蒙古族人群炎症和内皮功能标志与心脑血管病的关系
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摘要
研究目的:
1探讨内蒙古农牧区蒙古族人群中炎症和内皮功能异常与心血管病传统危险因素(高血压、超重和肥胖、血糖水平异常、血脂水平异常)的关联关系;2探讨炎症和内皮功能异常与心脑血管事件危险的关联关系。3探讨外源性感染与心脑血管事件的关联关系。
对象与方法:
1现况研究:于2002～2003年,选取内蒙古通辽市科左后旗朝鲁吐苏木乡和奈曼旗固日班花苏木乡作为研究现场,将其中20岁及以上蒙古族居民作为研究对象。采用统一编制的调查表,由经过培训的调查人员对研究对象进行调查,并测量血压、人体指标,采集血标本。现场调查内容包括:人口统计学特征、吸烟和饮酒情况、高血压病家族史等;现场测量指标包括:三次血压、身高、体重、腰围和臀围;实验室检测指标包括:甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)、空腹血糖、胰岛素、C-反应蛋白(CRP)、细胞间粘附分子(ICAM-1)、E选择素(E-selectin)、血管紧张素Ⅱ(AngⅡ)和肺炎衣原体(CP)、肺炎支原体(MP)、幽门螺杆菌(HP)及柯萨奇病毒(CV)Ig抗体的检测。
2巢氏病例对照研究:自2004年开始至2010年,对参与现况研究的2589人进行了连续的随访调查。以心脑血管事件作为结局事件(包括脑卒中和冠心病)。将入户调查和查阅医院病例档案相结合,采用统一设计的调查表对研究对象进行调查,收集随访期间发生心脑血管事件的有关资料。对随访研究中得到的脑卒中和冠心病新发病例,分别选取同性别、同年龄(±3岁)、并与病例居住邻近(邻居)的无心脑血管事件者作为对照,与病例1:1配对,进行巢式病例对照研究。
3统计分析:采用Epidata3.0软件建立数据库,所有数据经双遍录入。用SAS9.1进行统计分析。P=0.05作为显著性水准。
结果:
1炎症和内皮功能异常与心血管病传统危险因素的关系
1.1本研究共纳入2589名蒙古族人,其中男性1064人,女性1525人;年龄最小者为20岁,最大者为84岁,平均年龄为46.51岁。
1.2 AngⅡ、CRP、ICAM-1和E-selectin在高血压组的水平高于正常血压组,logistic回归分析结果显示,经多因素调整后,AngⅡ和CRP与高血压患病危险性之间存在着显著的关联关系,与AngⅡ和CRP最低水平者相比,其AngⅡ和CRP位于最高水平者患高血压的OR(95%CI)分别为1.87(1.43～2.46)和1.40(1.06～1.85)。
1.3多因素loistic回归分析结果表明,高腰围与高CRP存在着显著的关联关系(OR=1.46, 95%CI=1.21～1.76),高BMI与高E-selectin存在显著的关联关系(OR=1.30, 95%CI=1.08～1.55);与最低水平者相比,高CRP和高ICAM-1水平者空腹血糖异常或患糖尿病的危险性显著增加,其OR(95%CI)分别为2.93(2.39～3.59)和3.48(2.85～4.24);与正常者相比,TG、TC和LDL-C异常与高CRP存在显著的关联关系,其OR(95%CI)分别为3.36 (2.65～4.27)、1.87(1.40～2.48)和1.69(1.32～2.19);与HDL-C>1.04 mmol/L者相比,HDL-C≤1.04 mmol/L者的CRP水平升高的危险增加,其OR(95%CI)为1.79(1.47～2.19)。
2炎症和内皮功能异常与心脑血管事件的关系(巢氏病例对照研究)
2.1经多因素调整后,与基线CRP<3.95mg/L者相比,基线CRP≥11.39mg/L者发生脑卒中危险的OR(95%CI)为3.40(1.13～10.24)。无论是单因素分析还是多因素调整,基线血清AngⅡ、ICAM-1和E-selectin水平与脑卒中的发病危险均未发现有统计学关联,也未发现这些标志物与冠心病之间存在关联关系。
2.2高AngⅡ、高CRP、高ICAM-1和高E-selectin相互聚集与脑卒中发病有关,在脑卒中病例组,基线时有2个或2个以上炎症和内皮功能标志物水平升高的聚集率(51.06%)显著高于对照组(30.85%),P<0.05。以0个聚集者为参比,经多因素调整后,基线时有2个或2个以上指标聚集者的脑卒中发病危险的OR(95%CI)为10.76(2.54～45.63)。
2.3肺炎衣原体感染者发生脑卒中的危险是未感染者的3.09倍,其OR(95%CI)为3.09(1.20～7.94),经多因素调整后,这种关联仍有统计学意义,其OR(95%CI)为2.59(1.07～6.29)。多因素调整后,CV感染者与未感染者相比,发生冠心病的危险性显著增加,其OR(95%CI)为5.56(1.15～26.90)。
结论:
1具有高水平CRP和AngⅡ者,患高血压的危险性增加,提示炎症和内皮功能异常可能在高血压的发展过程中发挥了一定作用;
2高WC和高BMI与炎症和内皮功能标志物水平升高相关联;血脂各成分水平异常均与CRP水平升高相关联;炎症和内皮功能标志物水平升高与空腹血糖异常或糖尿病相关联。
3 CRP水平升高可增加脑卒中的发病危险,2个或2个以上高水平炎症和内皮功能标志物的聚集可增加脑卒中的发病危险。
4 CP感染可增加脑卒中的发病危险, CV感染可增加冠心病的发病危险。CP和CV感染可能分别是脑卒中和冠心病的危险因素。
5本研究结果提示炎症和内皮功能异常与其他心血管病危险因素一样,也是心脑血管病的重要危险因素,可能与其他心血管病危险因素有相互促进的作用,也可能是心脑血管病发病的重要机制之一。
Objective:1. To explore the association between inflammation and endothelial dysfunction and cardiovascular risk factors ( hypertension,obesity,hyperglycemia and dyslipidemia) among Mongolian population in agricultural and pastoral areas,Inner Mongolia. 2.To investigate relationship between inflammation and endothelial dysfunction and risk of cardio-cerebrovascular events. 3.To investigate the association between extraneous pathogen(Chlamydia pneumonia, Mycoplasma pneumonia, Helicobacter pylon, Coxackie Virus) infection and risk of cardio-cerebrovascular events.
Subjects and methods:
1. Baseline investigation: We conducted a cross-sectional study between 2002 and 2003 in Inner Mongolia, study participants aged 20 years and older were recruited from 32 villages in two adjacent townships located in Kezuohou Banner (county) and Naiman Banner.
Data on demographic information, lifestyle risk factors including smoking and alcohol drinking, family history of hypertension and personal medical history were obtained using a standard questionnaire administered by trained staff,and the related physical examination and blood samples collection were also conducted during field investigation. Body hight, weight, waist circumference,hip circumference and three times of blood pressures were measured for all participants.
Fasting plasma glucose(FPG), insulin, triglyceride(TG), total cholesterol(TC),
high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1(ApoA1), apolipoprotein B(ApoB), C-reactive protein(CRP), E-selectin, intercellular adhesion molecules-1(ICAM-1), angiotensinⅡ( AngⅡ) , and IgG antibodies for Chlamydia pneumonia, Mycoplasma pneumonia, Helicobacter pylori and Coxsackie virus were detected for all participants.
2. nest case-control study: Follow-up investigations had been conducted for the subjects involved in baseline study since year 2004. The cardio-cerebrovascular events (including stroke and coronary heart disease incidence) were the study outcome.We used household interview by designed questionnaires, monitoring data and hospital medical records to investigate cardio-cerebrovascular events. Based on follow-up investigations, a nested case-control study were conducted, and stroke and coronary heart disease patients occurred during follow-up period were served as the cases, and controls were selected from the participants without cardio-cerebrovascular events, matched by sex,age (±3 years) and residence address with cases.
3. Statistical analysis: The Epidata3.0 Software was used to build database. All data were checked after data entry for two times. SAS9.1 Software was used for statistical analysis, using P=0.05 as test level.
Results
1.A total of 2589 subjects aged 20-84 years old, 1064 males and 1525 females with average age of 46.51 years old, were included in the study.
2. AngⅡ, CRP, ICAM-1 and E-selectin in hypertension group were higher than that in normotensive group. Logistic regression analysis showed that AngⅡand CRP were positively and significantly associated with risk of hypertension, after adjustment for multivariate, compared with those with lowest AngⅡand CRP levels, the ORs (95% CIs) of hypertension were 1.87 (1.43-2.46) and 1.40 (1.06-1.85) for the participants with highest levels, respectively.
3. Multivariate logistic regression analysis showed that high WC was positively and significantly associated with risk of increased CRP (OR = 1.46, 95% CI = 1.21-1.76), high BMI was positively and significantly associated with risk of increased E-selectin (OR = 1.30, 95% CI = 1.08-1.55). impaired FPG or diabetes was positively and significantly associated with risks of increased CRP and ICAM-1, and compared with those without impaired FPG or diabetes, the ORs (95% CIs) of increased CRP and ICAM-1 were 2.93 (2.39-3.59) and 3.48 (2.85-4.24 ) for participants with impaired FPG or diabetes, respectively. High TG, high TC, high LDL-C and low HDL-C were positively and significantly associated with risk of increased CRP, and ORs (95% CIs) were 3.36(2.65-4.27), 1.87(1.40-2.48), 1.69(1.32-2.19) and 1.79(1.47-2.19) of increased CRP for participants with High TG, high TC, high LDL-C and low HDL-C respectively, compared with those with normal TG, TC, LDL-C and HDL-C.
4. Participants with CRP≥11. 39mg/L was almost 3 times the risk of stroke compared to participants with CRP<3.95mg/L , and OR (95%CI) was 3.40(1.13-10.24) , after multivariable adjustment, no matter whether unadjustment or multivariable adjustment, elevated AngⅡ, ICAM-1 and E-selectin levels were not significantly associated with increased risk for stroke incidence. The association of inflammation and endothelial dysfunction biomarkers with coronary heart disease incidence were not found in the present nest case-control study.
5. There was significant relationship between the clustering of elevated AngⅡ, CRP, ICAM-1 and E-selectin levels at baseline and stroke events, the proportion(51.06%) of≥2 elevated biomarkers was higher in the stroke cases than that in controls(30.85%), P<0.05. After multivariate adjustment, OR (95%CI) of stroke was 10.76 (2.54-45.63) for participants≥2 elevated biomarkers at baseline compared to those without elevated biomarker.
6. Participants infected with Chlamydia pneumoniae had 3.09 (1.20-7.94) times the risk of stroke compare to participants without Chlamydia pneumoniae infection under unadjustment for other variables, after multivariable adjustment, infection of Chlamydia pneumoniae was associated with increased risk for stroke, with OR (95%CI) of 2.59(1.07-6.29). After multivariable adjustment, OR (95%CI) of coronary heart disease was 5.56(1.15-26.90) for participants infected with coxsackie virus compare to those without coxsackie virus infection.
Conclusions:
1 Participants with elevated CRP level and AngⅡhad increased risk of hypertension, which indicate that inflammation and endothelial dysfunction may play a role in the development of hypertension.
2 High WC and BMI were associated with risk of elevated inflammation and endothelia biomarkers; abnormal levels of blood lipids were associated with elevated CRP; elevated inflammation and endothelial biomarkers was associated with impaired FPG or diabetes.
3 Elevated CRP might increase the risk of stroke incidence, 2 or more elevated inflammation and endothelial biomarkers might increase the risk for stroke incidence.
4 Participants infected with Chlamydia pneumonia had increased risk for stroke compared with those without Chlamydia pneumonia infection. Infection of Chlamydia pneumonia maybe a risk factor for stroke.Participants infected with coxsackie virus had increased risk for coronary heart disease compared with those without coxsackie virus infection. Infection of coxsackie virus maybe a risk factor for coronary heart disease.
5 The present study suggest that inflammation and endothelial dysfunction are also risk factors of cardio-cerebrovascular diseases as other cardiovascular risk factors, maybe inflammation and endothelial dysfunction and other cardiovascular risk factors promote them mutually or a mechanism in development cardio-cerebrovascular diseases.
