冠心病不稳定性心绞痛气虚血瘀证及炎症相关性研究
|
摘要
冠心病是多种危险因素所导致的慢性疾病。尽管很多因素(如年龄、吸烟、饮酒、肥胖、高血压、糖尿病、高血脂及遗传等)已被证明与冠心病的发生、发展有关,但还不能对所有冠心病的发生作出满意的解释。因此,对导致冠心病发生、发展的其他生物学标志物,尤其是炎症标志物(如白细胞计数、C反应蛋白、白细胞介素)等的研究已成为当前研究的热点。冠心病属中医“胸痹”、“心痛”范畴,中医学运用病证结合防治冠心病心绞痛具有独特优势,而中医辨证论治又是中医理论的核心和精髓。不同中医证候可能存在不同的生物学基础。本论文对125例冠心病不稳定性心绞痛患者进行中医证候调查,对其理化指标进行统计分析,并做白介素-1、6、肿瘤坏子因子-a、细胞间黏附因子-1、血清淀粉样蛋白A等炎症相关指标,旨在探讨冠心病不稳定性心绞痛患者证候分布特点及不同证候间是否存在不同理化指标及炎症相关因子的差异,并对冠心病不稳定性心绞痛不同中医证候与理化指标、炎症相关因子做相关性分析。为临床寻找简便、有效的判断冠心病不稳定性心绞痛不同证候及预后的指标。
结果：①125例冠心病不稳定性心绞痛患者中医证候特点：涵盖血瘀证、痰浊证、气滞证、寒凝证、气虚证、阴虚证、阳虚证等7个证候；其中单证31例,占24.60%,以血瘀证为主,占51.61%,其次气虚证,占12.90%；两证组合64例,占51.20%,以气虚血瘀证最多,占48.88%,其次痰瘀互阻证,占14.06%；三证组合22例,占16.80%,以气虚血瘀痰浊证最多,占28.57%,其次为气虚血瘀气滞证,占23.81%；四证组合和五证组合少见,各占4.76%和2.38%；从两证到五证组合在气虚血瘀证的基础上以气虚-阴虚-气滞为组合变化轴线；气虚血瘀并见者51例,占总病例数的40.80%；虚实兼夹证71例,占总病例数的56.80%；②证候与理化指标间Sperman相关分析显示：血瘀证与血清总胆固醇水平(TC)、载脂蛋白B(apoB100)、直接胆红素(DBIL)相关；气虚证与平均红细胞血红蛋白浓度(MCHC)、直接胆红素(DBIL)等相关；气虚血瘀证与外周血红细胞计数(RBC)、红细胞平均体积(MCV)、平均红细胞血红蛋白浓度(MCHC).直接胆红素(DBIL)等相关；Logistic回归结果显示：单核细胞(M)、胆红素、载脂蛋白B (apoB100).载脂蛋白AI(apoAI)、白细胞计数(WBC)等为血瘀证主要影响因素；气虚证主要影响因素依次为外周血红细胞计数(RBC)、平均红细胞血红蛋白含量(MCH)、红细胞平均体积(MCV)等；气虚血瘀证影响因素依次为胆红素、红细胞计数(RBC)、平均红细胞血红蛋白含量(MCH)、红细胞压积(HCT)、单核细胞(M)、红细胞平均体积(MCV)等；③证候与炎症相关性研究中结果显示：血瘀证与白细胞介素-6(IL-6)、肿瘤坏死因子-a(TNF-a).细胞间黏附因子-1(ICAM-1)及纤维蛋白原(FIB)相关；气虚证与白细胞介素-6(IL-6)、肿瘤坏死因子-a(TNF-a).细胞间黏附因子-1(ICAM-1)、超敏C反应蛋白(hs-CRP)及核因子-KB(NF-KB)相关；气虚血瘀证与白细胞介素-6(IL-6)、肿瘤坏死因子-a(TNF-a).细胞间黏附因子-1(ICAM-1)相关；④炎症指标间及血脂相关性分析结果显示：血清淀粉样蛋白A(SAA)与血清甘油三酯(TG)正相关(r=0.246,p=0.004)、与白细胞介素-1(IL-1)正相关(r==0.192,p=0.025),与载脂蛋白AI(apoAI)负相关(r=-0.182,p=0.034);超敏C反应蛋白(hs-CRP)与载脂蛋白AI(apoAI)负相关(r=-0.179,p=0.037),与载脂蛋白B100 (apoB100)负相关(r=-0.192,p=0.025),与细胞间黏附因子-1(ICAM-1)正相关(r=0.323,p=0.000);纤维蛋白原(FIB)与载脂蛋白AI(apoAI)负相关(r=-0.188,p=0.029),与白细胞介素-1(IL-1)、细胞间粘附因子-1(ICAM-1)正相关(r=0.301,p=0.000;r=0.339,p=0.000);白细胞介素-1(IL-1)与载脂蛋白(apoAI)负相关(r=-0.180,p=0.036);白细胞介素-6(IL-6)与载脂蛋白(apoAI)负相关(r=-0.178,p=0.039);细胞间黏附因子因子(ICAM-1)与高密度脂蛋白(HDL)负相关(r=-0.217,p=0.011)。
结论：①125例冠心病不稳定性心绞痛患者证候涵盖血瘀证、痰浊证、气滞证、寒凝证、气虚证、阴虚证、阳虚证等7个证候；证候组合以两证组合为主；从两证到五证组合在气虚血瘀证的基础上以气虚-阴虚-气滞为组合变化轴线；气虚血瘀为冠心病不稳定性心绞痛主要病机；②冠心病不稳定性心绞痛血瘀证与外周血白细胞、清总胆固醇水平、载脂蛋白B、胆红素水平相关；气虚证与外周血红细胞计数、平均血红蛋白浓度、血小板计数、胆红素水平相关；气虚血瘀证与外周血红细胞计数、平均血红蛋白浓度、白细胞计数、胆红素水平相关,提示冠心病不稳定性心绞痛患者不同证候有自己的生物学基础；③冠心病不稳定性心绞痛发生、发展与炎症相关,且冠心病不稳定性心绞痛患者不同中医证候存在炎症相关因子表达差异：血瘀证与肿瘤坏死因子-a、纤维蛋白原相关；气虚证与纤维蛋白原、超敏C反应蛋白、白细胞介素-6、肿瘤坏死因子-a、细胞间黏附因子-1、核因子-KB相关；气虚血瘀证与白细胞介素-1、6、肿瘤坏死因子-a、细胞间黏附因子-1相关；④各种炎症相关指标之间及炎症指标与血脂之间存在相关关系。
冠心病不稳定性心绞痛的发生、发展与炎症反应有关。冠心病不稳定性心绞痛血瘀证、气虚证、气虚血瘀证候与炎症反应有关。结果进一步支持了以动脉粥样硬化为基础的冠心病是一种慢性炎症过程这一理论假说。并提示冠心病不稳定性心绞痛不同证候中释放急性时相蛋白、炎症因子有一定的差异。
Coronary heart disease(CHD) is a chronic diseases caused by many risk factors. Although many factors (such as age, smoking, drinking, obesity, hypertension, hyperlipidemia, diabetes and genetic, etc.) has been proven with the occurrence of CHD, but also the occurrence of CHD can not be made for all satisfactory explanation. Therefore, leading to CHD and other biological markers, particularly, inflammatory markers (such as white blood cell count, C-reactive protein, interleukin) and other research has become a research hotspot. CHD are the category of "Chest", "heartache" in Traditional Chinese Medicine(TCM). The treatment according to syndrome differentiation is the core and essence of TCM theory. Different syndromes may exist in different biological basis. TCM have the unique advantages to put to use syndrome and disease to prevent and cure Unstable angina (UA).The study invests the syndromes of 125 patients in UA of CHD, makes statistical analysis of their biological parameter detections,and detects their IL-1, IL-6, TNF-a, cell adhesion molecule-1, serum amyloid A, etc. inflammation-related indexes.Aim to investigate the class distribution of different syndromes,and the relation between syndromes with biological parameter detections and inflammation-related indexes. To find simple and effective indexes to judge UA different syndromes to use for clinical.
