治疗前动态血压监测对非糖尿病的高血压病患者靶器官损害的预测价值
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摘要
前言
动态血压监测(ABPM)对高血压病(HP)患者血压监测有独特的优越性。ABPM可以提供白天、夜间和清晨血压的信息；排除了“白大衣效应”和“安慰剂效应”，更准确的反映真实的血压水平，重复性好；能显示出血压的昼夜节律、血压值的变异度、血压负荷等有价值的指标；对阵发性高血压、顽固性高血压、临界性高血压、“白大衣性正常血压”有特殊的诊断价值。而诊所血压因传统的汞柱式血压计无法实时、连续的进行血压的监测，又易于受体位、情绪、活动的影响，根据ELSA研究的结果，诊所血压和24h动态血压有一定的相关性，但相关系数很小，诊所血压并不能很好的反映24h血压的真实水平，因此只有动态血压才能敏感而客观地监测HP患者实际的血压水平。
由于靶器官损害(TOD)在评价高血压患者心血管危险方面的重要性，对每一
浙江大学硕士学位论文
个HP患者都应仔细寻找TOD的证据。2003年《欧洲高血压治疗指南》规定TOD包
括左室肥厚(LVH)、颈动脉内膜中层厚度(工MT)、M以、血清肌配浓度(Cr)
>l .snunol/L。在高血压患者中评价ABPM对TOD及各种心脑血管事件的预测价值己
经进行了一些研究，结论是24h平均血压值与靶器官损害有关，随着平均血压值
的增高，高血压对靶器官危害性增加。然而，由于同时存在代谢紊乱，有1/3左
右的高血压患者同时合并有2型糖尿病，而糖尿病对HP患者的各种靶器官的损害
以及预后都将产生重要的影响，而且其产生靶器官的损害的机制也不完全相同。
因此为了明确ABPM对高血压靶器官损害的预测价值需排除糖尿病的影响。而目前
国内外类似的研究大多未将研究范围限制在非糖尿病的HP患者。
目的
本研究以S2名未经降压治疗的非糖尿病的HP患者为研究对象，选择LVMI、
IMT、MCA为靶器官损害的指标，排除了糖尿病对结果的影响，进一步评价ABPM对
非糖尿病的HP患者TOD及今后发生CV事件的预测价值。
对象和方法
1对象和分组
选择2002年1月一2003年1月期间在金华市中心医院心内科住院的HP患者
52名(男性43名，女性39名)，年龄35~83(63士10)岁，平均高血压病程(7.98
士7 .94)年。
浙江大学硕士学位论文
1 .1入选标准:未经正规降压药物治疗的高血压患者或初诊的高血压病患者，符
合1999年WHo/IsH高血压诊断标准:不同日两次以上收缩压SBP)140mmHg
和(或)舒张压DBp妻90rnrnHgO
1 .2排除标准:排除各种继发性高血压、糖尿病(空腹血糖妻7.0~ol/L或餐后2h
血糖妻11.lmmol几)、泌尿系统疾病，有严重的心脑血管并发症的病史或体征(充
血性心衰、心肌梗塞、心绞痛、短暂脑缺血发作和中风)或肾功能损害(Cr>
1.5m留dl)。严重肺气肿和房颤患者因影响超声数据的收集也不列入研究。
1 .3分组方法:所有入选的患者根据入院后水银柱血压计测量的诊所血压值分为
两组，组l为血压<140/gommHg(n=26)，组2为血压)140/90mrnHg(n=56)。
所有患者再根据入院后24h动态血压值重新分组，组A平均血压值<130/85mmHg
(n=27)，组B平均血压值〕130/ 85mmHg(n=55)。
2方法
2.1诊所血压的测量用标准水银柱血压计完成诊所血压的测量，柯氏第一和第
五音作为收缩压与舒张压值。患者坐位或卧位休息10分钟以上，以卧位测量3次，
间隔2分钟分别读出3次收缩与舒张压后取平均值。所有的测量都在上午8一9点之
间完成，在同一侧受臂进行测量。诊所血压的测量时间与动态血压监测安排为同
一天。
2.2动态血压的测量以美国SpaceLabs 5200型24h动态血压检测系统进行动态
血压检测，白天及夜间均设置为每30min自动记录一次血压读数，测定平均收缩
压MSBP，平均舒张压MDBP，脉压(PP=MSBP一MDBP)，白天平均收缩压dDBP，
浙江大学硕士学位论文
白天平均舒张压dSBP，夜间平均收缩压nSBP，夜间平均舒张压nDBP。
2.3生化指标的测定:
(l)采用德国BECKMAN CXg生化分析仪测定血清空腹和餐后2h血糖(GLU)、
肌配(Cr)、总胆固醇(TC)浓度。
(2)采用特定蛋白分析仪测定尿微量白蛋白含量，乘以24h总尿量即为24h尿
微量白蛋白总量。连续测定两次取均值。M以定义为30一30Omg/24h
2.4采用美国惠普公司SONOS一5500型多普勒超声诊断仪，取胸骨旁左室长轴
切面用M型超声测量室间隔舒张末期厚度(Wsd)，左室后壁舒张末期厚度
(PWTd)，左室舒张末期内径(LVIDd)，采用美国超声协会推荐公式计算左室重
量LVM(g)=0.8又1 .04[(IVsT+LVIDd+Lpwp)3一LVIDd3]+0.6，左室重量指数LVMI
(g/m2)一LVM旧SA，左室肥厚(LVH)的诊断标准为LVMI男性>1 25 g/mZ女性