1探讨内蒙古农牧区蒙古族人群中炎症和内皮功能异常与心血管病传统危险因素(高血压、超重和肥胖、血糖水平异常、血脂水平异常)的关联关系;2探讨炎症和内皮功能异常与心脑血管事件危险的关联关系。3探讨外源性感染与心脑血管事件的关联关系。
对象与方法:
1现况研究:于2002～2003年,选取内蒙古通辽市科左后旗朝鲁吐苏木乡和奈曼旗固日班花苏木乡作为研究现场,将其中20岁及以上蒙古族居民作为研究对象。采用统一编制的调查表,由经过培训的调查人员对研究对象进行调查,并测量血压、人体指标,采集血标本。现场调查内容包括:人口统计学特征、吸烟和饮酒情况、高血压病家族史等;现场测量指标包括:三次血压、身高、体重、腰围和臀围;实验室检测指标包括:甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)、空腹血糖、胰岛素、C-反应蛋白(CRP)、细胞间粘附分子(ICAM-1)、E选择素(E-selectin)、血管紧张素Ⅱ(AngⅡ)和肺炎衣原体(CP)、肺炎支原体(MP)、幽门螺杆菌(HP)及柯萨奇病毒(CV)Ig抗体的检测。
2巢氏病例对照研究:自2004年开始至2010年,对参与现况研究的2589人进行了连续的随访调查。以心脑血管事件作为结局事件(包括脑卒中和冠心病)。将入户调查和查阅医院病例档案相结合,采用统一设计的调查表对研究对象进行调查,收集随访期间发生心脑血管事件的有关资料。对随访研究中得到的脑卒中和冠心病新发病例,分别选取同性别、同年龄(±3岁)、并与病例居住邻近(邻居)的无心脑血管事件者作为对照,与病例1:1配对,进行巢式病例对照研究。
3统计分析:采用Epidata3.0软件建立数据库,所有数据经双遍录入。用SAS9.1进行统计分析。P=0.05作为显著性水准。
结果:
1炎症和内皮功能异常与心血管病传统危险因素的关系
1.1本研究共纳入2589名蒙古族人,其中男性1064人,女性1525人;年龄最小者为20岁,最大者为84岁,平均年龄为46.51岁。
1.2 AngⅡ、CRP、ICAM-1和E-selectin在高血压组的水平高于正常血压组,logistic回归分析结果显示,经多因素调整后,AngⅡ和CRP与高血压患病危险性之间存在着显著的关联关系,与AngⅡ和CRP最低水平者相比,其AngⅡ和CRP位于最高水平者患高血压的OR(95%CI)分别为1.87(1.43～2.46)和1.40(1.06～1.85)。
1.3多因素loistic回归分析结果表明,高腰围与高CRP存在着显著的关联关系(OR=1.46, 95%CI=1.21～1.76),高BMI与高E-selectin存在显著的关联关系(OR=1.30, 95%CI=1.08～1.55);与最低水平者相比,高CRP和高ICAM-1水平者空腹血糖异常或患糖尿病的危险性显著增加,其OR(95%CI)分别为2.93(2.39～3.59)和3.48(2.85～4.24);与正常者相比,TG、TC和LDL-C异常与高CRP存在显著的关联关系,其OR(95%CI)分别为3.36 (2.65～4.27)、1.87(1.40～2.48)和1.69(1.32～2.19);与HDL-C>1.04 mmol/L者相比,HDL-C≤1.04 mmol/L者的CRP水平升高的危险增加,其OR(95%CI)为1.79(1.47～2.19)。
2炎症和内皮功能异常与心脑血管事件的关系(巢氏病例对照研究)
2.1经多因素调整后,与基线CRP<3.95mg/L者相比,基线CRP≥11.39mg/L者发生脑卒中危险的OR(95%CI)为3.40(1.13～10.24)。无论是单因素分析还是多因素调整,基线血清AngⅡ、ICAM-1和E-selectin水平与脑卒中的发病危险均未发现有统计学关联,也未发现这些标志物与冠心病之间存在关联关系。
2.2高AngⅡ、高CRP、高ICAM-1和高E-selectin相互聚集与脑卒中发病有关,在脑卒中病例组,基线时有2个或2个以上炎症和内皮功能标志物水平升高的聚集率(51.06%)显著高于对照组(30.85%),P<0.05。以0个聚集者为参比,经多因素调整后,基线时有2个或2个以上指标聚集者的脑卒中发病危险的OR(95%CI)为10.76(2.54～45.63)。
2.3肺炎衣原体感染者发生脑卒中的危险是未感染者的3.09倍,其OR(95%CI)为3.09(1.20～7.94),经多因素调整后,这种关联仍有统计学意义,其OR(95%CI)为2.59(1.07～6.29)。多因素调整后,CV感染者与未感染者相比,发生冠心病的危险性显著增加,其OR(95%CI)为5.56(1.15～26.90)。
结论:
1具有高水平CRP和AngⅡ者,患高血压的危险性增加,提示炎症和内皮功能异常可能在高血压的发展过程中发挥了一定作用;
2高WC和高BMI与炎症和内皮功能标志物水平升高相关联;血脂各成分水平异常均与CRP水平升高相关联;炎症和内皮功能标志物水平升高与空腹血糖异常或糖尿病相关联。
3 CRP水平升高可增加脑卒中的发病危险,2个或2个以上高水平炎症和内皮功能标志物的聚集可增加脑卒中的发病危险。
4 CP感染可增加脑卒中的发病危险, CV感染可增加冠心病的发病危险。CP和CV感染可能分别是脑卒中和冠心病的危险因素。
5本研究结果提示炎症和内皮功能异常与其他心血管病危险因素一样,也是心脑血管病的重要危险因素,可能与其他心血管病危险因素有相互促进的作用,也可能是心脑血管病发病的重要机制之一。
Objective:1. To explore the association between inflammation and endothelial dysfunction and cardiovascular risk factors ( hypertension,obesity,hyperglycemia and dyslipidemia) among Mongolian population in agricultural and pastoral areas,Inner Mongolia. 2.To investigate relationship between inflammation and endothelial dysfunction and risk of cardio-cerebrovascular events. 3.To investigate the association between extraneous pathogen(Chlamydia pneumonia, Mycoplasma pneumonia, Helicobacter pylon, Coxackie Virus) infection and risk of cardio-cerebrovascular events.
Subjects and methods:
1. Baseline investigation: We conducted a cross-sectional study between 2002 and 2003 in Inner Mongolia, study participants aged 20 years and older were recruited from 32 villages in two adjacent townships located in Kezuohou Banner (county) and Naiman Banner.
Data on demographic information, lifestyle risk factors including smoking and alcohol drinking, family history of hypertension and personal medical history were obtained using a standard questionnaire administered by trained staff,and the related physical examination and blood samples collection were also conducted during field investigation. Body hight, weight, waist circumference,hip circumference and three times of blood pressures were measured for all participants.
Fasting plasma glucose(FPG), insulin, triglyceride(TG), total cholesterol(TC),
high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1(ApoA1), apolipoprotein B(ApoB), C-reactive protein(CRP), E-selectin, intercellular adhesion molecules-1(ICAM-1), angiotensinⅡ( AngⅡ) , and IgG antibodies for Chlamydia pneumonia, Mycoplasma pneumonia, Helicobacter pylori and Coxsackie virus were detected for all participants.
2. nest case-control study: Follow-up investigations had been conducted for the subjects involved in baseline study since year 2004. The cardio-cerebrovascular events (including stroke and coronary heart disease incidence) were the study outcome.We used household interview by designed questionnaires, monitoring data and hospital medical records to investigate cardio-cerebrovascular events. Based on follow-up investigations, a nested case-control study were conducted, and stroke and coronary heart disease patients occurred during follow-up period were served as the cases, and controls were selected from the participants without cardio-cerebrovascular events, matched by sex,age (±3 years) and residence address with cases.
3. Statistical analysis: The Epidata3.0 Software was used to build database. All data were checked after data entry for two times. SAS9.1 Software was used for statistical analysis, using P=0.05 as test level.
Results
1.A total of 2589 subjects aged 20-84 years old, 1064 males and 1525 females with average age of 46.51 years old, were included in the study.
2. AngⅡ, CRP, ICAM-1 and E-selectin in hypertension group were higher than that in normotensive group. Logistic regression analysis showed that AngⅡand CRP were positively and significantly associated with risk of hypertension, after adjustment for multivariate, compared with those with lowest AngⅡand CRP levels, the ORs (95% CIs) of hypertension were 1.87 (1.43-2.46) and 1.40 (1.06-1.85) for the participants with highest levels, respectively.
3. Multivariate logistic regression analysis showed that high WC was positively and significantly associated with risk of increased CRP (OR = 1.46, 95% CI = 1.21-1.76), high BMI was positively and significantly associated with risk of increased E-selectin (OR = 1.30, 95% CI = 1.08-1.55). impaired FPG or diabetes was positively and significantly associated with risks of increased CRP and ICAM-1, and compared with those without impaired FPG or diabetes, the ORs (95% CIs) of increased CRP and ICAM-1 were 2.93 (2.39-3.59) and 3.48 (2.85-4.24 ) for participants with impaired FPG or diabetes, respectively. High TG, high TC, high LDL-C and low HDL-C were positively and significantly associated with risk of increased CRP, and ORs (95% CIs) were 3.36(2.65-4.27), 1.87(1.40-2.48), 1.69(1.32-2.19) and 1.79(1.47-2.19) of increased CRP for participants with High TG, high TC, high LDL-C and low HDL-C respectively, compared with those with normal TG, TC, LDL-C and HDL-C.
4. Participants with CRP≥11. 39mg/L was almost 3 times the risk of stroke compared to participants with CRP<3.95mg/L , and OR (95%CI) was 3.40(1.13-10.24) , after multivariable adjustment, no matter whether unadjustment or multivariable adjustment, elevated AngⅡ, ICAM-1 and E-selectin levels were not significantly associated with increased risk for stroke incidence. The association of inflammation and endothelial dysfunction biomarkers with coronary heart disease incidence were not found in the present nest case-control study.
5. There was significant relationship between the clustering of elevated AngⅡ, CRP, ICAM-1 and E-selectin levels at baseline and stroke events, the proportion(51.06%) of≥2 elevated biomarkers was higher in the stroke cases than that in controls(30.85%), P<0.05. After multivariate adjustment, OR (95%CI) of stroke was 10.76 (2.54-45.63) for participants≥2 elevated biomarkers at baseline compared to those without elevated biomarker.
6. Participants infected with Chlamydia pneumoniae had 3.09 (1.20-7.94) times the risk of stroke compare to participants without Chlamydia pneumoniae infection under unadjustment for other variables, after multivariable adjustment, infection of Chlamydia pneumoniae was associated with increased risk for stroke, with OR (95%CI) of 2.59(1.07-6.29). After multivariable adjustment, OR (95%CI) of coronary heart disease was 5.56(1.15-26.90) for participants infected with coxsackie virus compare to those without coxsackie virus infection.
Conclusions:
1 Participants with elevated CRP level and AngⅡhad increased risk of hypertension, which indicate that inflammation and endothelial dysfunction may play a role in the development of hypertension.
2 High WC and BMI were associated with risk of elevated inflammation and endothelia biomarkers; abnormal levels of blood lipids were associated with elevated CRP; elevated inflammation and endothelial biomarkers was associated with impaired FPG or diabetes.
3 Elevated CRP might increase the risk of stroke incidence, 2 or more elevated inflammation and endothelial biomarkers might increase the risk for stroke incidence.
4 Participants infected with Chlamydia pneumonia had increased risk for stroke compared with those without Chlamydia pneumonia infection. Infection of Chlamydia pneumonia maybe a risk factor for stroke.Participants infected with coxsackie virus had increased risk for coronary heart disease compared with those without coxsackie virus infection. Infection of coxsackie virus maybe a risk factor for coronary heart disease.
5 The present study suggest that inflammation and endothelial dysfunction are also risk factors of cardio-cerebrovascular diseases as other cardiovascular risk factors, maybe inflammation and endothelial dysfunction and other cardiovascular risk factors promote them mutually or a mechanism in development cardio-cerebrovascular diseases.
引文
1 Powles J, Day N. Interpreting the global burden of disease. Lancet 2002, 360: 1342.
2 Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data. Lancet 2005; 365: 217–223.
3 He J,Gu D,Wu X, et al. Major causes of death among men and women in China. N Engl J Med 2005; 353: 1124–1134.
4李立明,饶克勤.中国居民2002年营养与健康状况调查.中华流行病学杂志2005; 7:478-484.
5 Dekker JM, Girman C, Rhodes T, et al. Metabolic Syndrome and 10-Year Cardiovascular Disease Risk in the Hoorn Study. Circulation 2005; 112: 666-673.
6 Isomaa B,Almgren P, Tuomi T, et al. Cardiovascular Morbidity and Mortality Associated With the Metabolic Syndrome. Diabetes Care 2001; 24: 683-689.
7 de Jager J,Dekker JM, Kooy A, et al. Endothelial Dysfunction and Low-Grade Inflammation Explain Much of the Excess Cardiovascular Mortality in Individuals With Type 2 Diabetes: The Hoorn Study. Arterioscler Thromb Vasc Biol 2006; 26: 1086- 1093.