Result:①125 patients with UA patients with blood stasis syndrome, phlegm syndrome, and Qi stagnation syndrome, cold coagulation card syndrome, qi deficiency syndrome, yin deficiency syndrome, yang deficiency syndrome; documents 31 cases, accounting for 24.6%, mainly by blood stasis syndrome, accounting for 51.61%, followed by qi deficiency syndrome, accounting for 12.9%; two card combinations of 64 cases, accounting for 51.2%, up to Qi deficiency and blood stasis syndrome, accounting for 48.88%, followed by phlegm and blood stasis syndrome, accounting for 14.06%; three card combination 22 cases of qi deficiency、blood stasis and phlegm syndrome, accounting for 28.57%, followed by blood stasis and Qi stagnation syndrome, accounting for 23.81%; four card combinations and rare combination of five cards, accounting for 4.76% and 2.38%; On the basis of Qi deficiency and blood stasis syndrome,two to five card combination changes at Qi deficiency-yin Deficiency-Qi stagnation axis; 51 patients are Qi deficiency and blood stasis syndrome,which account for the total number of cases of 40.80%; 71 patients are actual situation and evidence folders, which account forthe total number of cases of 56.80%.②Syndrome associated with the biological parameter detections Sperman analysis and Lgistic stepwise regression analysis showed:blood stasis syndrome relate with CHO, DBIL and MCV; Qi deficiency syndrome relate with RBC, MCH, PLT, DBIL; Qi deficiency and blood stasis syndrome relate with RBC, MCH, PLT, DBIL. Logistic regression analysis showed:Mononuclear cells (M), bilirubin, apolipoprotein B (apoB100), apolipoprotein AI (apoAI), white blood cell count (WBC),etc are the main infiuence factors of blood stasis syndrome of CHD; the main infiuence factors of qi deficiency syndrome were red blood cell count (RBC), mean corpuscular hemoglobin (MCH), mean corpuscular volume (MCV), the infiuence factors of Qi deficiency and blood stasis syndrome were bilirubin, red blood cell count (RBC), mean corpuscular hemoglobin (MCH), hematocrit (HCT), monocytes (M), mean corpuscular volume (MCV),etc.③The result of relation between Syndrome with inflammation-related indexes showe:blood stasis syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1,FIB; Qi deficiency syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1, hs-CRP,NF-KB; Qi deficiency and blood stasis syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1.④Inflammation and lipid indexes correlation analysis showed that:SAA positive correlation with TG (r= 0.246, p= 0.004) and IL-1 (r= 0.192, p= 0.025), but negative correlation with apoAI (r=-0.182, p= 0.034); hs-CRP negative correlation with apoAI and B100 (r=-0.179, p= 0.037; r=-0.192, p= 0.025), but positively correlated with ICAM-1 (r = 0.323, p= 0.000); FIB negative correlation with apoAI (r=-0.188, p= 0.029), but positively correlation with IL-1, ICAM-1 (r= 0.301, p= 0.000; r= 0.339, p= 0.000). IL-1 negative correlation with apoAI (r=-0.180, p= 0.036); IL-6 negative correlation with apoAI (r=-0.178, p= 0.039); ICAM-1 negative correlation with HDL (r=-0.217, p= 0.011). Conclusion:①125 patients with UA patients with blood stasis syndrome, phlegm syndrome, and Qi stagnation syndrome, cold coagulation card syndrome, qi deficiency syndrome, yin deficiency syndrome, yang deficiency syndrome; On the basis of Qi deficiency and blood stasis syndrome,two to five card combination changes at Qi deficiency-yin Deficiency-Qi stagnation axis;Qi deficiency and blood stasis syndrome is the main pathogenesis.②The blood stasis syndrome of UA relate with CHO, DBIL and MCV; Qi deficiency syndrome relate with RBC, MCH, PLT, DBIL; Qi deficiency and blood stasis syndrome relate with RBC, MCH, PLT, DBIL.CHD blood stasis syndrome、qi deficiency syndrome、Qi deficiency and blood stasis syndrome have its own biology mechanism.③UA occurrence and development may be associated with inflammation, and the existence of different syndromes abnormal expression of inflammation-related factors. blood stasis syndrome relate with IL-1; Qi deficiency syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1, NF-KB.④There is correlation between various inflammation-related indicators,also between inflammation-related indicators and blood lipids.
CHD occurrence, development may be inflammation-related. Syndrome of blood stasis, qi deficiency, qi deficiency and blood stasis are inflammation-related. The results further support the Atherosclerosis is a chronic inflammatory process. Different syndromes of UA have the inflammatory process and release acute phase proteins.
结果：①125例冠心病不稳定性心绞痛患者中医证候特点：涵盖血瘀证、痰浊证、气滞证、寒凝证、气虚证、阴虚证、阳虚证等7个证候；其中单证31例,占24.60%,以血瘀证为主,占51.61%,其次气虚证,占12.90%；两证组合64例,占51.20%,以气虚血瘀证最多,占48.88%,其次痰瘀互阻证,占14.06%；三证组合22例,占16.80%,以气虚血瘀痰浊证最多,占28.57%,其次为气虚血瘀气滞证,占23.81%；四证组合和五证组合少见,各占4.76%和2.38%；从两证到五证组合在气虚血瘀证的基础上以气虚-阴虚-气滞为组合变化轴线；气虚血瘀并见者51例,占总病例数的40.80%；虚实兼夹证71例,占总病例数的56.80%；②证候与理化指标间Sperman相关分析显示：血瘀证与血清总胆固醇水平(TC)、载脂蛋白B(apoB100)、直接胆红素(DBIL)相关；气虚证与平均红细胞血红蛋白浓度(MCHC)、直接胆红素(DBIL)等相关；气虚血瘀证与外周血红细胞计数(RBC)、红细胞平均体积(MCV)、平均红细胞血红蛋白浓度(MCHC).直接胆红素(DBIL)等相关；Logistic回归结果显示：单核细胞(M)、胆红素、载脂蛋白B (apoB100).载脂蛋白AI(apoAI)、白细胞计数(WBC)等为血瘀证主要影响因素；气虚证主要影响因素依次为外周血红细胞计数(RBC)、平均红细胞血红蛋白含量(MCH)、红细胞平均体积(MCV)等；气虚血瘀证影响因素依次为胆红素、红细胞计数(RBC)、平均红细胞血红蛋白含量(MCH)、红细胞压积(HCT)、单核细胞(M)、红细胞平均体积(MCV)等；③证候与炎症相关性研究中结果显示：血瘀证与白细胞介素-6(IL-6)、肿瘤坏死因子-a(TNF-a).细胞间黏附因子-1(ICAM-1)及纤维蛋白原(FIB)相关；气虚证与白细胞介素-6(IL-6)、肿瘤坏死因子-a(TNF-a).细胞间黏附因子-1(ICAM-1)、超敏C反应蛋白(hs-CRP)及核因子-KB(NF-KB)相关；气虚血瘀证与白细胞介素-6(IL-6)、肿瘤坏死因子-a(TNF-a).细胞间黏附因子-1(ICAM-1)相关；④炎症指标间及血脂相关性分析结果显示：血清淀粉样蛋白A(SAA)与血清甘油三酯(TG)正相关(r=0.246,p=0.004)、与白细胞介素-1(IL-1)正相关(r==0.192,p=0.025),与载脂蛋白AI(apoAI)负相关(r=-0.182,p=0.034);超敏C反应蛋白(hs-CRP)与载脂蛋白AI(apoAI)负相关(r=-0.179,p=0.037),与载脂蛋白B100 (apoB100)负相关(r=-0.192,p=0.025),与细胞间黏附因子-1(ICAM-1)正相关(r=0.323,p=0.000);纤维蛋白原(FIB)与载脂蛋白AI(apoAI)负相关(r=-0.188,p=0.029),与白细胞介素-1(IL-1)、细胞间粘附因子-1(ICAM-1)正相关(r=0.301,p=0.000;r=0.339,p=0.000);白细胞介素-1(IL-1)与载脂蛋白(apoAI)负相关(r=-0.180,p=0.036);白细胞介素-6(IL-6)与载脂蛋白(apoAI)负相关(r=-0.178,p=0.039);细胞间黏附因子因子(ICAM-1)与高密度脂蛋白(HDL)负相关(r=-0.217,p=0.011)。
结论：①125例冠心病不稳定性心绞痛患者证候涵盖血瘀证、痰浊证、气滞证、寒凝证、气虚证、阴虚证、阳虚证等7个证候；证候组合以两证组合为主；从两证到五证组合在气虚血瘀证的基础上以气虚-阴虚-气滞为组合变化轴线；气虚血瘀为冠心病不稳定性心绞痛主要病机；②冠心病不稳定性心绞痛血瘀证与外周血白细胞、清总胆固醇水平、载脂蛋白B、胆红素水平相关；气虚证与外周血红细胞计数、平均血红蛋白浓度、血小板计数、胆红素水平相关；气虚血瘀证与外周血红细胞计数、平均血红蛋白浓度、白细胞计数、胆红素水平相关,提示冠心病不稳定性心绞痛患者不同证候有自己的生物学基础；③冠心病不稳定性心绞痛发生、发展与炎症相关,且冠心病不稳定性心绞痛患者不同中医证候存在炎症相关因子表达差异：血瘀证与肿瘤坏死因子-a、纤维蛋白原相关；气虚证与纤维蛋白原、超敏C反应蛋白、白细胞介素-6、肿瘤坏死因子-a、细胞间黏附因子-1、核因子-KB相关；气虚血瘀证与白细胞介素-1、6、肿瘤坏死因子-a、细胞间黏附因子-1相关；④各种炎症相关指标之间及炎症指标与血脂之间存在相关关系。