>1209/m。
2.5颈总动脉内膜一中层厚度(I MT)和动脉硬化斑块的测量:
(l)应用美国ATL 5000型B型超声诊断仪进行双侧颈总动脉IMT的测量。横纵
向观察颈总动脉，冻结颈动脉窦以下1。m处(无斑块部位)的图像，共测量5次IMT，
取10次左右侧测量值的平均值即为平均颈总动脉IMT。测定的IMT范围在0.50一
20mm间。IMT>0.9被认为是内膜增厚。
(2)颈动脉斑块测定:若发现斑块，横纵向冻结图像，并测量其厚度，若在同一
动脉段发现多个斑块，记录斑块数目，并测量
Measurements of ambulatory blood pressure as an adjunct to casual/clinic blood pressure measurements are widely used for the diagnosis and treatment of hypertension currently. It has uniformly demonstrated on a cross-sectional basis that average ambulatory blood pressure (ABP) is correlated to target-organ damage. Several event-based cohort studies have shown that ABP improves cardiovascular risk stratification over and beyond office BP. Most of these studies have been conducted in subjects with essential hypertension (EH) who were treated at the time of execution of ABP monitoring; other studies have been
conducted in subjects who were poorly controlled with treatment or in untreated hypertension patients. But few studies conducted in patients with non-diabetic EH, while Diabetes Mellitus is the most important risk factor of end-target damage and cardiovascular events.
Objectives
The objective of this study was to establish whether ambulatory blood pressure offered a better estimate of cardiovascular risk than its clinical blood pressure counterpart did in non-diabetic untreated essential hypertension subjects.
Objects and Methods
1. Patients and controls
82 untreated EH patients were included in the study. (43 male, 39 female, the mean age was 63 + 10 years and the mean history time was 7.98 7.94 years)
The inclusion criteria were as following: clinical diastolic BP was above 90 mmHg and (or) systolic BP was above 160mmHg.
Exclusion criteria were as following: patients with diabetes mellitus or secondary hypertension; patients had a history or sign of previous cardiovascular events, such as congestive heart failure, myocardial infarction, angina pectoris and stroke; patients had renal diseases, urine tract diseases and serum creatinine level above 1.5mmol/L; conditions preventing from data collection, such as atrial fibrillation and pulmonary emphysema.