8吴兆苏,姚崇华,赵东.我国人群脑卒中发病率、死亡率的流行病学研究.中华流行病学杂志2003; 24: 236-239.
9 Zhang C. The role of inflammatory cytokines in endothelial dysfunction. Basic Research in Cardiology 2008; 103:398-406.
10 Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation, Part I. Circulation 2003; 108: 1917-1923.
11 Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342: 836-843.
12 Schiffrin EL, Touyz RM. Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. J Am Coll Cardiol 2003; 42: 911-913.
13 Pastore L, Tessitore A, Martinotti S, et al. Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells andincreases soluble ICAM-1 release in vivo. Circulation 1999; 100: 1646-1652.
14 Schillaci G, Pirro M, Gemelli F, et al. Increased C-reactive protein concentrations in never-treated hypertension: the role of systolic and pulse pressures. J Hypertens 2003; 21: 1841-1846.
15 Bautista LE, Lópex-Jaramillo P, Vera LM, et al. Is C-reactive protein an independent risk factor for essential hypertension? J Hypertens 2001; 19: 857-861.
16 Sung KC, Suh JY, Kim BS, et al. High sensitivity C-reactive protein as an independent risk factor for essential hypertension. Am J Hypertens 2003; 16: 429-433.
17 Lakoski SG, Herrington DM, Siscovick DM, et al. C-reactive protein concentration and incident hypertension in young adults: the CARDIA study. Arch Intern Med. 2006; 166: 345-349.
18 Davey Smith G, Lawlor DA, Harbord R, et al. Association of C-reactive protein with blood pressure and hypertension life course confounding and Mendelian randomization tests of causality. Arterioscler Thromb Vasc Biol. 2005; 25: 1051-1056.
19 Bautista LE, Lopez-Jaramillo P, Vera LM, et al. Is C-reactive protein an independent risk factor for essential hypertension? J Hypertens 2001; 19: 857-861.
20 Sesso HD, Buring JE, Rifai N, et al. C-reactive protein and the risk of developing hypertension. JAMA 2003; 290: 2945-2951.
21 Miller MA, Kerry SM, Cook DG, et al. Cellular adhesion molecules and blood pressure interaction with sex in a multi-ethnic population. J Hypertens 2004; 22:705–711.
22 DeSouza CA, Dengel DR, Macko RF, et al. Elevated evels of circulating cell adhesion molecules in uncomplicated essential hypertension. Am J Hypertens 1997; 10: 1335-1341.
23 Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation, Part I. Circulation 2003; 108: 1917-1923.
24 Mulvihill NT, Foley JB. Inflammation in acute coronary syndromes. Heart 2002;87: 201-204.
25 Lindsberg PJ, Grau AJ. Inflammation and Infections as Risk Factors for Ischemic Stroke. Stroke 2003; 34: 2518-2532
26 Wakugawa Y, Kiyohara Y, Tanizaki Y, et al. C-Reactive Protein and Risk of First-Ever Ischemic and Hemorrhagic Stroke in a General Japanese Population. The Hisayama Study. Stroke 2006; 37: 27-32.
27 Bruno G, Fornengo P, Novelli G, et al. C-Reactive Protein and 5-Year Survival in Type 2 Diabetes. Diabetes 2009; 58: 926-933.
28 Lee C, Adler A, Sandhu M, et al. Association of C-reactive protein with type 2 diabetes: prospective analysis and meta-analysis. Diabetologia 2009; 52: 1040-1047.
29 Dehghan A, Kardys I, de Maat MPM, et al. Genetic Variation, C-Reactive Protein Levels, and Incidence of Diabetes. Diabetes 2007; 56: 872-878.
30 Wexler DJ, Hu FB, Manson JE, et al. Mediating Effects of Inflammatory Biomarkers on Insulin Resistance Associated with Obesity. Obesity 2005; 13: 1772- 1783.
31 Ye X, Franco OH, Yu Z, et al. Associations of inflammatory factors with glycaemic status among middle-aged and older Chinese people. Clinical Endocrinology 2009; 70: 854-862.
32 Miller MA, Cappuccio FP. Cellular adhesion molecules and their relationship with measures of obesity and metabolic syndrome in a multiethnic population. Int J Obes 2006; 30: 1176-1182.
33 Menke A, Muntner P, Wildman RP, et al. Measures of Adiposity and Cardiovascular Disease Risk Factors. Obesity 2007; 15: 785-795.
34 Esmaillzadeh A, Azadbakht L. Increased Levels of Inflammation among Women with Enlarged Waist and Elevated Triglyceride Concentrations. Ann Nutr Metab 2010; 57: 77-84.
1.中国成人血脂异常防治指南制订联合委员会.中国成人血脂异常防治指南.中华心血管病杂志2007, 35: 3902419.
2. Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance andβ2cell function from fasting plasma glucose and insulin concent rations in man. Diabetologia 1985; 28: 412-419.
1 Ridker PM. C-reactive protein and the prediction of cardiovascular events among those at intermediate risk. J Am Coll Cardiol 2007; 49:2129-2138.
2 Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation, part I.Circulation 2003; 108:1917-1923.
3 Pasceri V, Willerson JT, Yeh ETH. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000; 102:2165-2168.
4 Bautista LE, Lo′pex-Jaramillo P, Vera LM, et al. Is C-reactive protein an independent risk factor for essential hypertension?J Hypertens 2001; 19:857-861.
5 Sung KC, Suh JY, Kim BS, et al. High sensitivity C-reactive protein as an independent risk factor for essential hypertension.Am J Hypertens 2003; 16:429-433.
6 Lakoski SG, Herrington DM, Siscovick DM, et al. C-reactive protein concentration and incident hypertension in young adults: the CARDIA study. Arch Intern Med 2006; 166:345-349.
7 Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342:836-843.
8 DeSouza CA, Dengel DR, Macko RF, et al. Elevated levels of circulating cell adhesion molecules in uncomplicated essential hypertension. Am J Hypertens 1997;10:1335-1341.
9 Hlubocka Z, Umnerova V, Heller S, et al. Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors.J Human Hypertens 2002; 16:557-562.
10 Cottone S, Mule G, Nardi E, et al. C-reactive protein and intercellular adhesion molecule-1 are stronger predictors of oxidant stress than blood pressure in established hypertension. J Hypertens 2007; 25:423-428.
11 Miller MA, Kerry SM, Cook DG, et al. Cellular adhesion molecules and blood pressure interaction with sex in a multiethnic population. J Hypertens 2004; 22:705-711.
12 Schiffrin EL, Touyz RM. Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. J Am Coll Cardiol 2003; 42:911-913.
13 Pastore L, Tessitore A, Martinotti S, et al. Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells and increases soluble ICAM-1 release in vivo. Circulation 1999; 100:1646-1652.
14 Dzau VJ. Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis. Hypertension 2001; 37:1047-1052.
15 Liao TD, Yang XP, Liu YH, et al. Role of inflammation in the development of renal damage and dysfunction in angiotensin II-induced hypertension. Hypertension 2008; 52:256-263.
16 He J, Klag MJ, Appel LJ, et al. The renin-angiotensin system and blood pressure: differences between blacks and whites. Am J Hypertens 1999; 12:555-562.
17 Hwang SJ,Ballantyne CM,Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1 and E-selectin in carotid atherosclerosis and incident coronary heart disease cases.Circulation 1997;96:4219-4225.
18 Miller MA, Cappuccio FP. Cellular adhesion molecules and their relationship with measures of obesity and metabolic syndrome in a multiethnic population. Int J Obes 2006; 30: 1176-1182.
19 Bo?anskáL, Michalsky D, LacinováZ, et al. The influence of obesity and different fat depots on adipose tissue gene expression and protein levels of cell adhesion molecules. Physiol Res 2010;79:79-88
20 Ponthieux A, Herbeth B, Droesch S, et al. Biological determinants of serum ICAM-1, E-selectin, P-selectin and L-selectin levels in healthy subjects: the Stanislas study. Atherosclerosis 2004; 172: 299-308.
21 Kelly T, Yang W, Chen CS, et al. Global burden of obesity in 2005 and projections to 2030. Int J Obes 2008; 32: 1431-1437.
22 Adams KF, Schatzkin A, Harris TB, et al. Overweight, Obesity and Mortality in a Large Prospective Cohort of Persons 50 to 71 Years Old. N Engl J Med 2006; 355: 763-778.
23 Jee SH, Sull JW, Park J, et al. Body-Mass Index and Mortality in Korean Men and Women. N Engl J Med 2006; 355: 779-787.
24 Hu D, Xie J, Fu P, et al. Central Rather Than Overall Obesity Is Related to Diabetes in the Chinese Population: The InterASIA Study. Obesity 2007;15: 2809-2816.
25 Flegal KM, Graubard BI, Williamson DF, et al. Cause-Specific Excess Deaths Associated With Underweight, Overweight, and Obesity. JAMA 2007; 298: 2028-2037.
26 Pischon T, Boeing H, Hoffmann K, et al. General and Abdominal Adiposity and Risk of Death in Europe. N Engl J Med 2008; 359: 2105-2120.
27 Menke A, Muntner P, Wildman RP, et al. Measures of Adiposity and Cardiovascular Disease Risk Factors. Obesity 2007; 15: 785-795.
28 Reis JP, Araneta MR, Wingard DL, et al. Overall Obesity and Abdominal Adiposity as Predictors of Mortality in U.S. White and Black Adults. Annals of Epidemiology 2009;19:134-142.
29 Haslam DW, James WPT. Obesity. The Lancet 2005; 366: 1197-1209.
30 Panagiotakos DB, Pitsavos C, Yannakoulia M, et al. The implication of obesity and central fat on markers of chronic inflammation: The ATTICA study. Atherosclerosis 2005;183:308-315.
31 Zhang C. The role of inflammatory cytokines in endothelial dysfunction. Basic Research in Cardiology 2008; 103: 398-406.
32 Wang C, Li S, Weisel RD, et al. C-Reactive Protein Upregulates Angiotensin Type 1 Receptors in Vascular Smooth Muscle. Circulation 2003; 107: 1783-1790.
33 Festa A, D'Agostino R, Williams K, et al. The relation of body fat mass and distribution to markers of chronic inflammation. International Journal of Obesity & Related Metabolic Disorders 2001; 25: 1407.
34 Meigs JB, Hu FB, Rifai N, et al. Biomarkers of Endothelial Dysfunction and Risk of Type 2 Diabetes Mellitus. JAMA 2004; 291: 1978-1986.
35 Visser M, Bouter LM, McQuillan GM, et al. Elevated C-Reactive Protein Levels in Overweight and Obese Adults. JAMA 1999; 282: 2131-2135.
36 Kim K, Valentine RJ, Shin Y, et al. Associations of visceral adiposity and exercise participation with C-reactive protein, insulin resistance, and endothelial dysfunction in Korean healthy adults. Metabolism 2008; 57: 1181-1189.
37 Thorand B, Baumert J, D?ring A, et al. Sex differences in the relation of body composition to markers of inflammation. Atherosclerosis 2006; 184: 216-224.
38 Dehghan A, Kardys I, de Maat MPM, et al. Genetic Variation, C-Reactive Protein Levels, and Incidence of Diabetes. Diabetes 2007; 56: 872-878.
39 Ye X, Franco OH, Yu Z, et al. Associations of inflammatory factors with glycaemic status among middle-aged and older Chinese people. Clinical Endocrinology2009; 70: 854-862.
40 Lin J, Zhang M, Song F, et al. Association between C-reactive protein and pre-diabetic status in a Chinese Han clinical population. Diabetes/Metabolism Research and Reviews 2009; 25: 219-223.
41 Hu FB, Meigs JB, Li TY, et al. Inflammatory Markers and Risk of Developing Type 2 Diabetes in Women. Diabetes 2004; 53: 693-700.
42 Barzilay JI, Abraham L, Heckbert SR, et al. The Relation of Markers of Inflammation to the Development of Glucose Disorders in the Elderly. Diabetes 2001;50: 2384-2389.
43 Doi Y, Kiyohara Y, Kubo M, et al. Elevated C-Reactive Protein Is a Predictor of the Development of Diabetes in a General Japanese Population. Diabetes Care 2005; 28: 2497-2500.
44 Festa A, D'Agostino R, Tracy RP, et al. Elevated Levels of Acute-Phase Proteins and Plasminogen Activator Inhibitor-1 Predict the Development of Type 2 Diabetes. Diabetes 2002; 51: 1131-1137.
45 Freeman DJ, Norrie J, Caslake MJ, et al. C-Reactive Protein Is an Independent Predictor of Risk for the Development of Diabetes in the West of Scotland Coronary Prevention Study. Diabetes 2002; 51: 1596-1600.
46 Nakanishi S, Yamane K, Kamei N, et al. Elevated C-Reactive Protein Is a Risk Factor for the Development of Type 2 Diabetes in Japanese Americans. Diabetes Care 2003; 26: 2754-2757.