冠心病不稳定性心绞痛的发生、发展与炎症反应有关。冠心病不稳定性心绞痛血瘀证、气虚证、气虚血瘀证候与炎症反应有关。结果进一步支持了以动脉粥样硬化为基础的冠心病是一种慢性炎症过程这一理论假说。并提示冠心病不稳定性心绞痛不同证候中释放急性时相蛋白、炎症因子有一定的差异。
Coronary heart disease(CHD) is a chronic diseases caused by many risk factors. Although many factors (such as age, smoking, drinking, obesity, hypertension, hyperlipidemia, diabetes and genetic, etc.) has been proven with the occurrence of CHD, but also the occurrence of CHD can not be made for all satisfactory explanation. Therefore, leading to CHD and other biological markers, particularly, inflammatory markers (such as white blood cell count, C-reactive protein, interleukin) and other research has become a research hotspot. CHD are the category of "Chest", "heartache" in Traditional Chinese Medicine(TCM). The treatment according to syndrome differentiation is the core and essence of TCM theory. Different syndromes may exist in different biological basis. TCM have the unique advantages to put to use syndrome and disease to prevent and cure Unstable angina (UA).The study invests the syndromes of 125 patients in UA of CHD, makes statistical analysis of their biological parameter detections,and detects their IL-1, IL-6, TNF-a, cell adhesion molecule-1, serum amyloid A, etc. inflammation-related indexes.Aim to investigate the class distribution of different syndromes,and the relation between syndromes with biological parameter detections and inflammation-related indexes. To find simple and effective indexes to judge UA different syndromes to use for clinical.
Result:①125 patients with UA patients with blood stasis syndrome, phlegm syndrome, and Qi stagnation syndrome, cold coagulation card syndrome, qi deficiency syndrome, yin deficiency syndrome, yang deficiency syndrome; documents 31 cases, accounting for 24.6%, mainly by blood stasis syndrome, accounting for 51.61%, followed by qi deficiency syndrome, accounting for 12.9%; two card combinations of 64 cases, accounting for 51.2%, up to Qi deficiency and blood stasis syndrome, accounting for 48.88%, followed by phlegm and blood stasis syndrome, accounting for 14.06%; three card combination 22 cases of qi deficiency、blood stasis and phlegm syndrome, accounting for 28.57%, followed by blood stasis and Qi stagnation syndrome, accounting for 23.81%; four card combinations and rare combination of five cards, accounting for 4.76% and 2.38%; On the basis of Qi deficiency and blood stasis syndrome,two to five card combination changes at Qi deficiency-yin Deficiency-Qi stagnation axis; 51 patients are Qi deficiency and blood stasis syndrome,which account for the total number of cases of 40.80%; 71 patients are actual situation and evidence folders, which account forthe total number of cases of 56.80%.②Syndrome associated with the biological parameter detections Sperman analysis and Lgistic stepwise regression analysis showed:blood stasis syndrome relate with CHO, DBIL and MCV; Qi deficiency syndrome relate with RBC, MCH, PLT, DBIL; Qi deficiency and blood stasis syndrome relate with RBC, MCH, PLT, DBIL. Logistic regression analysis showed:Mononuclear cells (M), bilirubin, apolipoprotein B (apoB100), apolipoprotein AI (apoAI), white blood cell count (WBC),etc are the main infiuence factors of blood stasis syndrome of CHD; the main infiuence factors of qi deficiency syndrome were red blood cell count (RBC), mean corpuscular hemoglobin (MCH), mean corpuscular volume (MCV), the infiuence factors of Qi deficiency and blood stasis syndrome were bilirubin, red blood cell count (RBC), mean corpuscular hemoglobin (MCH), hematocrit (HCT), monocytes (M), mean corpuscular volume (MCV),etc.③The result of relation between Syndrome with inflammation-related indexes showe:blood stasis syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1,FIB; Qi deficiency syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1, hs-CRP,NF-KB; Qi deficiency and blood stasis syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1.④Inflammation and lipid indexes correlation analysis showed that:SAA positive correlation with TG (r= 0.246, p= 0.004) and IL-1 (r= 0.192, p= 0.025), but negative correlation with apoAI (r=-0.182, p= 0.034); hs-CRP negative correlation with apoAI and B100 (r=-0.179, p= 0.037; r=-0.192, p= 0.025), but positively correlated with ICAM-1 (r = 0.323, p= 0.000); FIB negative correlation with apoAI (r=-0.188, p= 0.029), but positively correlation with IL-1, ICAM-1 (r= 0.301, p= 0.000; r= 0.339, p= 0.000). IL-1 negative correlation with apoAI (r=-0.180, p= 0.036); IL-6 negative correlation with apoAI (r=-0.178, p= 0.039); ICAM-1 negative correlation with HDL (r=-0.217, p= 0.011). Conclusion:①125 patients with UA patients with blood stasis syndrome, phlegm syndrome, and Qi stagnation syndrome, cold coagulation card syndrome, qi deficiency syndrome, yin deficiency syndrome, yang deficiency syndrome; On the basis of Qi deficiency and blood stasis syndrome,two to five card combination changes at Qi deficiency-yin Deficiency-Qi stagnation axis;Qi deficiency and blood stasis syndrome is the main pathogenesis.②The blood stasis syndrome of UA relate with CHO, DBIL and MCV; Qi deficiency syndrome relate with RBC, MCH, PLT, DBIL; Qi deficiency and blood stasis syndrome relate with RBC, MCH, PLT, DBIL.CHD blood stasis syndrome、qi deficiency syndrome、Qi deficiency and blood stasis syndrome have its own biology mechanism.③UA occurrence and development may be associated with inflammation, and the existence of different syndromes abnormal expression of inflammation-related factors. blood stasis syndrome relate with IL-1; Qi deficiency syndrome relate with IL-6, TNF-a, intercellular adhesion molecule-1, NF-KB.④There is correlation between various inflammation-related indicators,also between inflammation-related indicators and blood lipids.
CHD occurrence, development may be inflammation-related. Syndrome of blood stasis, qi deficiency, qi deficiency and blood stasis are inflammation-related. The results further support the Atherosclerosis is a chronic inflammatory process. Different syndromes of UA have the inflammatory process and release acute phase proteins.
引文
[1]武阳丰.重视心血管病流行病学研究工作[J].中华流行病学杂志,2003,24(7):337.
[2]张晓东,姚映芷.冠心病心绞痛中医病机及治法研究概述[J].吉林中医药,2005,25(3)：56-58.
[3]姬生勤.冠心病心绞痛辨治思路与方法探析[J].中国中医药信息杂志,2003,10(10):48.