All the patients were first divided into two groups according to clinical blood pressure level. 26 Patients in group 1: BP below 140/90 mmHg. And 56 patients in group 2: BP level above 140/90mmHg. All the patients were then divided into another two groups according ABPM monitoring, 27 patients in group A : mean blood pressure below 130/85mmHg,and 55 patients in group B : mean blood pressure above 130/85mmHg. 2. Methods
2.1 BP was measured in a quiet environment with a mercury sphygmomanometer with the patient in a supine position after 10 minutes' rest, SBP and DBP (Korotkoff phase I and phase V, respectively) represented in each visit the mean of three different readings measured at 2-minute intervals.
2.2 ABPM was performed with the use of an oscillometric monitor
(Spacelabs 9200 ), recording began between 8:30 and 9:00 with readings every 30 minutes to 8:00 in the next morning. Recording mean systolic blood pressure(MSBP) mean diastolic blood pressure (MDBP) pulse pressure (PP=MSBP-MDBP), daytime mean systolic blood pressure (dSBP), daytime mean diastolic blood pressure(dDBP), night mean systolic blood pressure(nSBP), night mean diastolic blood pressure (nDBP).
2.3 Blood samples were obtained in the morning after a minimum of 8 hours fasting. Serum biochemical profiles were measured using an autoanalyzer system multianalyzer computer: creatinine, cholesterol and glucose.
Two separate 24-hour urine collections were measured using an immunonephelometric assay (BECKMAN ARRAY) to measure micro-albuminuria.
2.4 Echocardiography
Echocardiography were performed with SONOS-5500 Doppler Echocardiography instrument, left ventricle internal dimensions (LVIDd), posterior wall (LPWP) and interventricular septum thickness (IVST) were measured according to the recommendations of American Society of Echocardiography. Left ventricular mass (LVM) and Left ventricular mass index (LVMI) were calculated by the formula as following '?LVM(g)=0.8 X
1.04[(IVST+LVIDd+LPWP)3-LVIDd3]+0.6, LVMI (g/m2) =LVM/BSA
2.5 Intima media thickness (IMT) and plaque of the carotid artery
The
动态血压监测(ABPM)对高血压病(HP)患者血压监测有独特的优越性。ABPM可以提供白天、夜间和清晨血压的信息；排除了“白大衣效应”和“安慰剂效应”，更准确的反映真实的血压水平，重复性好；能显示出血压的昼夜节律、血压值的变异度、血压负荷等有价值的指标；对阵发性高血压、顽固性高血压、临界性高血压、“白大衣性正常血压”有特殊的诊断价值。而诊所血压因传统的汞柱式血压计无法实时、连续的进行血压的监测，又易于受体位、情绪、活动的影响，根据ELSA研究的结果，诊所血压和24h动态血压有一定的相关性，但相关系数很小，诊所血压并不能很好的反映24h血压的真实水平，因此只有动态血压才能敏感而客观地监测HP患者实际的血压水平。
由于靶器官损害(TOD)在评价高血压患者心血管危险方面的重要性，对每一
浙江大学硕士学位论文
个HP患者都应仔细寻找TOD的证据。2003年《欧洲高血压治疗指南》规定TOD包
括左室肥厚(LVH)、颈动脉内膜中层厚度(工MT)、M以、血清肌配浓度(Cr)
>l .snunol/L。在高血压患者中评价ABPM对TOD及各种心脑血管事件的预测价值己
经进行了一些研究，结论是24h平均血压值与靶器官损害有关，随着平均血压值
的增高，高血压对靶器官危害性增加。然而，由于同时存在代谢紊乱，有1/3左