47 Laaksonen DE, Niskanen L, Nyyss?nen K, et al. C-reactive protein and the development of the metabolic syndrome and diabetes in middle-aged men. Diabetologia 2004; 47: 1403-1410.
48 Pradhan AD, Manson JE, Rifai N, et al. C-Reactive Protein, Interleukin 6, and Risk of Developing Type 2 Diabetes Mellitus. JAMA 2001; 286: 327-334.
49 Tan KCB, Wat NMS, Tam SCF, et al. C-Reactive Protein Predicts the Deterioration of Glycemia in Chinese Subjects With Impaired Glucose Tolerance. Diabetes Care 2003; 26: 2323-2328.
50 Han TS, Sattar N, Williams K, et al. Prospective Study of C-Reactive Protein in Relation to the Development of Diabetes and Metabolic Syndrome in the Mexico City Diabetes Study. Diabetes Care 2002; 25: 2016-2021.
51 Thorand B, Baumert J, D?ring A, et al. Sex differences in the relation of bodycomposition to markers of inflammation. Atherosclerosis 2006; 184: 216-224.
52 Meigs JB, Hu FB, Rifai N, et al. Biomarkers of Endothelial Dysfunction and Risk of Type 2 Diabetes Mellitus. JAMA 2004; 291: 1978-1986.
53 Song Y, Manson JE, Tinker L, et al. Circulating Levels of Endothelial Adhesion Molecules and Risk of Diabetes in an Ethnically Diverse Cohort of Women. Diabetes 2007; 56: 1898-1904.
54 Festa A, Agostino R. Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome: The Insulin Resistance Atherosclerosis Study (IRAS). Circulation 2000; 102:42-47
55 Haverkate F, Thompson SG, Pyke SDM, et al. for the European Concerted Action on hrombosis and Disabilities Angina Pectoris StudyGroup. Production of C-reactive protein and risk of coronary events in stable and unstable angina. Lancet 1997;349:462-466.
56 Koenig W, Sund M. C-reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men. Circulation 1999;99:237-242.
57 Mendall MA, Patel P, Ballam L, et al. C Reactive protein and its relation to cardiovascular risk factors: a population based cross sectional study. BMJ 1996; 312: 1061-1065.
58 Tracy RP, Psaty BM, Macy E, et al. Lifetime smoking exposure affects the association of c-reactive protein with cardiovascular disease risk factors and subclinical disease in healthy elderly subjects. Arterioscler Thromb Vasc Biol 1997;17:2167-2176.
59 Yudkin JS, Stehouwer CDA, Emeis JJ, et al. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction. Arterioscler Thromb Vasc Biol 1999;19:972–978.
60 Esmaillzadeh A, Azadbakht L. Increased Levels of Inflammation among Women with Enlarged Waist and Elevated Triglyceride Concentrations. Ann Nutr Metab 2010 Aug 20;57:77-84.
61 da Silva IT, Sanches LB, Mello AP, et al. Impact of C-reactive protein on cardiovascular risk in adolescents. Arq Bras Cardiol 2010;94:585-591.
62 Verit FF. High sensitive serum C-reactive protein and its relationship with other cardiovascular risk factors in normoinsulinemic polycystic ovary patients withoutmetabolic syndrome. Arch Gynecol Obstet 2010; 281: 1009-1014.
63 Thomas P, Vinzenz Hombach, Jan Torzewski. C-Reactive Protein– Mediated Low Density Lipoprotein Uptake by Macrophages:Implications for Atherosclerosis. Circulation 2001;103:1194-1197
64 Sonia S, Fahad R. C-Reactive Protein as a Screening Test for Cardiovascular Risk in a Multiethnic Population. Arteriosclerosis, Thrombosis, and Vascular Biology 2004; 24: 1509.
65 Yoshiki M, Toshikazu H, Shusaku S, et al. Metabolic Syndrome is Strongly Associated With Chronic Subclinical Inflammation in Patients Achieving Optimal Low-Density Lipoprotein-Cholesterol Levels in Secondary Prevention of Cardiovascular Disease. Circ J 2008; 72: 2046–2050.
66 Wexler DJ, Hu FB, Manson JE, et al. Mediating Effects of Inflammatory Biomarkers on Insulin Resistance Associated with Obesity. Obesity 2005; 13: 1772-1783.
67.Mathieu P, Poirier P, Pibarot P, et al. Despres J-P. Visceral Obesit: The Link Among Inflammation, Hypertension, and Cardiovascular Disease. Hypertension 2009;53: 577-584.
68 Mendall MA, Goggin PM, Molineaux N, et al. Relationship of helicobacter pylori infection and coronary heart disease. Br heart J 1994;71:437-439.
69 Kowalski M. Helicobacter pylori infection in coronary artery disease: influence of H. pylori eradication on coronary artery lumen after percutaneous transluminal coronary angioplasty. The detection of H.pylori specific DNA in human coronary atherosclerotic plague. J physiol pharmacol 2001;52:3-31.
70.Martin-de-argila C, Boixeda D, Canton R, et al. High seroprevalence of helicobacter pylori infection in coronary heart disease. Lancet 1995;346:310.
71 Whincup PH, Mendall MA, Perry IJ, et al. Prospective relations between helicobacter pylori infection, coronary heart disease and stroke in middle aged men. Heart 1996;75:568-572.
72 Danesh J, Collins R, Peto R. chronoc infections and coronary heart disease: is there a link? Lancet 1997;350:430-436.
73 Yukihiko M, Hiroaki T, Haruo N. Association of Mycoplasma pneumoniae infection with coronary artery disease and its interaction with chlamydial infection. Atheroslerosis 2004;9:139-144.
74 Basinkevich AB, Shakhnovich RM, Martynova VR, et al. Role of Chlamydia, mycoplasma and cytomegalovirus infection in the development of coronary artery disease. Cardio 2003;43:4-9.
75 Negh J, Gupta S, Goodbourn C, et al. Mycoplasma pneumoniae in elderly patients with stroke. A case-control study on the seroprevalence of M. pneumoniae in elderly patients with acute cerebrovascular disease-the M-PEPS study. Cerebrovasc Dis 2004;17:314-319.
76 Saikku P, Leinonen M, Tenkanen L, et al. Chronic chlamydia pneumoniae and clinical course in patients with unstable angina pectoris. Atherosclerosis 2000;153:499-504.
77 Thoms DH, Grayston JT, Siscovick DS, et al. Association of prior infection with chlamydia pneumoniae and angiographically demonstrated coronary artery disease.JAMA 1992; 268: 68-72.
78 Ericson K, Salden GP, Lindquist O, et al. Relationship of chlamydia pneumoniae infection to severity of human coronary atherosclerosis. Circulation 2000;101:2568-2571.
79张大庆,赵水平.肺炎衣原体与冠心病的关系.中国动脉粥样硬化杂志2002; 10: 274-276.
80 Roivainen M, Alfthan G, Jousilahti P, et al. Entrovirus infection as a possible risk factor for myocardial infarction. Circulation 1998;98:2534.
81孙余华,鞠振宇,吴永键,等.肺炎衣原体感染增加糖尿病患冠心病的危险性.中华心血管病杂志2003;3:169-172.
82 Huber S A , Kupperman H. Hormonal regulation of CD4( + ) T2cell responses in coxsackievirus B32 induced myocarditis in mice. J Virol 1999;73: 4689-4695.
83 Huber S A , Stone J E, Wagner D H, et al. Gamma delta + T cells regulate major histocompatibility complex class II (IA and IE) dependent susceptibility to coxsackievirus B32 induced autoimmune myocarditis. J Virol 1999;73 :5630-5636.
84 Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation 2003;107:363-369.
85 Libby P, Ridker PM. Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice. Journal of the American College of Cardiology 2006; 48: A33-A46.
86 Pearson TA, Mensah GA, Alexander RW, et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499-511.
87 Andersson J, Johansson L, Ladenvall P, et al. C-reactive protein is a determinant of first-ever stroke:prospective nested case-referent study. Cerebrovasc Dis 2009; 27: 544-551.
88 Makita S, Nakamura M, Satoh K, et al. Serum C-reactive protein levels can be used to predict future ischemic stroke and mortality in Japanese men from the general population. Atherosclersis 2009;204:234-238.
89 Tanne D, Benderly M, Goldbourt U, et al. C-Reactive Protein as a Predictor of Incident Ischemic Stroke Among Patients With Preexisting Cardiovascular Disease. Stroke 2006; 37: 1720-1724.
90 Ye X, Franco OH, Yu Z, et al. Associations of inflammatory factors with glycaemic status among middle-aged and older Chinese people. Clinical Endocrinology 2009; 70: 854-862.
91 Lin J, Zhang M, Song F, et al. Association between C-reactive protein and pre-diabetic status in a Chinese Han clinical population. Diabetes/Metabolism Research and Reviews 2009; 25: 219-223.
92 Yamada S, Gotoh T, Nakashima Y, et al. Distribution of Serum C-Reactive Protein and Its Association with Atherosclerotic Risk Factors in a Japanese Population. American Journal of Epidemiology 2001; 153: 1183-1190.
93 Otsuka T, Kawada T, Katsumata M, et al. High-sensitivity C-reactive protein is Associated with the risk of coronary heart disease as estimated by the Framingham Risk Score in middle-aged Japanese men. International Journal of Cardiology 2008; 129:245-250.
94 Sung KC, Suh JY, Kim BS, et al. High sensitivity c-reactive protein as an independent risk factor for essential hypertension. Am J Hypertens 2003;16: 429-433.
95 Kilpatrick EL, Bunk DM. Development of a Reference Measurement Procedure for C-Reactive Protein in Human Serum. Anal Chem 2009;81:8610-8616.
96 Pearson TA, Mensah GA, Alexander RW, et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statementfor Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499-511.
97 Ridker PM, Cook N. Clinical Usefulness of Very High and Very Low Levels of C-Reactive Protein Across the Full Range of Framingham Risk Scores. Circulation 2004; 109: 1955-1959.
98 Hickling S, Hung J, Knuiman M, et al. Are the associations between diet and C-reactive protein independent of obesity? Preventive Medicine 2008; 47:71-76.
99 Baena D, Alvarez P. Association between clustering of cardiovascular risk factors and the risk of cardiovascular disease. Rev Esp Salud Publica 2002;76:7-15.
100左惠娟,苏江莲,姚崇华.非瓣膜性房颤患者缺血性脑卒中危险因素暴露水平与聚集分析.中华流行病学杂志2008;29:819-822.
1 Powles J, Day N. Interpreting the global burden of disease. Lancet 2002; 360: 1342.
2田凤华.心脑血管疾病的预防.中国自然医学杂志2008; 10: 191-192.
3 Blake GJ, Ridker PM. High sensitivity C-reactive protein for protein for predicting cardiovascular diseades: An inflammatory hypothesis. Eur Heat J 2001; 22:349-352.
4 Ross R. Atherosclerosis : An inflammatory disease. N Engl J Med 1999;340:115-126.
5 Rosenson RS, Koenig W. Utility of inflammatory markers in the management of coronary artery disease. Am J Cardiol 2003; 92: 10-18.
6 Reiss AB, Glass AD. Atherosclerosis: immune and inflammatory aspects. J Investig Med 2006; 54: 123-131.
7李志强,郑兴.炎症与冠心病.中国心血管病研究杂志2006;4:233-235.
8 Lowe GD. The association between elevated levels of inflammation biomarkers and coronary artery disease and death. CMA J 2006; 174: 479-480.
9 Tillett W, Francis TJ. Serological reactions in pneumonia with a non protein somatic fraction of pneumococcus. J exp MED 1930; 52: 561-585
10 Ivashchenko Y, Kramer F, Schater S, et al. Protein kinase C pathway is involved in transcriptional regulation of c-reactive protein synthesis in human hepatocytes. Arterioscler Thromb Vasc Biol 2005; 25: 186-192.
11 J Szalai. The biological functions of C-reactive protein.Vase Pharmaca1 2002;39: 105-107.
12 Gambino R. C-reactive protein–undervalued underutilized. Clin Chem 1997;43: 2017-20l8.
13 Woloshin S, Schwartz LM. Distraction of c-reactive protein values in the united states. N Engl J Med 2005; 352: 1611-1613.
14 Meier-Ewert HK, Ridker PM, Rifai N, et al. Absence of diurnal variation of c-reactive protein concentrations in healthy human subjects. Clin Chem 2001; 47: 426-430.
15 Frohlich M, Sund M, Thorand B, et al. Lack of seasonal variation in c-reactive protein. Clin Chem 2002; 48: 575-577.
16 Libby P, Ridker PM. Novel inflammatory markers of coronary risk: theory versus practice. Circulation 1999; 100: 1148-1150.