[4]李宝同,张庆宏,石磊.中医药治疗冠心病研究进展[J].长春中医药大学学报,2007,23(1)：75-76.
[5]李芳,樊相军.胸痹诱发因素与辩证分型的调查分析[J].人民军医,2001,44(8):484-486.
[6]吴辉,于扬文,吴伟.116例冠心病患者中医证候及病因分析[J].江苏中医,2004,25(10)：30.
[7]杨利,邓铁涛.“冠心三论”[J].湖南中医药导报,2004,10(6)：8-10.
[8]吴以岭.从络病学说论治冠心病心绞痛[J].中国中医基础医学杂志,2001,7(4)：71
[9]1980年全国冠心病辨证论治研究座谈会.冠心病中医辨证试行标准[S].中医杂志,1980,(8)：46.
[10]陈贵延,薛赛琴.最新国内外疾病诊疗标准[S].北京：学苑出版社,1992.209-212, 678.
[11]中西医结合心血管学会.冠心病的中医辨证标准[S].中西医结合杂志,1991,11(5)：257.
[12]卫生部.中药新药治疗胸痹心痛的临床研究指导原则[S].1993.41
[13]郑筱萸.中药新药临床研究指导原则[S].北京：中国医药科技出版社,2002.
[14]王永炎.中医内科学[M].上海：上海科学技术出版社,1997.
[15]郭志华.冠心病心绞痛2432例中医辨证分型综合统计分析[J].湖南中医杂志,1998,14(2)：7.
[16]衷敬柏,董绍英,王阶,王永炎.2689例冠心病心绞痛证候要素的文献统计分析.[J]中国中医药信息杂志,2006,13(5):100-101.
[17]王阶,邢雁伟,姚魁武,李军.冠心病心绞痛中医证候要素研究及临床应用[J].湖北中医学院学报,2009,11(3):3-5.
[18]王晓才,林谦,王晓宝,农一兵.胸痹中医证候影响因素的回归分析.[J]北京中医,2007,26(4):218-220.
[19]文川,程伟.206例冠心病心绞痛患者问诊资料与中医辨证关系的探讨[J].湖北中医杂志,2002,(10)：3.
[20]王阶,李军,姚魁武,衷敬柏.冠心病心绞痛证候要素和冠脉病变的Logistic回归分析[J].辽宁中医杂志,2007,34(9):1209-1211.
[21]吴旸,金刚,崔杰,彭建军,任文林.冠心病中医证候特点的回归分析[J].中医药学报,2008,36(4):4-6.
[22]王永霞,胡宇才,朱明军,高传玉.冠心病心绞痛中医证候分布相关性研究[J].世界中西医结合杂志,2008,3(12):714-719.
[23]张敏州,邹旭,李新梅.胸痹心痛证冠状动脉造影100例临床分析[J].浙江中西医结合杂志,2001,11(8)：472-475.
[24]褚福永,王阶,姚魁武,李志忠.冠心病不稳定型心绞痛中医辨证分型与血脂及冠脉造影结果的相关性研究.[J]北京中医药2009,28(12)：918-921.
[25]邹旭,邓铁涛.冠状动脉成型术后再狭窄的中医证候初探[J].广州中医药大学学报,2001,18(4)：293.
[26]马晓昌,尹太英,陈可冀.冠心病中医辨证分型与冠状动脉造影所见相关性比较研究[J].中国中西医结合杂志,2001,21(9)：654-656.
[27]李佃贵,李俊峡,李振彬.冠心病患者病变程度与中医证型的关系[J].中国中医药信息杂志,2001,8(12)：57-58.
[28]张惠贞,张鸿文,贺莉清.心律失常与胸痹心痛证型关系的探讨[J].河南中医学刊,1996,11(4)：39-41.
[29]赵亚莉,杨幼新.冠心病心电图与中医辨证分型的关系[J].江苏中医,2001,22(9):20-
[30]陈伯钧,张文清,张敏州.冠心病中医分型与心律失常及心功能关系分析[J].现代中西医结合杂志,2000,9(19):1857-1858.
[31]张宁宁.气滞血瘀、气虚血瘀心绞痛患者心率变异性与心肌缺血指数相关性探讨[J].山东中医药大学学报,2003,27(2)：123.
[32]王阶,何庆勇,施展,刑雁伟.冠心病证候要素组合与心功能及血脂的相关性[J].中西医结合学报,2008,6(9)：897-901.
[33]周英.心血管病表现心虚证患者左心室舒张功能观察[J].中国中西医结合杂志,1995,15(1)：13.
[34]王硕仁,赵明镜,吕希滢.冠心病心气虚证与左心室功能及心肌缺血相关性的临床研究[J].中国中西医结合杂志,1998,18(8)：457-460.
[35]王阶,何庆勇,施展,邢雁伟,李霁,房玉涛,汤艳莉.冠心病证候要素组合与心功能及血脂的相关性.[J]中西医结合学报,2008,6(9):897-901.
[36]袁肇凯,田松,黄献平,胡志希,孙贵香,陈清华,莫莉,简维雄.冠心病痰瘀证候血脂指标的Meta分析。[J]云南中医学院学报,2008,31(5):1-8.
[37]金志刚,周端,顾仁樱.冠心病血瘀证与血清脂蛋白(a)含量的临床观察.河南中医药学刊,1995,10(3)：28
[38]孙锡印,杨妻琳.冠心病气滞血瘀与气虚血瘀证型间血载脂蛋白的异同及辨治影响[J].江苏中医,1997,18(6)：40.
[39]李俊,李小敏,刘映峰.冠心病冠状动脉造影结果与中医证型及血脂、脂蛋白关系的研究[J].中国中医急症,2000,9(3)：123-125.
[40]何剑平,李小敏,张瞥.冠心病中医辨证与血脂脂蛋白关系的探析[J].辽宁中医杂志,1998,25(11)：505-507.
[41]熊尚全,许少锋,郭云庚.冠心病本虚标实辨证与脂蛋白(a)关系的初步研究[J].福建中医学院学报,1998,8(1)：1-3.
[42]詹萍,施卿卿,郭云庚.不稳定心绞痛中医分型与胰岛素抵抗的关系[J].福建中医药,2001,3(2)：3.
[43]李俊,王天伟,严夏.冠心病不稳定型心绞痛中医证候与C反应蛋白和基质金属蛋白酶-9关系的研究[J].辽宁中医药大学学报,2008,10(2)：102-103.
[44]杨徐杭,汶医宁,魏敏慧.冠心病中医辨证与血清C反应蛋白的相关性研究[J].中医药学刊,2004,22(9)：1649.
[45]卢玉俊,石磊.冠心病中医证型与血浆同型半胱氨酸水平相关性的研究[J].浙江中医药大学学报,2009,33(1)：103-104.
[46]林凯旋,安辉,廖灿铭.冠心病血瘀证与同型半胱氨酸的相关性研究[J].中医研究,2007,20(2)：32-33.
[47]方建伟,黄源鹏,林求诚.冠心病中医证型与血浆ET、TXA2-PGI2的关系[J].实用中医药杂志,2005,21(9)：519.
[48]黄献平.心病气血辨证瘀血清锌铜铁钙含量的关系[J].辽宁中医杂志,1997,24(4)：149.
[49]江帆.左归饮加减治疗心肾阳虚型胸痹心痛50例[J].吉林中药,2006,3(3):271.
[50]刘亚光.现代自然科学与中医理论[M].福州：福建科学技术出版社,1983:247.
[51]王霭平.从肺论治胸痹心痛的临床观察[J].上海针灸杂志,2004,4(4):251.
[52]王中平.以活血化瘀法治疗冠心病心绞痛[J].中华实用中西医杂志,2002,2(15)：501.
[53]张跃林.中医活血化瘀法治疗冠心病心绞痛84例观察,中国医学杂志,2007,5(11):19-20.
[54]胥春梅.中医药治疗冠心病心绞痛30例[J].现代中医药,2003(2):28-29.
[55]贺敬波,黄绵清,张勤.加减暖肝煎胶囊治疗不稳定型心绞痛的临床研究及理论探讨[J].中国中医基础医学杂志,2003,9(9):55-56.