右的高血压患者同时合并有2型糖尿病，而糖尿病对HP患者的各种靶器官的损害
以及预后都将产生重要的影响，而且其产生靶器官的损害的机制也不完全相同。
因此为了明确ABPM对高血压靶器官损害的预测价值需排除糖尿病的影响。而目前
国内外类似的研究大多未将研究范围限制在非糖尿病的HP患者。
目的
本研究以S2名未经降压治疗的非糖尿病的HP患者为研究对象，选择LVMI、
IMT、MCA为靶器官损害的指标，排除了糖尿病对结果的影响，进一步评价ABPM对
非糖尿病的HP患者TOD及今后发生CV事件的预测价值。
对象和方法
1对象和分组
选择2002年1月一2003年1月期间在金华市中心医院心内科住院的HP患者
52名(男性43名，女性39名)，年龄35~83(63士10)岁，平均高血压病程(7.98
士7 .94)年。
浙江大学硕士学位论文
1 .1入选标准:未经正规降压药物治疗的高血压患者或初诊的高血压病患者，符
合1999年WHo/IsH高血压诊断标准:不同日两次以上收缩压SBP)140mmHg
和(或)舒张压DBp妻90rnrnHgO
1 .2排除标准:排除各种继发性高血压、糖尿病(空腹血糖妻7.0~ol/L或餐后2h
血糖妻11.lmmol几)、泌尿系统疾病，有严重的心脑血管并发症的病史或体征(充
血性心衰、心肌梗塞、心绞痛、短暂脑缺血发作和中风)或肾功能损害(Cr>
1.5m留dl)。严重肺气肿和房颤患者因影响超声数据的收集也不列入研究。
1 .3分组方法:所有入选的患者根据入院后水银柱血压计测量的诊所血压值分为
两组，组l为血压<140/gommHg(n=26)，组2为血压)140/90mrnHg(n=56)。
所有患者再根据入院后24h动态血压值重新分组，组A平均血压值<130/85mmHg
(n=27)，组B平均血压值〕130/ 85mmHg(n=55)。
2方法
2.1诊所血压的测量用标准水银柱血压计完成诊所血压的测量，柯氏第一和第
五音作为收缩压与舒张压值。患者坐位或卧位休息10分钟以上，以卧位测量3次，
间隔2分钟分别读出3次收缩与舒张压后取平均值。所有的测量都在上午8一9点之
间完成，在同一侧受臂进行测量。诊所血压的测量时间与动态血压监测安排为同
一天。
2.2动态血压的测量以美国SpaceLabs 5200型24h动态血压检测系统进行动态
血压检测，白天及夜间均设置为每30min自动记录一次血压读数，测定平均收缩
压MSBP，平均舒张压MDBP，脉压(PP=MSBP一MDBP)，白天平均收缩压dDBP，
浙江大学硕士学位论文
白天平均舒张压dSBP，夜间平均收缩压nSBP，夜间平均舒张压nDBP。
2.3生化指标的测定:
(l)采用德国BECKMAN CXg生化分析仪测定血清空腹和餐后2h血糖(GLU)、
肌配(Cr)、总胆固醇(TC)浓度。
(2)采用特定蛋白分析仪测定尿微量白蛋白含量，乘以24h总尿量即为24h尿
微量白蛋白总量。连续测定两次取均值。M以定义为30一30Omg/24h
2.4采用美国惠普公司SONOS一5500型多普勒超声诊断仪，取胸骨旁左室长轴
切面用M型超声测量室间隔舒张末期厚度(Wsd)，左室后壁舒张末期厚度
(PWTd)，左室舒张末期内径(LVIDd)，采用美国超声协会推荐公式计算左室重
量LVM(g)=0.8又1 .04[(IVsT+LVIDd+Lpwp)3一LVIDd3]+0.6，左室重量指数LVMI
(g/m2)一LVM旧SA，左室肥厚(LVH)的诊断标准为LVMI男性>1 25 g/mZ女性
>1209/m。
2.5颈总动脉内膜一中层厚度(I MT)和动脉硬化斑块的测量:
(l)应用美国ATL 5000型B型超声诊断仪进行双侧颈总动脉IMT的测量。横纵
向观察颈总动脉，冻结颈动脉窦以下1。m处(无斑块部位)的图像，共测量5次IMT，
取10次左右侧测量值的平均值即为平均颈总动脉IMT。测定的IMT范围在0.50一
20mm间。IMT>0.9被认为是内膜增厚。
(2)颈动脉斑块测定:若发现斑块，横纵向冻结图像，并测量其厚度，若在同一
动脉段发现多个斑块，记录斑块数目，并测量
Measurements of ambulatory blood pressure as an adjunct to casual/clinic blood pressure measurements are widely used for the diagnosis and treatment of hypertension currently. It has uniformly demonstrated on a cross-sectional basis that average ambulatory blood pressure (ABP) is correlated to target-organ damage. Several event-based cohort studies have shown that ABP improves cardiovascular risk stratification over and beyond office BP. Most of these studies have been conducted in subjects with essential hypertension (EH) who were treated at the time of execution of ABP monitoring; other studies have been
conducted in subjects who were poorly controlled with treatment or in untreated hypertension patients. But few studies conducted in patients with non-diabetic EH, while Diabetes Mellitus is the most important risk factor of end-target damage and cardiovascular events.
