and its inhibitors in calcific aortic stenosis. Ann Thorac Surg.2003;76:681-688
    [25]Kaden JJ, Dempfle CE, Grobholz R, et al. Inflammatory regulation of extracellularmatrix remodeling in calcific aortic valve stenosis. Cardiovasc Pathol.2005;14:80-87.
    [26]Helske S, Lindstedt KA, Laine M, et al. Induction of local angiotensin II producingsystems in stenotic aortic valves. J Am Coll Cardiol.2004;44:1859-1866.
    [27]Rosenhek R, Rader F, Loho N, et al. Statins but not angiotensin-converting enzymeinhibitors delay progression of aortic stenosis. Circulation.2004;110:1291-1295.
    [28]Cagirci G, Cay S, Karakurt O, et al. Paraoxonase activity might be predictive of theseverity of aortic valve stenosis. J Heart Valve Dis.2010;19:453-458.
    [29]Rajamannan NM. Bicuspid aortic valve disease:the role of oxidative stress in Lrp5bone formation. Cardiovasc Pathol.2011;20:168-176.
    [30]Garg V, Muth AN, Ransom JF, et al. Mutations in NOTCH1cause aortic valvedisease. Nature.2005;437:270-274.
    [31]Novaro GM, Sachar R, Pearce GL, et al. Association between apolipo-protein Ealleles and calcific valvular heart disease. Circulation.2003;108:1804-1808.
    [32]Ortlepp JR, Hoffmann R, Ohme F, et al. The vitamin D receptor geno-typepredisposes to the development of calcific aortic valve stenosis. Heart.2001;85:635-638.
    [33]Singh R, Strom JA, Ondrovic L, et al. Age-related changes in the aortic valve affectleaflet stress distributions:implications for aortic valve degeneration. J Heart ValveDis.2008;17:290-298.
    [34]Matsumoto Y, Adams V, Walther C, et al. Reduced number and function ofendothelial progenitor cells in patients with aortic valve stenosis:a novel concept forvalvular endothelial cell repair. Eur Heart J.2009;30:346-355.
    [35]Vahanian A, Baumgartner H, Bax J, et al. Guidelines on the management of valvularheart disease. The Task Force on the Management of Val-vular Heart Disease of theEuropean Society of Cardiology. Eur Heart J2007;28:230-268.
    [36]Carabello BA, Paulus WJ. Aortic stenosis. Lancet.2009;373:956-966.
    [37]Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valvestenosis EAE/ASE recommendations of clinical practice. J Am Soc Echocardiogr.2009;22:1-23.
    [38]Islam S, Islam E, Cevik C, et al. Aortic stenosis and angiodysplastic gastrointestinalbleeding:Heyde’s disease. Heart Lung.2011Oct11.[Epub ahead of print].
    [39]Vincentelli A, Susen S, Le Tourneau T, et al. Acquired vonWillebrand syndrome inaortic stenosis. N Engl J Med.2003;349:343-349.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700