[56]刘慎柏.温心通脉方配合西药治疗不稳定性心绞痛60例临床观察[J].湖南中医药导报,2003,9(6)：22-23.
[57]张华伟.络脉舒通颗粒对不稳定型心绞痛疗效的临床观察[J].临床军医杂志,2004,32(6):8-9.
[58]洪永敦,黄衍寿,陈宇鹏,吴辉.清热化痰活血法治疗冠心病不稳定性心绞痛临床研究[J].辽宁中医杂志,2005,32(7)：625-627.
[59]彭桂阳.加减参脉汤治疗冠心病心绞痛60例总结[J].湖南中医杂志,2004,20(4)：14-15.
[60]李浩,崔玲,崔天红.益心通脉颗粒剂治疗阳癖心痛的临床研究[J].中国中医药信息,1999,6(10)：45-47.
[61]藕二祥.益气滋阴、活血通络法对不稳定性心绞痛血小板活化功能的影响[J].江苏中医药,2006,27(9)：24-25.
[62]叶建芳,刘文胜.健脾化痰活血法治疗不稳定性心绞痛50例疗效观察[J].新中医,2005,39(7)：36-37.
[63]唐其柱.补阳还五汤对不稳定心绞痛患者血小板功能和纤溶活性的影响[J].中国中西医结合杂志,1997,17(9)：523-525.
[64]姚槐芳.益气活血汤治疗不稳定性心绞痛32例[J].临床中老年保健,2001,4(3):174-175.
[65]金力华.补虚扶正法治疗冠心病心绞痛医案50例[J].山西中医,2003,19(1)：3132.
[66]欧阳智新,欧阳博文.补肾固本对治疗冠心病的作用[J].中国中医药信息杂志,2002,9(4)：7-8.
[67]张晓梅,张幼筠,梁来军.调肝舒心冲剂治疗冠心病心绞痛的临床疗效及实验研究[J].实用中西医结合杂志,1997,11(4):294-295.
[68]杨丁友,段学忠.舒心益脉胶囊对冠心病不稳定性心绞痛患者血小板活化功能的影响[J].中国实验方剂学杂志,2001,7(4)：50-51.
[69]刘海波,高润霖.C反应蛋白与冠心病患者冠状动脉斑块形态的关系[J].中国循环杂志,2002,17(2)：130-133.
[70]王显刚,张文高.益气活血解毒法对不稳定性心绞痛患者血管内皮保护与抑制血小板活化作用[J].山东生物医学工程,2002,21(1):24-26.
[71]吴同和.清热解毒法对不稳定性心绞痛患者C反应蛋白的影响[J].吉林中医药,2006,26(11)：43-44.
[1]R idker PM. Clinical app lication of C-reactive p roteinfor cardiovascular disease detection and p revention[J]. Circulation,2003,107 (3):363-369.
[2]R idker PM,Morrow D,M PH. H igh sensitivity C-reaction p rotein and cardiovascular risk:rational forscreening and p rimary p revention [J]. Am J Cardiol,2003,92 (Supp 1): 17-22.
[3]ZairisMN,M anousak is SJ, StefanidisA S. C-reactive p rotein and rap idly p rogressive coronary artery disease is there any relation? [J]. Clin Card iol,2003,26 (2):85-90.
[4]Eren E, Yilmaz N, Pence S. D iagnostic value ofC-reactive p rote in patients with angiograph ically documented coronary heart disease [J]. Acta Med ica,2002,45 (4): 155-160.
[5]Ridker P M, Buring J F, Shih J. Prospcctive study of C-reactive protein and the risk of future cardiovascularevente among apparently healthy women[J]. Circulation,1998,98: 731-733.
[6]Balbay Y, Tikiz H, Baptiste RJ. Circulating interleukin-1 beta, interleukin-6, tumornecrosis factor-alpha, and soluble ICAM-1 in patients with chronic stable angina and myocardial infarction. Angiology,2001,52 (2):109-114.
[7]Dinarello CA. Modalities for reducing interleukin-1 activity in disease.Immunol Today,1993,14(6):260-264.
[8]Ikesa U, Ikwda M, Ohara T. Interleukin-6stimulates the growth of vascular smooth muscle cells in thePDGF2dependen manner[J]. Am J Phydiol,1991,260:1713.
[9]CruIickshanka M, Oldroyd K, Cobbe S, et al.Serum interleukin-6 in suspected myocardial infarction[J].Lancet,1994,343:974.
[10]陈绍宇.急性心肌梗死患者血清TNF. IL-6和sIL-2水平的变化[J].临床心血管病杂志,1999,15(9):4251.
[11]Masashi S, Kenj IU, Masako H. Effect ofmagnesium sulfate pretreatment and dignificance of matrixmetal loproteinase-1 and interleukin-6 levels in coronaryreperfusion therapy for patients with acute myocardialinfarction[J]. Angiol, 1999,50:573.
[12]Paul M, Ridker N R, Meir J S. Plasmaconcentration of interleukin-6 and the risk of futuremyocardial infarction among apparently healthy men [J].Circulation,2000,18 (5):17671
[13]Ridker P M, Hennekens C H, BuringJ E. C-reactive protein and other markers of inflammation in theprediction of cardiovascular disease in women[J]. N Eng J Med, 2000,342:836-843.
[14]Yamashita H, Shlimada K, Seki E. Concentrations of interleukins, interferon, and C-reactiveprotein in stable and unstable angina pectoris [J]. Am JArdiol,2003, 91:133-136.
[15]李艳,杨超,黄从新.白细胞介素6基因2174G/C和2634C/G多态性与冠心病的相关性研究[J].中华检验医学杂志,2005,28(4):369-372.
[16]Lyon H, Lange C, Lake S. IL-10 gene polymorphisms are associatedwith asthma phenotypes in children. Genet Epidemiol,2004,26(2):155-165.
[17]Henke PK,DeBrunye LA, Strieter RM. Viral IL-10 gene transferdecreases inflammation and cell adhesion molecule expression in a rat model of venous thrombosis.J Immunol,2000,164(4):2131-2141.
[18]Morise Z, Eppihimer M, Granger DN. Effects of lipopolysaccharideon endothelial cell adhesion molecule expression ininterleukin-10 deficient mice. Inflammation,1999, 23(2):99-110.
[19]Uyemura K, Demer LL,Castle SC. Cross-regulatory roles of interleukin(IL)-12 and IL-10 in atherosclerosis. J Clin Invest,1996,97(9):2130-2138.
[20]Mallat Z, Henry P, Fressonnet R. Increased plasma concentrations of interleukin-18 in acute coronary syndromes. Heart,2002,88 (5):467-469.
[21]Gupta S, Pablo AM, Jiang X. IFN-gamma potentiates atherosclerosisin Apo E knockout mice. J Clin Invest,1997,99(11):2752-2761.
[22]Blankenberg S, Tiret L, Bickel C. Interleukin-18 is a strong predictor of cardiovascular death in stable and unstable angina. Circulation,2002,106 (1):24-30.
[23]Elhage R, Jawien J, Rudling M. Reduced atherosclerosis in interleukin-18 deficient apolipoprotein E knock2out mice. Cardiovasc Res,2003,59 (1):234-240.
[24]Ridker PM, Rifai N, Pfeffer MA. Long-term effects of pravastatinon plasma concentration of C-reactive protein:TheCholesteroland Recurrent Events (CARE) Investigators [J].Circulation,1999,100(3):230-235.
[25]Ridker PM,Cushman M,Stampfer MJ. Inflammation,aspirin,andrisks of cardiovascular disease in apparently healthy men [J]. NEng JMed,1997,336(14): 973-979.
[26]Meek R L, Urieli2Shoval S,Benditt E P. Expression ofapolipoprotein serum amyloid A mRNA inhumanatherosclerotic lesions and cultured vascular cells:implica-tions for serum amyloid A function. Proc Natl Acad SciUSA,1994,91:3186-3190.
[27]Johnson B D, Kip K E, Marroquin O C. Serumamyloid A as a predictor of coronary artery disease and car-diovascular outcome in women:the National Heart, Lung,and Blood Institute-Sponsored Women's Ischemia Syn-drome Evaluation (WISE). Circulation,2004,109:726-732.