17 Ross R. Atherosclerosis - an inflammatory disease. N Engl J Med 1999; 340: 115-126.
18 Libby P. Molecular bases of the acute coronary syndromes. Circulation 1995;91: 2844-2850.
19 Torzewski M, Risi C, Mortensen RF, et al. C-reactive protein in the arterial intima. Aterioscler thromb Vac Bio 2000; 20: 2094-2099.
20 Fichtlscherer S, Rosenberger G, Walter DH, et al. Elevated C-reactive protein levels and impaired endothelial vasoreactivity in patients with coronary artery disease. Circulation 2000;102:1000-1006.
21 Luigi M, Biasucci, LM, Liuzzo G. Elevated Levels of c-reactive protein at discharge in patients with unstable angina predict recurrent instability. Circulation 1999;99:855-860.
22 Pearson TA, Mensah GA, Alexander RW, et al. Makers of information and Cardiovascular disease. Application to clinical and public health practice: a statement for healthcare professional from the Centers for Disease control and Prevention and the Ameriean Heart Association.Circulation 2003;107:499-511.
23 Ridker PM, Cushman M, Stampfer MJ, et al. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease.Circulation 1998;97: 425-428.
24 Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of c-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med 1994; 331: 417-424.
25 Morrow DA, Rifai N, Antman EM, et al. C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI IIA sub study. J Am Coll Cardiol 1998, 31:1460-1465.
26 Bevilacqua M, strengelin S, Gimbrone M, et al. Endothelial leukocyte adhesion molecule 1:An inducible receptor for neutrophils related to complement regulatory proteins and lectins. Science 1989; 243: 1160.
27 Seman H B, Gurbel P A,Amderson J L, et al. Circulating cell adhesion molecules and death in patients with coronary artery disease. Circulation 2001;104:1336-1342.
28窦肇华,张远强,郭顺根,等.免疫细胞学与疾病.北京:中国医药科技出版社, 2004: 932-955.
29 Kansas GS. Selectins and their ligands:current concepts and controcersies. Blood 1996; 88: 3259-3287.
30 Haraldsen G, Kvale D, Uen B, et al. Cytokine-regulated expression of E-selectin, intercellular adhesion molecule-1(ICAM-1) , and vascular cell adhesion molecule-1 (VCAM-1) in human microvascular endothelial cells. J Immunol 1996; 156: 2558-2565.
31 Atalar E, Aytemir K, Haznedaroglu l, et al. Increased plasma levels of soluble selectins in patients with unstable angina.Int J Cardiol 2001; 78: 69-73.
32 Cockerill GW, Huehns TY, et al. Elevation of plasma high-density lipoprotein concentration reduces interleukin-1- induced expression of E-selectin in an in vivo model of acute inflammation.Circulation 2001; 103: 108-112.
33 Forlow SB, White EJ, Barlow SC, et al. Severe inflammatory defect and reduced viability in CD18 and E-selectin doieble mutant mice. Clin Invest 2000; 106 : 1457.
34华琦,李梅,刘力松等.高血压病患者脉压与内皮功能损害的相关性.中华内科杂志2003; 42: 574.
35段留法,郑秋甫,张丽萍等.自发性高血压大鼠内皮细胞功能不全发生机理实验研究.中国康复理论与实践2005; 11: 413.
36 Kuroda YT, Komamura K, Tatsumi R, et al . Vascular cell adhesion moleule-1 as a biochemical marker of left ventricular mass in the patients with hypertension. Am J Hypertens 2001, 14:868-872.
37 Blann AD, Tse W, Maxwell SJ, et al. Increased levels of the soluble adhesion molecule E - selectin in essential hypertension. J Hypertens 1994;12:925-928.
38沈庆乐,李培英,张存琪,等.选择素家族在老年冠心病和高血压中的临床意义.心血管康复医学杂志2001; 10:112-113.
39 Kozuka K, Kohryama T, Nomura E, et al. Endothelial markers and adhension molecules in acute ischemicstroke-equcntial change and differences in stroke subtype. Atherosclerosis 2002; 161: 161-168.
40 Mussack T, Biberthaler P, Steppert C, et al . Early Cellular brain damage and systemic inflammatory response after cardiopulmonary resuscitation on isolated severe headtrauma; a comparative pilot study on common pathomechanisms. Resuscitation 2001;49:193-199.
41 Omi H, Okayama N, Shimizum, et al. Participation of high glucose concentrations in neut rophil adhension and surface expression of adhension molecules on cultured human endothelial cells. Diabetes Complication 2002; 16: 201-208.
42 Soriano S, Lipton S, Wang Y, et al. Intercellular adhension molecule defiant mice are less susceptible to cerebral ischemia-reperfusion injury. Ana Neurol 1996; 39:618-624.
43 Bitsch A, Klene W, Murtada L, et al. A longitudinal prospective study of soluble adhesion molecules in acute stroke. Stroke 1998; 29: 2129-2135.
44 Akisu M, Kutursay N. Platelet-activating factor is an important mediator in hypoxie ischemic brain injury in the newborn rat . Flunarint and Ginkgo biloba extrat PAF concentration in the brain. Biol Neonate 1998; 74: 439-440.
45 Atalar E, Aytemir K, Haznedaroglu I, et al . Increased plasma levels of soluble selectin in patients with unstable angina. Int J Cardiol 2001;78: 69-73.
46 Semaan HB, Gurbel PA, Anderson JL, et al . Soluble VCAM-1 and E-selectin,but not ICAM-1 discriminate endothelial injury in patients with documented coronary artery disease. Cardiology 2000;93:7-10.
47田乃亮,陈清枝,李东野,等.血清Es和白细胞CD11b/CD18在冠心病中的意义.临床心血管病杂志200;20:7-9.
48沈庆乐,邓水泉,李培英,等.冠心病患者选择素P, L, E,一氧化氮及超氧化歧化酶水平变化及其相关性.中国心血管杂志2002;7:177-178.
49 Fang L, Wei H, Mak KH, et al. Marker of low-grade inflammation and soluble eell adhesion molecules in Chinese patients with coronary artery disease. Can J Cardiol 2004;20:1433-1 438.
50杨立森,林媛豪,石学宁,等.可溶性E-选择素对冠心病心绞痛的诊断意义.临床心血管病杂志2003;19:272-274.
51 Rothlein R, Dustin ML, Marlin SD, et al. A human intercellular adhesion molecule (ICAM-1) distinct from LFA-1. J Immunol 1986; 137: 1270-1274
52 Marlin SD, Spring TA. Purified intercellular adhesion molecule-1(ICAM-1) is aligand for lymphocyte function-associate antigen-1(LFA-1). Cell 1987;51: 813-819.
53何球藻,吴厚生.细胞与分子免疫学.上海科学技术文献出版社1997,104-120.
54 Leeuwenberg J. E-selectin and intercellular adhesion molecule-1 are released by activated human endothelial cells in vitro. Immunology 1992,77: 543-549.
55 Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases: the Atherosclerosis Risk In Cornmunities (ARIC)study. Circulation, 1997, 96: 4219-4225.
56 Blankenberg S, Barbaux S, Tiret L. Adhesion molecules and atherosclerosis. Atherosclerosis,2003; 170: 191-203.
57 Dustin ML, Rothlein R, Bahn AK, et al. Induction by IL-1 and IFN-γ. Tissue distribution, biochemistry and function of a natural adherence molecule (ICAM-1). J Immunol 1986;137:245-254.
58黄岚.细胞间粘附分子-1与心功能不全的临床意义.国外医学心血管疾病分册2000; 27: 5-7.
59 Poston RN, Johnson-Tidey RR. Localized adhesion of monocytes to human atherosclerotic plaques demons trated in vitro:Implications for atherogenesis.Am J Pathol 1996;149:73-80.
60 Haim M, Tanne D, Boyko V, et al. Solubele intercellular, adhesion molecule-1 and long-term risk of acute coronary events in patients with chronic coronary heart disease. J Am Coil Cardiol 2002;39:1133-1138.
61 Ikata J, Wakat S, Oishi Y, et al. Leukocyte counts and concent ration of soluble ashesion molecules as predictors of coronary atherosc1erosis. Coron Artery Dis 2000;11:445-449.
62 Mehta PK, Griendling KK. AngiotensinⅡcell signaling: physiological and pathological effects in the cardiovascular system. Am J Physiol Cell Physiol 2007;292: C82-97.
63 Johnston C, Risvanis J. Preclinical pharmacology of angiotensinⅡreceptor antagonists: Update and outstanding issues. Am J Hypertens 1997; 10: 306-310.
64 Schiffrin EL, Touyz RM. Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. J Am Coll Cardiol 2003; 42:911-913.
65 Pastore L, Tessitore A, Martinotti S, et al. Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells and increases soluble ICAM-1 release in vivo. Circulation 1999; 100:1646-1652.
66 Dzau VJ. Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis. Hypertension 2001; 37:1047-1052.
67 Liao TD, Yang XP, Liu YH, et al. Role of inflammation in the development of renal damage and dysfunction in angiotensin II-induced hypertension. Hypertension 2008; 52:256-263.
68 Gattullo D, Pagliaro P, Marsh NA, et al. New insights into nitricoxide and coronary circulation. Life Sci 1999; 65: 2167- 2174.
69 Liu HQ, Wei XB, Sun R, Cai YW, Lou HY, Wang JW, Chen AF, Zhang XM. Angiotensin II stimulates intercellular adhesion molecule-1 via an AT1 receptor/nuclear factor-kappaB pathway in brain microvascular endothelial cells. Life Sci. 2006;78:1293-8.
70 Wang CH, Li SH, Weisel RD, Fedak PW, Dumont AS, Szmitko P,etal. C-reactive protein upregulates angiotensin type 1 receptors in vascular smooth muscle. Circulation 2003;107:1783–1790.
71 Powell JS, Muller RK. Inhibitors of angiotension-converting enzyme prevent myointimal proliferation aftervascular injury. Science 1989;245:186-188.
72 Monton M, Castilla MA, et al. Effects of angiotensinⅡon endonthelial cell growth:role of AT-1 and AT-2 receptors. J Am Soc Nephrol 1998;9:969-974.
73陈良海,李刚,李代渝,等.幽门螺杆菌感染对心血管病患者脂代谢的影响.中国煤炭工业医学杂志2001;4:93-94.
74 Satmnalkopi K, Valto.en V, Kerttule Y, et al. Changes in serum lipoprotein pattern induced by acute infections. Metabolism 1988;37:859-861.
75 Rathbone B, Martin D, Stephens J, et al. Helicobacter pylori seropositivity in subjects with acute myocardial infarction. Heart 1996;76:308-311.
76 Yukihiko M, Hiroaki T, Haruo N. Association of Mycoplasma pneumoniae infection with coronary artery disease and its interaction with chlamydial infection. Atheroslerosis 2004;9:139-144.
77 Basinkevich AB, Shakhnovich RM, Martynova VR, et al. Role of Chlamydia, mycoplasma and cytomegalovirus infection in the development of coronary arterydisease. Cardio 2003;43:4-9.
78 Negh J, Gupta S, Goodbourn C, et al. Mycoplasma pneumoniae in elderly patients with stroke. A case-control study on the seroprevalence of M. pneumoniae in elderly patients with acute cerebrovascular disease-the M-PEPS study. Cerebrovasc dis 2004;17:314-319.
79 Thoms DH, Grayston JT, Siscovick DS, et al. Association of prior infection with chlamydia pneumoniae and angiographically demonstrated coronary artery disease. JAMA 1992;268:68-72.
80 Ericson K, Salden GP, Lindquist O, et al. Relationship of chlamydia pneumoniae Infection to severity of human coronary atherosclerosis. Circulation 2000;101: 2568-2571.
81孙余华,鞠振宇,吴永键等.肺炎衣原体感染增加糖尿病患冠心病的危险性.中华心血管病杂志2003;3:169-172.
82 Kalayoglu MV, Libby P, Byrne GI. Chlamydia pneumoniae as an emerging risk factor in cardiovascular disease. JAMA 2002;288:2724-2731.
83 Lau RC. Coxsackie B virus - specific IgMresponses in coronary care unit patients. Med Vird 1986;18:193-198.
2 Kearney PM, Whelton M, Reynolds K, et al. Global burden of hypertension: analysis of worldwide data. Lancet 2005; 365: 217–223.
3 He J,Gu D,Wu X, et al. Major causes of death among men and women in China. N Engl J Med 2005; 353: 1124–1134.
4李立明,饶克勤.中国居民2002年营养与健康状况调查.中华流行病学杂志2005; 7:478-484.
5 Dekker JM, Girman C, Rhodes T, et al. Metabolic Syndrome and 10-Year Cardiovascular Disease Risk in the Hoorn Study. Circulation 2005; 112: 666-673.