Objectives
The objective of this study was to establish whether ambulatory blood pressure offered a better estimate of cardiovascular risk than its clinical blood pressure counterpart did in non-diabetic untreated essential hypertension subjects.
Objects and Methods
1. Patients and controls
82 untreated EH patients were included in the study. (43 male, 39 female, the mean age was 63 + 10 years and the mean history time was 7.98 7.94 years)
The inclusion criteria were as following: clinical diastolic BP was above 90 mmHg and (or) systolic BP was above 160mmHg.
Exclusion criteria were as following: patients with diabetes mellitus or secondary hypertension; patients had a history or sign of previous cardiovascular events, such as congestive heart failure, myocardial infarction, angina pectoris and stroke; patients had renal diseases, urine tract diseases and serum creatinine level above 1.5mmol/L; conditions preventing from data collection, such as atrial fibrillation and pulmonary emphysema.
All the patients were first divided into two groups according to clinical blood pressure level. 26 Patients in group 1: BP below 140/90 mmHg. And 56 patients in group 2: BP level above 140/90mmHg. All the patients were then divided into another two groups according ABPM monitoring, 27 patients in group A : mean blood pressure below 130/85mmHg,and 55 patients in group B : mean blood pressure above 130/85mmHg. 2. Methods
2.1 BP was measured in a quiet environment with a mercury sphygmomanometer with the patient in a supine position after 10 minutes' rest, SBP and DBP (Korotkoff phase I and phase V, respectively) represented in each visit the mean of three different readings measured at 2-minute intervals.
2.2 ABPM was performed with the use of an oscillometric monitor
(Spacelabs 9200 ), recording began between 8:30 and 9:00 with readings every 30 minutes to 8:00 in the next morning. Recording mean systolic blood pressure(MSBP) mean diastolic blood pressure (MDBP) pulse pressure (PP=MSBP-MDBP), daytime mean systolic blood pressure (dSBP), daytime mean diastolic blood pressure(dDBP), night mean systolic blood pressure(nSBP), night mean diastolic blood pressure (nDBP).
2.3 Blood samples were obtained in the morning after a minimum of 8 hours fasting. Serum biochemical profiles were measured using an autoanalyzer system multianalyzer computer: creatinine, cholesterol and glucose.
Two separate 24-hour urine collections were measured using an immunonephelometric assay (BECKMAN ARRAY) to measure micro-albuminuria.
2.4 Echocardiography
Echocardiography were performed with SONOS-5500 Doppler Echocardiography instrument, left ventricle internal dimensions (LVIDd), posterior wall (LPWP) and interventricular septum thickness (IVST) were measured according to the recommendations of American Society of Echocardiography. Left ventricular mass (LVM) and Left ventricular mass index (LVMI) were calculated by the formula as following '?LVM(g)=0.8 X
1.04[(IVST+LVIDd+LPWP)3-LVIDd3]+0.6, LVMI (g/m2) =LVM/BSA
2.5 Intima media thickness (IMT) and plaque of the carotid artery
The
引文
[1]Zanchetti A, Bond MG,, Hennig M, et al. Calcium antagonist lacidipine slows down progression of asymptomatic carotid atherosclerosis: principal results of the European Lacidipine Study on Atherosclerosis (ELSA), a randomized, double-blind, long-term trial.. Circulation.. 2002. 5, 106(19): 2422-7.