[28]Coetzee G A, Strachan A F,van-der-Westhuyzen D R. Serum amyloid A-containing human high density lipoprotein 3:density,size and apolipoprotein composition.J Biol Chem,1986,261:9644-9651.
[29]丁云秋.心脑血管疾病多重危险因素控制会议概述.中华内科志,2000,39(12):858-859.
[30]Artl A, Marsche G, Lestavel S. Role of serum amy-loid A during metabolism of acute-phase HDL bymacrophages. Arterioscler Thromb Vasc Biol,2000,20:763-772.
[31]Migita K, Kawabe Y, Tominaga M. Serum amyloid Aprotein induces production of matrix metalloproteinases by human synovial fibroblasts. Lab Invest,1998,78:535-539.
[32]Daughterty A, Dunn JL, Rateri DL. Myeloperoxidase,a catalyst for lipoprotein oxidation, is expressed in human atheroscletoticlesions.J Clin Invest,1994,94 (1):437.
[33]Zhang R, Brennum ML, Fu X. Associa2tion between myeloperoxidase levels and riskof coronary artery disease. JAMA,2001,286(17): 2136-142.
[34]Nikpoor B, Turecki G, Fournier C. Afunctional myeloperoxidase polymorphic vari2ant is asscociated with coronary artery diseasein Frencn2Canadians. Am Heart J, 2001,142(2):336-339.
[35]Bekesi G, Magyar Z, Kakuss R. Changes in the myeloperoxidase activity of hu2man neutrophinic granulocytes and the amountof enzyme deriving from them under the effectof estrogenl. Orv Hetil,1999,140 (29):324-344.
[37]PostonR N, Haskard D O, Coucher J R. Expression of intercellularad-hesion molecule-1 in atherosclerotic plaques[J]. Am J Patho,1992,140:889-896.
[38]MaliK I, DanesH J, WhincuP P. Solubleadhesion molecules and prediction of coronary heart disease:a prospective study and meta-analysis [J].Lancet,2001,358:971-975.
[39]Blankenberg S, Rupprecht H J, Bickel C. Circulating cell adhesion molecules and death in patients with coronary artery disease [J]. Circulation,2001,104(12) 1336-1342.
[40]Haim M, Tanne D, Boyko V. Solubleintercellular adhesion molecule-1 and long-term risk of acutcoronary events in patients with chronic coronary heartdisease[J]. J Am Coll Cardiol,2002,39(7):1133-1138.
[41]Giesen PL, U Rauch, B Bohrmann. Blood-brone tissue factor:another view of thrombosis[J].Proc Natl Acad Sci USA,1999,96:2311-2315.
[42]Berg K. A new serum type system in men—the lipop rotein system [J].Acta PatholMicrobiol Scand,1963,59:369-382.
[43]Darvies MJ. Reactive oxygen species, metalloproteinases, and plaquesta-bility[J]. Circulation,1998,97(24):2382-2383.
[44]Ritchie ME. Nuclear factor-KB is selectively and markedly activated in humans with unstable angina pectoris[J]. Circulation,1998,98 (17):1707-1713.
[45]陈在嘉,高润霖.脂蛋白(α)与动脉粥样硬化[J].冠心病,2003,5(2)：133-135.
[46]Boerwinkle E, Leffert CC, L in J. Apolipop rotein(a) gene accounts for greater than 90% of the variation in p lasma lipop rotein (a) concentrations[J]. J Clin Invest,1992, 90 (1):52-60.
[47]Dahlen G H. Lipoprotein (a) in cardiovascular disease.Atherosclerosis,1994,108:111-120.
[48]Dahlen CH. Lp (a) lipop rotein in cardiovascular disease [J]. Athero-sclerosis,2001, 108:111.
[49]Mary S,Ayrs S,Humphris S. Lipoprotein(a) as predictor of myocardial infarction in middle-aged men. [J]Am J Med,2001,110(1):22-27.
[50]Von Eckardstein,Schulte H,Cullen P,oteet al.Lipoprotein(a) farther increase the risk of coronary events in men with high global cardiovascular risk.[J]Am Coll Cardiol,2001,37(2):434-439.
[51]刘毅,姜敏辉,高敏.c反应蛋白、心肌肌钙蛋白I对急性冠脉综合征的诊断价值[J].南通医学院学报,2003:23(4):419.
[52]戴秋艳,孙宝贵.脉压与冠心病患者左室肥厚的相关分析[J].中华国际医学杂志,2002:2(4)：301.
[53]盛富强.肌钙蛋白在诊断心肌损伤中的临床应用[J].郧阳医学院学报,2003:22(6):376.
[1]丁邦晗,马长生,张敏州.胸痹胸痛病人375例的冠脉病变程度及证型分析[J].中医药学刊,2004,22(6)：1096-1097.
[2]马晓昌,尹太英,陈可冀.冠心病中医辨证分型与冠状动脉造影所见相关性比较研究[J].中国中西医结合杂志,2001,21(9)：654-656.
[3]邢雁伟,王阶,衷敬柏,李海霞,高永红,何庆勇.采用聚类分析和对应相关方法研究1069例冠心病心绞痛证候应证组合规律[J],中华中医药杂志,2007,22(11):747-750.
[4]贾振华,王永军,吴以岭.基于熵的复杂系统分划方法与冠心病心绞痛证候要素提取及其分布规律[J].第二军医大学学报,2007,28(7):775-777.
[5]王阶,李军,姚魁武,等.冠心病心绞痛证候要素与应证组合研究[J].中医杂志,2007,48(10)：920-922.
[6]吴焕林,阮新民,杨小波.319例冠心病患者证候分布规律分析[J].中国中西医结合志,2007,27(6)：498-500.
[7]李江,赵水平.冠心病整体危险因素评估的方法及临床意义[J].中国循环杂志,2001：235-236.
[8]Taddei S, Virdis A, Mattei P. Unstable Angina/Myocardial Infarction/Atherosclerosis: Aging and Endothelial Function in Normotensive Subjects and Patients With Essential Hypertension. [Article]. Circulation April 1,1995,91(7):1981-1987.
[9]王小平.女性冠心病临床特征的分析.中国心血管杂志,2005,2:132-134.
[10]宋小虎,蔡学究,张德云.女性冠心病的发病特征及一级康复干预.中国临床康复,2005,19:154-155.
[11]Jensen J, Eriksson SV, Lindvall Bc. Women react with more myocardial ischemia and angina pectoris during elective percutaneous transluminal coronary angioplasty. [Miscellaneous Article]. Coronary ArteryDisease October 2000,11(7):527-535.
[12]Murphy NF, Simpson CR, MacIntyre K. Prevalence, incidence, primary care burden and medical treatment of angina in Scotland:age, sex and socioeconomic disparities:a population-based study. [Miscellaneous]. HeartAugust 2006,92(8):1047-1054.
[13]陈武,王邦宁,高世明.老中青年急性心肌梗塞的临床特点及相关因素分析[J].疾病控制杂志,2005,2:175-176.
[14]Gebara OCE, Mittleman MA, Sutherland P. Unstable Angina/Myocardial Infarction/Atherosclerosis:Association Between Increased Estrogen Status andIncreased Fibrinolytic Potential in the Framingham Offspring Study. [Article].Circulation April 1, 1995,91(7):1952-1958.
[15]Jousilahti P, Vartiainen E, Tuomilehto J. Sex, age, cardiovascular risk factors, and coronary heart disease:a prospective follow-up study of 14 786 middle-aged men and women in Finland. Circulation,1999,9:1165-1172.
[16]文川,程伟.206例冠心病心绞痛患者问诊资料与中医辨证关系的探讨[J].湖北中医杂志,2002,(10):3.
[17]赵慧辉,王伟,郭淑贞.冠心病不稳定性心绞痛血瘀证的蛋白质组学[J].中国动脉硬化杂志,2008,16(7):545-548.
[18]姚魁武,杨戈,王阶.高血压病血瘀证患者血液学指标判别分析[J].世界科学技术-中医药现代化基础研究,2006,8(5):30-42.