6 Isomaa B,Almgren P, Tuomi T, et al. Cardiovascular Morbidity and Mortality Associated With the Metabolic Syndrome. Diabetes Care 2001; 24: 683-689.
7 de Jager J,Dekker JM, Kooy A, et al. Endothelial Dysfunction and Low-Grade Inflammation Explain Much of the Excess Cardiovascular Mortality in Individuals With Type 2 Diabetes: The Hoorn Study. Arterioscler Thromb Vasc Biol 2006; 26: 1086- 1093.
8吴兆苏,姚崇华,赵东.我国人群脑卒中发病率、死亡率的流行病学研究.中华流行病学杂志2003; 24: 236-239.
9 Zhang C. The role of inflammatory cytokines in endothelial dysfunction. Basic Research in Cardiology 2008; 103:398-406.
10 Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation, Part I. Circulation 2003; 108: 1917-1923.
11 Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342: 836-843.
12 Schiffrin EL, Touyz RM. Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. J Am Coll Cardiol 2003; 42: 911-913.
13 Pastore L, Tessitore A, Martinotti S, et al. Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells andincreases soluble ICAM-1 release in vivo. Circulation 1999; 100: 1646-1652.
14 Schillaci G, Pirro M, Gemelli F, et al. Increased C-reactive protein concentrations in never-treated hypertension: the role of systolic and pulse pressures. J Hypertens 2003; 21: 1841-1846.
15 Bautista LE, Lópex-Jaramillo P, Vera LM, et al. Is C-reactive protein an independent risk factor for essential hypertension? J Hypertens 2001; 19: 857-861.
16 Sung KC, Suh JY, Kim BS, et al. High sensitivity C-reactive protein as an independent risk factor for essential hypertension. Am J Hypertens 2003; 16: 429-433.
17 Lakoski SG, Herrington DM, Siscovick DM, et al. C-reactive protein concentration and incident hypertension in young adults: the CARDIA study. Arch Intern Med. 2006; 166: 345-349.
18 Davey Smith G, Lawlor DA, Harbord R, et al. Association of C-reactive protein with blood pressure and hypertension life course confounding and Mendelian randomization tests of causality. Arterioscler Thromb Vasc Biol. 2005; 25: 1051-1056.
19 Bautista LE, Lopez-Jaramillo P, Vera LM, et al. Is C-reactive protein an independent risk factor for essential hypertension? J Hypertens 2001; 19: 857-861.
20 Sesso HD, Buring JE, Rifai N, et al. C-reactive protein and the risk of developing hypertension. JAMA 2003; 290: 2945-2951.
21 Miller MA, Kerry SM, Cook DG, et al. Cellular adhesion molecules and blood pressure interaction with sex in a multi-ethnic population. J Hypertens 2004; 22:705–711.
22 DeSouza CA, Dengel DR, Macko RF, et al. Elevated evels of circulating cell adhesion molecules in uncomplicated essential hypertension. Am J Hypertens 1997; 10: 1335-1341.
23 Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation, Part I. Circulation 2003; 108: 1917-1923.
24 Mulvihill NT, Foley JB. Inflammation in acute coronary syndromes. Heart 2002;87: 201-204.
25 Lindsberg PJ, Grau AJ. Inflammation and Infections as Risk Factors for Ischemic Stroke. Stroke 2003; 34: 2518-2532
26 Wakugawa Y, Kiyohara Y, Tanizaki Y, et al. C-Reactive Protein and Risk of First-Ever Ischemic and Hemorrhagic Stroke in a General Japanese Population. The Hisayama Study. Stroke 2006; 37: 27-32.
27 Bruno G, Fornengo P, Novelli G, et al. C-Reactive Protein and 5-Year Survival in Type 2 Diabetes. Diabetes 2009; 58: 926-933.
28 Lee C, Adler A, Sandhu M, et al. Association of C-reactive protein with type 2 diabetes: prospective analysis and meta-analysis. Diabetologia 2009; 52: 1040-1047.
29 Dehghan A, Kardys I, de Maat MPM, et al. Genetic Variation, C-Reactive Protein Levels, and Incidence of Diabetes. Diabetes 2007; 56: 872-878.
30 Wexler DJ, Hu FB, Manson JE, et al. Mediating Effects of Inflammatory Biomarkers on Insulin Resistance Associated with Obesity. Obesity 2005; 13: 1772- 1783.
31 Ye X, Franco OH, Yu Z, et al. Associations of inflammatory factors with glycaemic status among middle-aged and older Chinese people. Clinical Endocrinology 2009; 70: 854-862.
32 Miller MA, Cappuccio FP. Cellular adhesion molecules and their relationship with measures of obesity and metabolic syndrome in a multiethnic population. Int J Obes 2006; 30: 1176-1182.
33 Menke A, Muntner P, Wildman RP, et al. Measures of Adiposity and Cardiovascular Disease Risk Factors. Obesity 2007; 15: 785-795.
34 Esmaillzadeh A, Azadbakht L. Increased Levels of Inflammation among Women with Enlarged Waist and Elevated Triglyceride Concentrations. Ann Nutr Metab 2010; 57: 77-84.
1.中国成人血脂异常防治指南制订联合委员会.中国成人血脂异常防治指南.中华心血管病杂志2007, 35: 3902419.
2. Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance andβ2cell function from fasting plasma glucose and insulin concent rations in man. Diabetologia 1985; 28: 412-419.
1 Ridker PM. C-reactive protein and the prediction of cardiovascular events among those at intermediate risk. J Am Coll Cardiol 2007; 49:2129-2138.
2 Szmitko PE, Wang CH, Weisel RD, et al. New markers of inflammation and endothelial cell activation, part I.Circulation 2003; 108:1917-1923.
3 Pasceri V, Willerson JT, Yeh ETH. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000; 102:2165-2168.
4 Bautista LE, Lo′pex-Jaramillo P, Vera LM, et al. Is C-reactive protein an independent risk factor for essential hypertension?J Hypertens 2001; 19:857-861.
5 Sung KC, Suh JY, Kim BS, et al. High sensitivity C-reactive protein as an independent risk factor for essential hypertension.Am J Hypertens 2003; 16:429-433.
6 Lakoski SG, Herrington DM, Siscovick DM, et al. C-reactive protein concentration and incident hypertension in young adults: the CARDIA study. Arch Intern Med 2006; 166:345-349.
7 Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342:836-843.
8 DeSouza CA, Dengel DR, Macko RF, et al. Elevated levels of circulating cell adhesion molecules in uncomplicated essential hypertension. Am J Hypertens 1997;10:1335-1341.
9 Hlubocka Z, Umnerova V, Heller S, et al. Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors.J Human Hypertens 2002; 16:557-562.
10 Cottone S, Mule G, Nardi E, et al. C-reactive protein and intercellular adhesion molecule-1 are stronger predictors of oxidant stress than blood pressure in established hypertension. J Hypertens 2007; 25:423-428.
11 Miller MA, Kerry SM, Cook DG, et al. Cellular adhesion molecules and blood pressure interaction with sex in a multiethnic population. J Hypertens 2004; 22:705-711.
12 Schiffrin EL, Touyz RM. Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. J Am Coll Cardiol 2003; 42:911-913.
13 Pastore L, Tessitore A, Martinotti S, et al. Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells and increases soluble ICAM-1 release in vivo. Circulation 1999; 100:1646-1652.
14 Dzau VJ. Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis. Hypertension 2001; 37:1047-1052.
15 Liao TD, Yang XP, Liu YH, et al. Role of inflammation in the development of renal damage and dysfunction in angiotensin II-induced hypertension. Hypertension 2008; 52:256-263.
16 He J, Klag MJ, Appel LJ, et al. The renin-angiotensin system and blood pressure: differences between blacks and whites. Am J Hypertens 1999; 12:555-562.
17 Hwang SJ,Ballantyne CM,Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1 and E-selectin in carotid atherosclerosis and incident coronary heart disease cases.Circulation 1997;96:4219-4225.
18 Miller MA, Cappuccio FP. Cellular adhesion molecules and their relationship with measures of obesity and metabolic syndrome in a multiethnic population. Int J Obes 2006; 30: 1176-1182.
19 Bo?anskáL, Michalsky D, LacinováZ, et al. The influence of obesity and different fat depots on adipose tissue gene expression and protein levels of cell adhesion molecules. Physiol Res 2010;79:79-88
20 Ponthieux A, Herbeth B, Droesch S, et al. Biological determinants of serum ICAM-1, E-selectin, P-selectin and L-selectin levels in healthy subjects: the Stanislas study. Atherosclerosis 2004; 172: 299-308.
21 Kelly T, Yang W, Chen CS, et al. Global burden of obesity in 2005 and projections to 2030. Int J Obes 2008; 32: 1431-1437.
22 Adams KF, Schatzkin A, Harris TB, et al. Overweight, Obesity and Mortality in a Large Prospective Cohort of Persons 50 to 71 Years Old. N Engl J Med 2006; 355: 763-778.
23 Jee SH, Sull JW, Park J, et al. Body-Mass Index and Mortality in Korean Men and Women. N Engl J Med 2006; 355: 779-787.
24 Hu D, Xie J, Fu P, et al. Central Rather Than Overall Obesity Is Related to Diabetes in the Chinese Population: The InterASIA Study. Obesity 2007;15: 2809-2816.
25 Flegal KM, Graubard BI, Williamson DF, et al. Cause-Specific Excess Deaths Associated With Underweight, Overweight, and Obesity. JAMA 2007; 298: 2028-2037.
26 Pischon T, Boeing H, Hoffmann K, et al. General and Abdominal Adiposity and Risk of Death in Europe. N Engl J Med 2008; 359: 2105-2120.
27 Menke A, Muntner P, Wildman RP, et al. Measures of Adiposity and Cardiovascular Disease Risk Factors. Obesity 2007; 15: 785-795.
28 Reis JP, Araneta MR, Wingard DL, et al. Overall Obesity and Abdominal Adiposity as Predictors of Mortality in U.S. White and Black Adults. Annals of Epidemiology 2009;19:134-142.
29 Haslam DW, James WPT. Obesity. The Lancet 2005; 366: 1197-1209.
30 Panagiotakos DB, Pitsavos C, Yannakoulia M, et al. The implication of obesity and central fat on markers of chronic inflammation: The ATTICA study. Atherosclerosis 2005;183:308-315.
31 Zhang C. The role of inflammatory cytokines in endothelial dysfunction. Basic Research in Cardiology 2008; 103: 398-406.
32 Wang C, Li S, Weisel RD, et al. C-Reactive Protein Upregulates Angiotensin Type 1 Receptors in Vascular Smooth Muscle. Circulation 2003; 107: 1783-1790.
33 Festa A, D'Agostino R, Williams K, et al. The relation of body fat mass and distribution to markers of chronic inflammation. International Journal of Obesity & Related Metabolic Disorders 2001; 25: 1407.
34 Meigs JB, Hu FB, Rifai N, et al. Biomarkers of Endothelial Dysfunction and Risk of Type 2 Diabetes Mellitus. JAMA 2004; 291: 1978-1986.
35 Visser M, Bouter LM, McQuillan GM, et al. Elevated C-Reactive Protein Levels in Overweight and Obese Adults. JAMA 1999; 282: 2131-2135.
36 Kim K, Valentine RJ, Shin Y, et al. Associations of visceral adiposity and exercise participation with C-reactive protein, insulin resistance, and endothelial dysfunction in Korean healthy adults. Metabolism 2008; 57: 1181-1189.
37 Thorand B, Baumert J, D?ring A, et al. Sex differences in the relation of body composition to markers of inflammation. Atherosclerosis 2006; 184: 216-224.
38 Dehghan A, Kardys I, de Maat MPM, et al. Genetic Variation, C-Reactive Protein Levels, and Incidence of Diabetes. Diabetes 2007; 56: 872-878.
39 Ye X, Franco OH, Yu Z, et al. Associations of inflammatory factors with glycaemic status among middle-aged and older Chinese people. Clinical Endocrinology2009; 70: 854-862.
40 Lin J, Zhang M, Song F, et al. Association between C-reactive protein and pre-diabetic status in a Chinese Han clinical population. Diabetes/Metabolism Research and Reviews 2009; 25: 219-223.
41 Hu FB, Meigs JB, Li TY, et al. Inflammatory Markers and Risk of Developing Type 2 Diabetes in Women. Diabetes 2004; 53: 693-700.
42 Barzilay JI, Abraham L, Heckbert SR, et al. The Relation of Markers of Inflammation to the Development of Glucose Disorders in the Elderly. Diabetes 2001;50: 2384-2389.
43 Doi Y, Kiyohara Y, Kubo M, et al. Elevated C-Reactive Protein Is a Predictor of the Development of Diabetes in a General Japanese Population. Diabetes Care 2005; 28: 2497-2500.