[2]Cuspid C, Ambrosioni E, Mancia G,, et al. Role of echocardiogaphy and carotid ultrasonography in stratifying risk in patients with essential hypertension; The Assessment of Prognostic Risk Observation Survay. J. Hypertens. 2002, 20: 1307-1314.
[3]Roberto P, Antonella S, Maura R, et al. Prevalence and Clinical Correlates of Microalbuminuria in Essential Hypertensio.The MAGIC Study. Hypertension.. 1997, 30: 1135-1143.
[4]2003 European Society of Hypertension—European Society of Cardiology Guideline for the Management of arterial hypertension. Guideline committee. Journal of Hypertension. 2003, 21: 1011-1053.
[5]Giuseppe M, Alberto Z , Enrico A, et al. Ambulatory Blood Pressure Is Superior to Clinic Blood Pressure in Predicting Treatment-induced Regression of Left Ventricular Hypertrophy. Circulation. 1997, 95: 1464-1470.
[6]Mallion J-M, Baguet J-P, SichéJ-P, Tremel F, De Gaudemaris R. Clinical value of ambulatory blood pressure monitoring. J Hypertens. 1999;17:585-595.
[7]Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Porcellati C. Prognostic significance of the white-coat effect. Hypertension. 1997;29:1218-1224.[
[8]Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Pede S, Porcellati C. Ambulatory pulse pressure: a potent predictor of total cardiovascular risk in hypertension. Hypertension. 1998;32:983-988.
[9]王瑞冬、汪兰珍，老年高血压的动态血压监测，中华老年医学杂志1997，16(3)：159-161
[10]张传玉、阮萍、马建群等。动态血压负荷对高血压并靶器官损害的评价。临床心血管杂志1997，13(5)，286-288
[11]Dervereux R, Alonao E, Lutas E, et al. Echocardiography assessment of left ventricular hypertrophy Comparism to necropsy findings. Am J Cardiol, 1986, 57:450-458.
[12]张维忠，邱慧丽，范明昌等。高血压左心室肥厚的诊断探讨—5437例超声心动图资料分析。中国高血压杂志，1993，1(1)：5-7．
[13]Hoegholm A, Bangle L, Kristensen K, et al. Microalbuminuria in 411 untreated individuals with established hypertension 、 white -coat hypertension and normotension . Hypertension, 1994, 24: 101-105.
[14]Giaconi S, Levanti C, Fommei E, et al. Microalbuminuria and causal and ambulatory blood pressure monitoring in normotensives and in patients with bordline and mild essential hypertension. Am J Hypertense, 1989, 2: 259-261.
[15]Bianchi S, Bigazzi R, Amoroso A,et al.Silent ischemia is more prevalent among hypertensive patients with microalbuminuria and salt sensitivity. J Hum Hypertens. 2003 Jan; 17(1):13-20.
[16]Bianchi S, Bigazzi R, Campese VM. Microalbuminuria inessential hypertension: significance, pathophysiology, andtherapeutic implications. Am J Kidney Dis 1999;34:973-995.
[17]Roberto P, Giuseppe P, Giulia D, et al. Microalbuminuria and Transcapillary Albumin Leakage in Essential Hypertension Hypertension. 1999;34:491-495.
[18]Mogensen CE, Keane WF, Bennet et al. Prevention of diabeticrenal disease with special reference to mikroalbuminuria. Lancet. 1995;346:1080-4.
[19]G Viberti .Mechanism of hypertension-mediated end-organ damage in diabetes Endocrine Abstracts. 2003, 6: 221-224.