[19]丘瑞香,罗致强,朱雅宜,秦鉴。冠心病血瘀证血液理化特性与中医相关性研究[J].中医杂志,2002,43(5):378-379.
[20]丁邦晗,严夏,林晓忠,李松.血脂异常与胸痹心痛基本证型的相关性分析[J].辽宁中医杂志,2006,33(10):1261-1262.
[21]李松,丁邦晗,张敏州,蚁楷宏,陈伯钧,林晓忠,刘泽银.365例胸痹心痛患者证型血脂分析[J].广州中医药大学学报,2005,22(2):87-97.
[22]褚福永,王阶,姚魁武,李志忠.冠心病不稳定型心绞痛中医辨证分型与血脂及冠脉造影结果的相关性研究.[J]北京中医药2009,28(12):918-921.
[23]袁肇凯,田松,黄献平,胡志希,孙贵香,陈清华,莫莉,简维雄.冠心病痰瘀证候血脂指标的Meta分析[J].云南中医学院学报,2008,31(5):1-8.
[24]王阶,何庆勇,施展,邢雁伟,李霁,房玉涛,汤艳莉.冠心病证候要素组合与心功能及血脂的相关性[J].中西医结合学报,2008,6(9):897-901.
[25]Schwertner HA, Jackson WQ Tolan G Association oflow serum concentration of bilirubin with increased risk ofcoronary artery disease. Clin Chem,1994,40(1):18-23.
[26]林燕,黄维义.氧化应激致动脉粥样硬化作用的研究进展[J].黑龙江医学,2004,28:517-520.
[27]Mayer M. Association of serum bilirubin concerntrationwith risk of coronary artery disease [J]. ClinChem,2000,46(11):1723-1727.
[28]黄维义,曹林生,贺立群.冠心病患者胆红素浓度变化及其对低密度脂蛋白氧化修饰水平的影响.中国实用内科杂志,2001,21:23-24.
[29]李熹娟.胆红素与冠心病相关性的研究进展[J].心血管病学进展,2005,26:646-649.
[30]Peytonkj, Reynasv, Chapmangb. Hemeoxygenasel derived carbon monoxideisanautocrineinhibitorofvascularSmooth musclecell growth[J]. Blood,2002,99: 444-448.
[31]Sharma HS, Das DK, Verdouw PD. Enhanced expressionand localization of heme oxygenase-1 during recovery phaseof porcine stunned myocardium. Mol Cell Biochem,1999,196(1-2):133-139.
[32]李静,张继东,刘同涛.血清胆红素与冠脉病变程度、血脂及冠心病中医证型关系[J].南京中医药大学学报,2006,22(2):77-79.
[33]Hillis GS, Dalsey WC, Terregino C A. Altered CD18 leukocyteintegrin expression and adhesive function in patients with acute coronarysyntrome. Heart,2001,85:702-704.
[34]Shah P K. Mechanisms of plaque nulnerability and rupture. J Am CollCardiol, 2003,41:S15-22.
[35]Avanzas P, Arroyo2Espliguero R, Cosin Sales J. Multiplecomplex stenoses,high neutrophil count and C-reactive protein levels inpatients with chronic stable angina. Atherosclerosis,2004,175:151-157.
[36]蓝景生,黄照河,潘兴寿.外周血白细胞分类计数与冠心病及其危险因素聚集性的关系[J].中国全科医学,2008,11.(10)：1844-1845.
[37]卫任龙,杨志健,贾恩志,王连生,朱铁兵,陈波,曹克将,马文珠.外周血白细胞计数与冠状动脉狭窄的相关性[J].中国介入心脏病学杂志,2005,13(4):241-243.
[38]洪永敦,黄衍寿,吴辉,陈宇鹏,李斐媛,莫鸿辉.冠心病中医证候与炎症因子关系的临床研究[J].2005,,22(2)：81-86.
[39]Wolfgang Volker, Borszewski A,Unruh V. Copperinduced in flammatory of rat corotid arteries mimic restenosis arterosclerosislikeneointima formation. Atherosclerosis,1997,130:29.
[40]Lowe G, Rumley A, Norrie J. Blood rheology,cardiovascular risk factors and cardiovascular disease:the west of Scotland coronary prevention study. Thromb Haemost,2000,84 (4):553.
[41]张一娜,崔璨,张亚清.老年心脑血管疾病、糖尿病血液流变学改变[J].中国微循环杂志,2002,6(3)：167.
[42]冯永钦,谢传英,张清平.心脑血管疾病血液流变学指标的分析[J].中国血液流变学杂志,2002,12(1):22.
[43]何静脉,谭笑江,李巍.血液黏度检验中几个参数意义的探讨[J].大连医科大学学报,2000,22(2)：139.
[44]沈琪琳.老年冠心病患者血液流变学及血细胞参数的观察.中国慢性病预防与控制,2000,8(6)：252.
[45]Carallo C, Pujia A, Irace C. Whole blood viscosity andhaematocrit are associated with internal carotid atherosclerosisin men. Coron Artery Dis,1998,9 (2-3):113.
[46]Baskurt OK, Edremitlioglu M,Temiz A, Effect of ervthrocvte deformabilitv on myocardial hematocrit gradient. Am J Physiol,1995,268(lpt2):H:260-264.
[47]Gustavsson CG, Pwrsson SU, Larsson H. Changed blood rheology in patients with idiopathic dilated cardiomyopathy. Angioogy 1994,45(2):107-111.
[48]Syoten OKA. Cardiovas cular haemorheology [M]. Cambridge University Press,1983.
[49]潘瑞彭,王鸿利主编.血液学及血液学检验[M].北京：人民卫生出版社,1990.
[50]翁维良,廖福龙,吴云鹏.血液流变学研究方法及其应用[M].北京：科学出版社,1989.96-99.
[51]Walport MJ, Schifferli JA, Walza. the change of immunologic function of erythrocyte in the patients with coronary heart disease[J]. Clin. Immunol. EXP,1998,56:536-542.
[52]Kunapuli S P. ADP receptors:targetsfor developing antithrombotic agents [J].Curr Pharm,2003,9:2303-2316.
[53]Day CP. Br Heart J 1990,63:342.
[54]曹济民,王向东.急性心肌缺血时心室易颤期的变化趋势.中国应用生理学杂志,1992；8(1)：85
[55]陈良细.OT离散度评价心肌梗塞预后的临床意义.医学综述,1997;3(8):378
[1]Ross R. A therosclerosis an inflammatory disease [J].N Engl J Med,1999,340:115-126.
[2]Buffon A, Biasucci LM, Liuzzo G. Widespread coronary inflammationin unstable angina. NEngl J Med,2002,347(1):5-12.
[3]Mulvihill NT, Foley JB. Inflammation in acute coronary syndromes.Heart,2002,87(3):201-204.
[4]Rohde L E, Hennekens CH, Ridker P M. Survey of C-reactive protein and cardiovascular risk factor in apparently healthy men[J]. Am J Cardiol,1999,84:1018-1022.
[5]Ridker P M, Buring J F, Shih J. Prospcctive study of C-reactive protein and the risk of future cardiovascularevente among apparently healthy women[J]. Circulation,1998,98: 731-733.
[6]Liuzzo G, Biasucci L M, Gallimore L R. The prognostic value of C-reactive protein and serum amyloid A protein in seruere unstable angina[J]. N Engl J Med,1994,331:417-424.
[7]Anderson J L, Carlquist J F, Muhlestein J B. Evaluation of C-reactive protein, an inflammation and myocardialinfectins serology as risk factors for coronary artery disease and myocardial infarction[J]. J Am Coll Cardiol,1998,32:35-41.
[8]赵慧辉、王伟、郭淑贞.冠心病不稳定型心绞痛血瘀证的蛋白质组学[J].中国动脉硬化杂志,2008,16(7)：545-548.
[9]Coetzee G A, Strachan A F,van-der-Westhuyzen D R. Serum amyloid A-containing human high densitylipoprotein:density,size and apolipoprotein composition.J Biol Chem,1986,261:9644-9651.
[10]丁云秋.心脑血管疾病多重危险因素控制会议概述[J].中华内科志,2000,39(12)：858-859.