44 Festa A, D'Agostino R, Tracy RP, et al. Elevated Levels of Acute-Phase Proteins and Plasminogen Activator Inhibitor-1 Predict the Development of Type 2 Diabetes. Diabetes 2002; 51: 1131-1137.
45 Freeman DJ, Norrie J, Caslake MJ, et al. C-Reactive Protein Is an Independent Predictor of Risk for the Development of Diabetes in the West of Scotland Coronary Prevention Study. Diabetes 2002; 51: 1596-1600.
46 Nakanishi S, Yamane K, Kamei N, et al. Elevated C-Reactive Protein Is a Risk Factor for the Development of Type 2 Diabetes in Japanese Americans. Diabetes Care 2003; 26: 2754-2757.
47 Laaksonen DE, Niskanen L, Nyyss?nen K, et al. C-reactive protein and the development of the metabolic syndrome and diabetes in middle-aged men. Diabetologia 2004; 47: 1403-1410.
48 Pradhan AD, Manson JE, Rifai N, et al. C-Reactive Protein, Interleukin 6, and Risk of Developing Type 2 Diabetes Mellitus. JAMA 2001; 286: 327-334.
49 Tan KCB, Wat NMS, Tam SCF, et al. C-Reactive Protein Predicts the Deterioration of Glycemia in Chinese Subjects With Impaired Glucose Tolerance. Diabetes Care 2003; 26: 2323-2328.
50 Han TS, Sattar N, Williams K, et al. Prospective Study of C-Reactive Protein in Relation to the Development of Diabetes and Metabolic Syndrome in the Mexico City Diabetes Study. Diabetes Care 2002; 25: 2016-2021.
51 Thorand B, Baumert J, D?ring A, et al. Sex differences in the relation of bodycomposition to markers of inflammation. Atherosclerosis 2006; 184: 216-224.
52 Meigs JB, Hu FB, Rifai N, et al. Biomarkers of Endothelial Dysfunction and Risk of Type 2 Diabetes Mellitus. JAMA 2004; 291: 1978-1986.
53 Song Y, Manson JE, Tinker L, et al. Circulating Levels of Endothelial Adhesion Molecules and Risk of Diabetes in an Ethnically Diverse Cohort of Women. Diabetes 2007; 56: 1898-1904.
54 Festa A, Agostino R. Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome: The Insulin Resistance Atherosclerosis Study (IRAS). Circulation 2000; 102:42-47
55 Haverkate F, Thompson SG, Pyke SDM, et al. for the European Concerted Action on hrombosis and Disabilities Angina Pectoris StudyGroup. Production of C-reactive protein and risk of coronary events in stable and unstable angina. Lancet 1997;349:462-466.
56 Koenig W, Sund M. C-reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men. Circulation 1999;99:237-242.
57 Mendall MA, Patel P, Ballam L, et al. C Reactive protein and its relation to cardiovascular risk factors: a population based cross sectional study. BMJ 1996; 312: 1061-1065.
58 Tracy RP, Psaty BM, Macy E, et al. Lifetime smoking exposure affects the association of c-reactive protein with cardiovascular disease risk factors and subclinical disease in healthy elderly subjects. Arterioscler Thromb Vasc Biol 1997;17:2167-2176.
59 Yudkin JS, Stehouwer CDA, Emeis JJ, et al. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction. Arterioscler Thromb Vasc Biol 1999;19:972–978.
60 Esmaillzadeh A, Azadbakht L. Increased Levels of Inflammation among Women with Enlarged Waist and Elevated Triglyceride Concentrations. Ann Nutr Metab 2010 Aug 20;57:77-84.
61 da Silva IT, Sanches LB, Mello AP, et al. Impact of C-reactive protein on cardiovascular risk in adolescents. Arq Bras Cardiol 2010;94:585-591.
62 Verit FF. High sensitive serum C-reactive protein and its relationship with other cardiovascular risk factors in normoinsulinemic polycystic ovary patients withoutmetabolic syndrome. Arch Gynecol Obstet 2010; 281: 1009-1014.
63 Thomas P, Vinzenz Hombach, Jan Torzewski. C-Reactive Protein– Mediated Low Density Lipoprotein Uptake by Macrophages:Implications for Atherosclerosis. Circulation 2001;103:1194-1197
64 Sonia S, Fahad R. C-Reactive Protein as a Screening Test for Cardiovascular Risk in a Multiethnic Population. Arteriosclerosis, Thrombosis, and Vascular Biology 2004; 24: 1509.
65 Yoshiki M, Toshikazu H, Shusaku S, et al. Metabolic Syndrome is Strongly Associated With Chronic Subclinical Inflammation in Patients Achieving Optimal Low-Density Lipoprotein-Cholesterol Levels in Secondary Prevention of Cardiovascular Disease. Circ J 2008; 72: 2046–2050.
66 Wexler DJ, Hu FB, Manson JE, et al. Mediating Effects of Inflammatory Biomarkers on Insulin Resistance Associated with Obesity. Obesity 2005; 13: 1772-1783.
67.Mathieu P, Poirier P, Pibarot P, et al. Despres J-P. Visceral Obesit: The Link Among Inflammation, Hypertension, and Cardiovascular Disease. Hypertension 2009;53: 577-584.
68 Mendall MA, Goggin PM, Molineaux N, et al. Relationship of helicobacter pylori infection and coronary heart disease. Br heart J 1994;71:437-439.
69 Kowalski M. Helicobacter pylori infection in coronary artery disease: influence of H. pylori eradication on coronary artery lumen after percutaneous transluminal coronary angioplasty. The detection of H.pylori specific DNA in human coronary atherosclerotic plague. J physiol pharmacol 2001;52:3-31.
70.Martin-de-argila C, Boixeda D, Canton R, et al. High seroprevalence of helicobacter pylori infection in coronary heart disease. Lancet 1995;346:310.
71 Whincup PH, Mendall MA, Perry IJ, et al. Prospective relations between helicobacter pylori infection, coronary heart disease and stroke in middle aged men. Heart 1996;75:568-572.
72 Danesh J, Collins R, Peto R. chronoc infections and coronary heart disease: is there a link? Lancet 1997;350:430-436.
73 Yukihiko M, Hiroaki T, Haruo N. Association of Mycoplasma pneumoniae infection with coronary artery disease and its interaction with chlamydial infection. Atheroslerosis 2004;9:139-144.
74 Basinkevich AB, Shakhnovich RM, Martynova VR, et al. Role of Chlamydia, mycoplasma and cytomegalovirus infection in the development of coronary artery disease. Cardio 2003;43:4-9.
75 Negh J, Gupta S, Goodbourn C, et al. Mycoplasma pneumoniae in elderly patients with stroke. A case-control study on the seroprevalence of M. pneumoniae in elderly patients with acute cerebrovascular disease-the M-PEPS study. Cerebrovasc Dis 2004;17:314-319.
76 Saikku P, Leinonen M, Tenkanen L, et al. Chronic chlamydia pneumoniae and clinical course in patients with unstable angina pectoris. Atherosclerosis 2000;153:499-504.
77 Thoms DH, Grayston JT, Siscovick DS, et al. Association of prior infection with chlamydia pneumoniae and angiographically demonstrated coronary artery disease.JAMA 1992; 268: 68-72.
78 Ericson K, Salden GP, Lindquist O, et al. Relationship of chlamydia pneumoniae infection to severity of human coronary atherosclerosis. Circulation 2000;101:2568-2571.
79张大庆,赵水平.肺炎衣原体与冠心病的关系.中国动脉粥样硬化杂志2002; 10: 274-276.
80 Roivainen M, Alfthan G, Jousilahti P, et al. Entrovirus infection as a possible risk factor for myocardial infarction. Circulation 1998;98:2534.
81孙余华,鞠振宇,吴永键,等.肺炎衣原体感染增加糖尿病患冠心病的危险性.中华心血管病杂志2003;3:169-172.
82 Huber S A , Kupperman H. Hormonal regulation of CD4( + ) T2cell responses in coxsackievirus B32 induced myocarditis in mice. J Virol 1999;73: 4689-4695.
83 Huber S A , Stone J E, Wagner D H, et al. Gamma delta + T cells regulate major histocompatibility complex class II (IA and IE) dependent susceptibility to coxsackievirus B32 induced autoimmune myocarditis. J Virol 1999;73 :5630-5636.
84 Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation 2003;107:363-369.
85 Libby P, Ridker PM. Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice. Journal of the American College of Cardiology 2006; 48: A33-A46.
86 Pearson TA, Mensah GA, Alexander RW, et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499-511.
87 Andersson J, Johansson L, Ladenvall P, et al. C-reactive protein is a determinant of first-ever stroke:prospective nested case-referent study. Cerebrovasc Dis 2009; 27: 544-551.
88 Makita S, Nakamura M, Satoh K, et al. Serum C-reactive protein levels can be used to predict future ischemic stroke and mortality in Japanese men from the general population. Atherosclersis 2009;204:234-238.
89 Tanne D, Benderly M, Goldbourt U, et al. C-Reactive Protein as a Predictor of Incident Ischemic Stroke Among Patients With Preexisting Cardiovascular Disease. Stroke 2006; 37: 1720-1724.
90 Ye X, Franco OH, Yu Z, et al. Associations of inflammatory factors with glycaemic status among middle-aged and older Chinese people. Clinical Endocrinology 2009; 70: 854-862.
91 Lin J, Zhang M, Song F, et al. Association between C-reactive protein and pre-diabetic status in a Chinese Han clinical population. Diabetes/Metabolism Research and Reviews 2009; 25: 219-223.
92 Yamada S, Gotoh T, Nakashima Y, et al. Distribution of Serum C-Reactive Protein and Its Association with Atherosclerotic Risk Factors in a Japanese Population. American Journal of Epidemiology 2001; 153: 1183-1190.
93 Otsuka T, Kawada T, Katsumata M, et al. High-sensitivity C-reactive protein is Associated with the risk of coronary heart disease as estimated by the Framingham Risk Score in middle-aged Japanese men. International Journal of Cardiology 2008; 129:245-250.
94 Sung KC, Suh JY, Kim BS, et al. High sensitivity c-reactive protein as an independent risk factor for essential hypertension. Am J Hypertens 2003;16: 429-433.
95 Kilpatrick EL, Bunk DM. Development of a Reference Measurement Procedure for C-Reactive Protein in Human Serum. Anal Chem 2009;81:8610-8616.
96 Pearson TA, Mensah GA, Alexander RW, et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statementfor Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003; 107: 499-511.
97 Ridker PM, Cook N. Clinical Usefulness of Very High and Very Low Levels of C-Reactive Protein Across the Full Range of Framingham Risk Scores. Circulation 2004; 109: 1955-1959.
98 Hickling S, Hung J, Knuiman M, et al. Are the associations between diet and C-reactive protein independent of obesity? Preventive Medicine 2008; 47:71-76.
99 Baena D, Alvarez P. Association between clustering of cardiovascular risk factors and the risk of cardiovascular disease. Rev Esp Salud Publica 2002;76:7-15.
100左惠娟,苏江莲,姚崇华.非瓣膜性房颤患者缺血性脑卒中危险因素暴露水平与聚集分析.中华流行病学杂志2008;29:819-822.
1 Powles J, Day N. Interpreting the global burden of disease. Lancet 2002; 360: 1342.
2田凤华.心脑血管疾病的预防.中国自然医学杂志2008; 10: 191-192.
3 Blake GJ, Ridker PM. High sensitivity C-reactive protein for protein for predicting cardiovascular diseades: An inflammatory hypothesis. Eur Heat J 2001; 22:349-352.
4 Ross R. Atherosclerosis : An inflammatory disease. N Engl J Med 1999;340:115-126.
5 Rosenson RS, Koenig W. Utility of inflammatory markers in the management of coronary artery disease. Am J Cardiol 2003; 92: 10-18.
6 Reiss AB, Glass AD. Atherosclerosis: immune and inflammatory aspects. J Investig Med 2006; 54: 123-131.
7李志强,郑兴.炎症与冠心病.中国心血管病研究杂志2006;4:233-235.
8 Lowe GD. The association between elevated levels of inflammation biomarkers and coronary artery disease and death. CMA J 2006; 174: 479-480.
9 Tillett W, Francis TJ. Serological reactions in pneumonia with a non protein somatic fraction of pneumococcus. J exp MED 1930; 52: 561-585
10 Ivashchenko Y, Kramer F, Schater S, et al. Protein kinase C pathway is involved in transcriptional regulation of c-reactive protein synthesis in human hepatocytes. Arterioscler Thromb Vasc Biol 2005; 25: 186-192.
11 J Szalai. The biological functions of C-reactive protein.Vase Pharmaca1 2002;39: 105-107.
12 Gambino R. C-reactive protein–undervalued underutilized. Clin Chem 1997;43: 2017-20l8.
13 Woloshin S, Schwartz LM. Distraction of c-reactive protein values in the united states. N Engl J Med 2005; 352: 1611-1613.