[20]Lery D, Garrison R, Savage D, et al. Prognostic implications of echocardiographically determined Left Ventricular mass in the Framingham Heart Study.. Engl J Med, 1990, 322:1561-1566.
[21]Koren M, Devereux R, Casale P, et al. Relation of Left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann IntemMed 1991, 114: 342-352.
[22]Muler G , Nardi E, Andronico G, et al.Relationships between 24h blood pressure and target organ damage in patients with mild-to morderate essential hypertension Blood Press Monit, 2001, 6 (3): 115-123
[23]Sander D, Kukla C, Klingeh O, et al。 Relationships between blood pressure pattens and progression of early carotid atherosclerosis: a 3-year follow-up study, Circulation, 2000, 102 (13): 1536-1541
[24]Amar J, Bieler L, Salvador M et al.Intima media thickness of the carotid artery in white coat and ambulatory hypertension. Arch Mal Coeur Vaiss. 1997 Aug;90(8): 1075-1078
[25]孙刚，闫旭龙 王峰等。老年原发性高血压患者心脑血管事件与动态血压的关系。中国循环杂志，2000，10(15)280-282
[26]Imai Y, Nagnai K, Sakuma M, et al. Ambulatory blood pressure of adults in Ohasma.. Japan Hypertension, 1993, 22: 900-912.
[27]Redon J, Campos C, Narciso ML, et al, Prognostic value of ambulatory blood pressure monitoring inrefractory hypertension:a prospective study. Hypertension.. 1998, 31(2): 712-8..
[28]Staessen J, Thijs L, Fagard R, et al. Predicting cardiovascular risk using conventional vs ambulatory blood pressure in older patients with systolic hypertension, Systolic Hypertension in Europe Trial Investigators, JAMA, 1999, 282: 539-546.
[29]Franklin S, Lanson M, Khan S, et alo Does the relation of blood pressure to coronary heart disease risk change with age ? The Framgham heart study, Circulation, 2001, 103: 1245-1249
[30]Prospective studies collaboration Age-specific relevance of usual blood pressure to vascular mortablity: a meta—analysis of individual data for one million adults in 61 prospective studies, Lancet, 2002, 360.. 1903-1913
[2]Cuspid C, Ambrosioni E, Mancia G,, et al. Role of echocardiogaphy and carotid ultrasonography in stratifying risk in patients with essential hypertension; The Assessment of Prognostic Risk Observation Survay. J. Hypertens. 2002, 20: 1307-1314.
[3]Roberto P, Antonella S, Maura R, et al. Prevalence and Clinical Correlates of Microalbuminuria in Essential Hypertensio.The MAGIC Study. Hypertension.. 1997, 30: 1135-1143.
[4]2003 European Society of Hypertension—European Society of Cardiology Guideline for the Management of arterial hypertension. Guideline committee. Journal of Hypertension. 2003, 21: 1011-1053.
[5]Giuseppe M, Alberto Z , Enrico A, et al. Ambulatory Blood Pressure Is Superior to Clinic Blood Pressure in Predicting Treatment-induced Regression of Left Ventricular Hypertrophy. Circulation. 1997, 95: 1464-1470.
[6]Mallion J-M, Baguet J-P, SichéJ-P, Tremel F, De Gaudemaris R. Clinical value of ambulatory blood pressure monitoring. J Hypertens. 1999;17:585-595.
[7]Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Porcellati C. Prognostic significance of the white-coat effect. Hypertension. 1997;29:1218-1224.[
[8]Verdecchia P, Schillaci G, Borgioni C, Ciucci A, Pede S, Porcellati C. Ambulatory pulse pressure: a potent predictor of total cardiovascular risk in hypertension. Hypertension. 1998;32:983-988.
[9]王瑞冬、汪兰珍，老年高血压的动态血压监测，中华老年医学杂志1997，16(3)：159-161
[10]张传玉、阮萍、马建群等。动态血压负荷对高血压并靶器官损害的评价。临床心血管杂志1997，13(5)，286-288
[11]Dervereux R, Alonao E, Lutas E, et al. Echocardiography assessment of left ventricular hypertrophy Comparism to necropsy findings. Am J Cardiol, 1986, 57:450-458.