14 Meier-Ewert HK, Ridker PM, Rifai N, et al. Absence of diurnal variation of c-reactive protein concentrations in healthy human subjects. Clin Chem 2001; 47: 426-430.
15 Frohlich M, Sund M, Thorand B, et al. Lack of seasonal variation in c-reactive protein. Clin Chem 2002; 48: 575-577.
16 Libby P, Ridker PM. Novel inflammatory markers of coronary risk: theory versus practice. Circulation 1999; 100: 1148-1150.
17 Ross R. Atherosclerosis - an inflammatory disease. N Engl J Med 1999; 340: 115-126.
18 Libby P. Molecular bases of the acute coronary syndromes. Circulation 1995;91: 2844-2850.
19 Torzewski M, Risi C, Mortensen RF, et al. C-reactive protein in the arterial intima. Aterioscler thromb Vac Bio 2000; 20: 2094-2099.
20 Fichtlscherer S, Rosenberger G, Walter DH, et al. Elevated C-reactive protein levels and impaired endothelial vasoreactivity in patients with coronary artery disease. Circulation 2000;102:1000-1006.
21 Luigi M, Biasucci, LM, Liuzzo G. Elevated Levels of c-reactive protein at discharge in patients with unstable angina predict recurrent instability. Circulation 1999;99:855-860.
22 Pearson TA, Mensah GA, Alexander RW, et al. Makers of information and Cardiovascular disease. Application to clinical and public health practice: a statement for healthcare professional from the Centers for Disease control and Prevention and the Ameriean Heart Association.Circulation 2003;107:499-511.
23 Ridker PM, Cushman M, Stampfer MJ, et al. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease.Circulation 1998;97: 425-428.
24 Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of c-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med 1994; 331: 417-424.
25 Morrow DA, Rifai N, Antman EM, et al. C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI IIA sub study. J Am Coll Cardiol 1998, 31:1460-1465.
26 Bevilacqua M, strengelin S, Gimbrone M, et al. Endothelial leukocyte adhesion molecule 1:An inducible receptor for neutrophils related to complement regulatory proteins and lectins. Science 1989; 243: 1160.
27 Seman H B, Gurbel P A,Amderson J L, et al. Circulating cell adhesion molecules and death in patients with coronary artery disease. Circulation 2001;104:1336-1342.
28窦肇华,张远强,郭顺根,等.免疫细胞学与疾病.北京:中国医药科技出版社, 2004: 932-955.
29 Kansas GS. Selectins and their ligands:current concepts and controcersies. Blood 1996; 88: 3259-3287.
30 Haraldsen G, Kvale D, Uen B, et al. Cytokine-regulated expression of E-selectin, intercellular adhesion molecule-1(ICAM-1) , and vascular cell adhesion molecule-1 (VCAM-1) in human microvascular endothelial cells. J Immunol 1996; 156: 2558-2565.
31 Atalar E, Aytemir K, Haznedaroglu l, et al. Increased plasma levels of soluble selectins in patients with unstable angina.Int J Cardiol 2001; 78: 69-73.
32 Cockerill GW, Huehns TY, et al. Elevation of plasma high-density lipoprotein concentration reduces interleukin-1- induced expression of E-selectin in an in vivo model of acute inflammation.Circulation 2001; 103: 108-112.
33 Forlow SB, White EJ, Barlow SC, et al. Severe inflammatory defect and reduced viability in CD18 and E-selectin doieble mutant mice. Clin Invest 2000; 106 : 1457.
34华琦,李梅,刘力松等.高血压病患者脉压与内皮功能损害的相关性.中华内科杂志2003; 42: 574.
35段留法,郑秋甫,张丽萍等.自发性高血压大鼠内皮细胞功能不全发生机理实验研究.中国康复理论与实践2005; 11: 413.
36 Kuroda YT, Komamura K, Tatsumi R, et al . Vascular cell adhesion moleule-1 as a biochemical marker of left ventricular mass in the patients with hypertension. Am J Hypertens 2001, 14:868-872.
37 Blann AD, Tse W, Maxwell SJ, et al. Increased levels of the soluble adhesion molecule E - selectin in essential hypertension. J Hypertens 1994;12:925-928.
38沈庆乐,李培英,张存琪,等.选择素家族在老年冠心病和高血压中的临床意义.心血管康复医学杂志2001; 10:112-113.
39 Kozuka K, Kohryama T, Nomura E, et al. Endothelial markers and adhension molecules in acute ischemicstroke-equcntial change and differences in stroke subtype. Atherosclerosis 2002; 161: 161-168.
40 Mussack T, Biberthaler P, Steppert C, et al . Early Cellular brain damage and systemic inflammatory response after cardiopulmonary resuscitation on isolated severe headtrauma; a comparative pilot study on common pathomechanisms. Resuscitation 2001;49:193-199.
41 Omi H, Okayama N, Shimizum, et al. Participation of high glucose concentrations in neut rophil adhension and surface expression of adhension molecules on cultured human endothelial cells. Diabetes Complication 2002; 16: 201-208.
42 Soriano S, Lipton S, Wang Y, et al. Intercellular adhension molecule defiant mice are less susceptible to cerebral ischemia-reperfusion injury. Ana Neurol 1996; 39:618-624.
43 Bitsch A, Klene W, Murtada L, et al. A longitudinal prospective study of soluble adhesion molecules in acute stroke. Stroke 1998; 29: 2129-2135.
44 Akisu M, Kutursay N. Platelet-activating factor is an important mediator in hypoxie ischemic brain injury in the newborn rat . Flunarint and Ginkgo biloba extrat PAF concentration in the brain. Biol Neonate 1998; 74: 439-440.
45 Atalar E, Aytemir K, Haznedaroglu I, et al . Increased plasma levels of soluble selectin in patients with unstable angina. Int J Cardiol 2001;78: 69-73.
46 Semaan HB, Gurbel PA, Anderson JL, et al . Soluble VCAM-1 and E-selectin,but not ICAM-1 discriminate endothelial injury in patients with documented coronary artery disease. Cardiology 2000;93:7-10.
47田乃亮,陈清枝,李东野,等.血清Es和白细胞CD11b/CD18在冠心病中的意义.临床心血管病杂志200;20:7-9.
48沈庆乐,邓水泉,李培英,等.冠心病患者选择素P, L, E,一氧化氮及超氧化歧化酶水平变化及其相关性.中国心血管杂志2002;7:177-178.
49 Fang L, Wei H, Mak KH, et al. Marker of low-grade inflammation and soluble eell adhesion molecules in Chinese patients with coronary artery disease. Can J Cardiol 2004;20:1433-1 438.
50杨立森,林媛豪,石学宁,等.可溶性E-选择素对冠心病心绞痛的诊断意义.临床心血管病杂志2003;19:272-274.
51 Rothlein R, Dustin ML, Marlin SD, et al. A human intercellular adhesion molecule (ICAM-1) distinct from LFA-1. J Immunol 1986; 137: 1270-1274
52 Marlin SD, Spring TA. Purified intercellular adhesion molecule-1(ICAM-1) is aligand for lymphocyte function-associate antigen-1(LFA-1). Cell 1987;51: 813-819.
53何球藻,吴厚生.细胞与分子免疫学.上海科学技术文献出版社1997,104-120.
54 Leeuwenberg J. E-selectin and intercellular adhesion molecule-1 are released by activated human endothelial cells in vitro. Immunology 1992,77: 543-549.
55 Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases: the Atherosclerosis Risk In Cornmunities (ARIC)study. Circulation, 1997, 96: 4219-4225.
56 Blankenberg S, Barbaux S, Tiret L. Adhesion molecules and atherosclerosis. Atherosclerosis,2003; 170: 191-203.
57 Dustin ML, Rothlein R, Bahn AK, et al. Induction by IL-1 and IFN-γ. Tissue distribution, biochemistry and function of a natural adherence molecule (ICAM-1). J Immunol 1986;137:245-254.
58黄岚.细胞间粘附分子-1与心功能不全的临床意义.国外医学心血管疾病分册2000; 27: 5-7.
59 Poston RN, Johnson-Tidey RR. Localized adhesion of monocytes to human atherosclerotic plaques demons trated in vitro:Implications for atherogenesis.Am J Pathol 1996;149:73-80.
60 Haim M, Tanne D, Boyko V, et al. Solubele intercellular, adhesion molecule-1 and long-term risk of acute coronary events in patients with chronic coronary heart disease. J Am Coil Cardiol 2002;39:1133-1138.
61 Ikata J, Wakat S, Oishi Y, et al. Leukocyte counts and concent ration of soluble ashesion molecules as predictors of coronary atherosc1erosis. Coron Artery Dis 2000;11:445-449.
62 Mehta PK, Griendling KK. AngiotensinⅡcell signaling: physiological and pathological effects in the cardiovascular system. Am J Physiol Cell Physiol 2007;292: C82-97.
63 Johnston C, Risvanis J. Preclinical pharmacology of angiotensinⅡreceptor antagonists: Update and outstanding issues. Am J Hypertens 1997; 10: 306-310.
64 Schiffrin EL, Touyz RM. Multiple actions of angiotensin II in hypertension: benefits of AT1 receptor blockade. J Am Coll Cardiol 2003; 42:911-913.
65 Pastore L, Tessitore A, Martinotti S, et al. Angiotensin II stimulates intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells and increases soluble ICAM-1 release in vivo. Circulation 1999; 100:1646-1652.
66 Dzau VJ. Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis. Hypertension 2001; 37:1047-1052.
67 Liao TD, Yang XP, Liu YH, et al. Role of inflammation in the development of renal damage and dysfunction in angiotensin II-induced hypertension. Hypertension 2008; 52:256-263.
68 Gattullo D, Pagliaro P, Marsh NA, et al. New insights into nitricoxide and coronary circulation. Life Sci 1999; 65: 2167- 2174.
69 Liu HQ, Wei XB, Sun R, Cai YW, Lou HY, Wang JW, Chen AF, Zhang XM. Angiotensin II stimulates intercellular adhesion molecule-1 via an AT1 receptor/nuclear factor-kappaB pathway in brain microvascular endothelial cells. Life Sci. 2006;78:1293-8.
70 Wang CH, Li SH, Weisel RD, Fedak PW, Dumont AS, Szmitko P,etal. C-reactive protein upregulates angiotensin type 1 receptors in vascular smooth muscle. Circulation 2003;107:1783–1790.
71 Powell JS, Muller RK. Inhibitors of angiotension-converting enzyme prevent myointimal proliferation aftervascular injury. Science 1989;245:186-188.
72 Monton M, Castilla MA, et al. Effects of angiotensinⅡon endonthelial cell growth:role of AT-1 and AT-2 receptors. J Am Soc Nephrol 1998;9:969-974.
73陈良海,李刚,李代渝,等.幽门螺杆菌感染对心血管病患者脂代谢的影响.中国煤炭工业医学杂志2001;4:93-94.
74 Satmnalkopi K, Valto.en V, Kerttule Y, et al. Changes in serum lipoprotein pattern induced by acute infections. Metabolism 1988;37:859-861.
75 Rathbone B, Martin D, Stephens J, et al. Helicobacter pylori seropositivity in subjects with acute myocardial infarction. Heart 1996;76:308-311.
76 Yukihiko M, Hiroaki T, Haruo N. Association of Mycoplasma pneumoniae infection with coronary artery disease and its interaction with chlamydial infection. Atheroslerosis 2004;9:139-144.
77 Basinkevich AB, Shakhnovich RM, Martynova VR, et al. Role of Chlamydia, mycoplasma and cytomegalovirus infection in the development of coronary arterydisease. Cardio 2003;43:4-9.
78 Negh J, Gupta S, Goodbourn C, et al. Mycoplasma pneumoniae in elderly patients with stroke. A case-control study on the seroprevalence of M. pneumoniae in elderly patients with acute cerebrovascular disease-the M-PEPS study. Cerebrovasc dis 2004;17:314-319.
79 Thoms DH, Grayston JT, Siscovick DS, et al. Association of prior infection with chlamydia pneumoniae and angiographically demonstrated coronary artery disease. JAMA 1992;268:68-72.
80 Ericson K, Salden GP, Lindquist O, et al. Relationship of chlamydia pneumoniae Infection to severity of human coronary atherosclerosis. Circulation 2000;101: 2568-2571.
81孙余华,鞠振宇,吴永键等.肺炎衣原体感染增加糖尿病患冠心病的危险性.中华心血管病杂志2003;3:169-172.
82 Kalayoglu MV, Libby P, Byrne GI. Chlamydia pneumoniae as an emerging risk factor in cardiovascular disease. JAMA 2002;288:2724-2731.
83 Lau RC. Coxsackie B virus - specific IgMresponses in coronary care unit patients. Med Vird 1986;18:193-198.