[12]张维忠，邱慧丽，范明昌等。高血压左心室肥厚的诊断探讨—5437例超声心动图资料分析。中国高血压杂志，1993，1(1)：5-7．
[13]Hoegholm A, Bangle L, Kristensen K, et al. Microalbuminuria in 411 untreated individuals with established hypertension 、 white -coat hypertension and normotension . Hypertension, 1994, 24: 101-105.
[14]Giaconi S, Levanti C, Fommei E, et al. Microalbuminuria and causal and ambulatory blood pressure monitoring in normotensives and in patients with bordline and mild essential hypertension. Am J Hypertense, 1989, 2: 259-261.
[15]Bianchi S, Bigazzi R, Amoroso A,et al.Silent ischemia is more prevalent among hypertensive patients with microalbuminuria and salt sensitivity. J Hum Hypertens. 2003 Jan; 17(1):13-20.
[16]Bianchi S, Bigazzi R, Campese VM. Microalbuminuria inessential hypertension: significance, pathophysiology, andtherapeutic implications. Am J Kidney Dis 1999;34:973-995.
[17]Roberto P, Giuseppe P, Giulia D, et al. Microalbuminuria and Transcapillary Albumin Leakage in Essential Hypertension Hypertension. 1999;34:491-495.
[18]Mogensen CE, Keane WF, Bennet et al. Prevention of diabeticrenal disease with special reference to mikroalbuminuria. Lancet. 1995;346:1080-4.
[19]G Viberti .Mechanism of hypertension-mediated end-organ damage in diabetes Endocrine Abstracts. 2003, 6: 221-224.
[20]Lery D, Garrison R, Savage D, et al. Prognostic implications of echocardiographically determined Left Ventricular mass in the Framingham Heart Study.. Engl J Med, 1990, 322:1561-1566.
[21]Koren M, Devereux R, Casale P, et al. Relation of Left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann IntemMed 1991, 114: 342-352.
[22]Muler G , Nardi E, Andronico G, et al.Relationships between 24h blood pressure and target organ damage in patients with mild-to morderate essential hypertension Blood Press Monit, 2001, 6 (3): 115-123
[23]Sander D, Kukla C, Klingeh O, et al。 Relationships between blood pressure pattens and progression of early carotid atherosclerosis: a 3-year follow-up study, Circulation, 2000, 102 (13): 1536-1541
[24]Amar J, Bieler L, Salvador M et al.Intima media thickness of the carotid artery in white coat and ambulatory hypertension. Arch Mal Coeur Vaiss. 1997 Aug;90(8): 1075-1078
[25]孙刚，闫旭龙 王峰等。老年原发性高血压患者心脑血管事件与动态血压的关系。中国循环杂志，2000，10(15)280-282
[26]Imai Y, Nagnai K, Sakuma M, et al. Ambulatory blood pressure of adults in Ohasma.. Japan Hypertension, 1993, 22: 900-912.
[27]Redon J, Campos C, Narciso ML, et al, Prognostic value of ambulatory blood pressure monitoring inrefractory hypertension:a prospective study. Hypertension.. 1998, 31(2): 712-8..
[28]Staessen J, Thijs L, Fagard R, et al. Predicting cardiovascular risk using conventional vs ambulatory blood pressure in older patients with systolic hypertension, Systolic Hypertension in Europe Trial Investigators, JAMA, 1999, 282: 539-546.
[29]Franklin S, Lanson M, Khan S, et alo Does the relation of blood pressure to coronary heart disease risk change with age ? The Framgham heart study, Circulation, 2001, 103: 1245-1249
[30]Prospective studies collaboration Age-specific relevance of usual blood pressure to vascular mortablity: a meta—analysis of individual data for one million adults in 61 prospective studies, Lancet, 2002, 360.. 1903-1913