[11]Artl A, Marsche G, Lestavel S. Role of serum amy-loid A during metabolism of acute-phase HDL bymacrophages. Arterioscler Thromb Vasc Biol,2000,20:763-772.
[12]Migita K, Kawabe Y, Tominaga M. Serum amyloid Aprotein induces production of
matrix metalloproteinases by human synovial fibroblasts. Lab Invest,1998,78:535-539.
[13]Ridker PM, Morrow D, M PH. High sensitivity C-reaction protein and cardiovascular risk: rational forscreening and p rimary p revention [J]. Am J Card iol,2003,92 (Supp 1):17-22.
[14]Zwaka TP, Hombach V, Torzewski J. C-reactive Protein mediated low density lipoprotein uptake by macrophages:implicationsfor at herosclersis[J]. Circulation 2001,103:1194-1197.
[14]Nakagomi A, Freedman SB, Geczy CL. Interferon-gamma andlipopolysaccharide potentiate monocyte tissue factor inductionby C-reactive protein:relationship wit h age, sex,and hormonereplacement t reatment [J]. Circulation,2000,101:1784-1791.
[15]Bickel C, Rupprecht HJ, Blankenberg S. Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease[J].Am J Cardiol,2002,89(1):12-17.
[16]Woodward M, Low e G D, Rum ley A. Fibrinogen as a risk factor for coronary heart disease and mortality in middle-aged men and women-The Scottish heart Health Studu[J]Eur Heart J,1998,19(1):55-62.
[17]毛以林,李旭,彭素娟,罗昌国.冠心病血瘀证与高敏c反应蛋白相关性研究[J].中国中医药信息杂志,2007,17(6):26-27.
[18]商秀洋,石洁.冠心病中医辨证与血清高敏c反应蛋白的关系研究[J].现代中西医结合杂志,2008,17(6):818-819.
[19]托马斯.临床实验诊断学[M].第1版.上海：上海科学技术出版社,2004,575.
[20]Robins S J, Collins D, Wittes J T. Relation of gemfibrozil treatmenttreatmentand lipid levels with major coronary events:VA-HIT:a randomizedcontrolled trial[J]. JAMA, 2001,285:1585-1591.
[21]Von Fckardstein A, Hersberger M, Rohrer L. Current understandingof the metabolism and biological actions of HDL[J]. Curr Opin Clin NutrMetab Care,2005,8:147-152.
[22]Lee JM,Okumura MJ, Davis MM. Prevalence and determinants of insulin resistance among US adolescents:a population-bases study[J]. Diabetes Care,2006,29(11) 2427-2432.
[23]Nakagomi A, Freedman SB, Geczy CL. Interferon-gamma andlipopolysaccharide potentiate monocyte tissue factor inductionby C-reactive protein:relationship wit h age, sex,and hormonereplacement treatment [J]. Circulation,2001,103:1194-1197.
[24]Masashi S, Kenj IU, Masako H. Effect ofmagnesium sulfate pretreatment and dignificance of matrixmetal loproteinase-1 and interleukin-6 levels in coronaryreperfusion therapy for patients with acute myocardialinfarction[J]. Angiol 1999,50：573.
[25]洪永敦,黄衍寿,吴辉,陈宇鹏.冠心病中医证候与炎症因子关系的临床研究[J].广州中医药大学学报,2005,22(2):81-86.
[26]Ridker PM, Rifai N, Pfeffer M, et al. Elevation oftumor necrosis factor-alpha and increased risk of recurrentcoronary events after myocardial infarction [J].Circulation, 2000,101:2149-2153.
[27]毛以林,谭光波,袁肇凯,黄献平.高敏C反应蛋白和可溶性细胞间黏附分子-1与冠心病血瘀证的相关性研究[J].新中医,2007,39(3):25-26.
[28]朱青霞.冠心病中医证型与血清可溶性细胞间黏附分子的相关性研究[J].中国中医基础医学杂志,2007,13(11):842-843.
[39]Hao Y, Qiu Q Y, W J. Effect of astragaius polysaccharin(APS) on ymphocyte-endothelium adhesion and the moiecular mechanism [J]. Immunnol Ji：免疫学学杂志),2000,16(3):206-209.
[30]Peng Q,Wei Z, Lau BH. Pycnogenol inhibits tumor necrosis factor-alphainduced nuclear factor kappa B activation and adhesion molecule expressionin human vascular endothelial cells[J]. Cell Mol Life scj,2000,57 (5):834-41.
[31]Nakagomi A, Freedman SB, Geczy CL. Interferon-gamma andlipopolysaccharide potentiate monocyte tissue factor inductionby C-reactive protein:relationship wit h age, sex,and hormonereplacement t reatment [J]. Circulation,2000,101:1784-1791.
[32]Yasojima K, Schwab C, Mcgeer EG. Generation of C-reactive Protein and complment component s in at herosclerotic plaques[J]. Am J Pat hol,2001,158:1039-1049.
[33]柏正平,谭光波,卜献春,孙春林.冠心病中医辨证分型与细胞黏附分子的关系[J].中西医结合心脑血管病杂志,2006,4(2)：108-109.
[34]杨徐杭,汶医宁,党琳,魏敏慧.冠心病中医辨证与E-选择素、细胞间黏附分子-1的关系的研究[J].四川中医,2008,26(1)：61-62.
[35]丁邦晗,严夏,林晓忠,李松.血脂异常与胸痹心痛基本证型的相关性分析[J].辽宁中医杂志,2006,33(10)：1261-1262.
[36]Simonini A, Moscuci M, Muller DW. IL-8 is an angiogenicfactor in human coronary atheretonry tissue. Circulation,2000,101:1519-1526.
[37]Hearse DJ. Myocardial protection during ischemia and reperfusion.Mol Cell Biochem, 1998,186:177-184.
[38]Giesen PL, U Rauch, B Bohrmann. Blood-brone tissue factor:another view of thrombosis[J]. Proc Natl Acad Sci USA,1999,96:2311-2315.
[39]Lee SH, Wolf PL, Eseudero R. Early expression of angiogenesisfactors in acute myocardial ischemia and infarction. N Engl J Med,2000,342:626-633.
[40]Ritchie ME. Nuclear factor-κB is selectively and markedly activated in humans with unstable angina pectoris[J]. Circulation,1998,98 (17):1707-1713.
[41]Darvies MJ. Reactive oxygen species, metalloproteinases, and plaquesta-bility[J]. Circulation,1998,97(24):2382-2383.
[42]Wilson SH, Best PJ, Edwards WD. Nuclear factor-kappa-B immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectovis. Atheroscl-rosis,2002,160:147-53
[43]Calabresi L,Villa B,Omobom L. Soluble cellular adhesion molecules are increased in patients with low HDL-cholesterol [J]. Atherosclerosis,2000,151(1):216-226.
[44]Park SH, Park JH, Kang JS. Involvement of transcrip tion factors in p lasmaHDL protection against TNF-alpha induced vascular cell adhesion molecule-lexp ression[J]. IntB iochem CellB iol,2003,35 (2):168-182.
[45]James AL, David AM, Marc SS.Association Between Plasma Levels of Monocyte Chemoattractant Protein-1 and Long-Term Clinical Outcomes in Patients With Acute Coronary Syndromes [J]. Circulation,2003,107:690-695.
[46]Masamichi K, Kensuke E,Shiro K.Role of Monocyte Chemoattractant Protein-1 in Cardiovascular Remodeling Induced by Chronic Blockade of Nitric Oxide Synthesis[J].Circulation;2000,102:2243-2248.
[47]Peng Q,Wei Z, Lau BH. Pycnogenol inhibits tumor necrosis factor-alphainduced nuclear factor kappa B activation and adhesion molecule expressionin human vascular endothelial cells[J]. Cell Mol Life scj,2000,57 (5):834-41.
[48]Darvies MJ. Reactive oxygen species, metalloproteinases, and plaquesta-bility[J]. Circulation,1998,97(24):2382-2383.
[2]张晓东,姚映芷.冠心病心绞痛中医病机及治法研究概述[J].吉林中医药,2005,25(3)：56-58.
[3]姬生勤.冠心病心绞痛辨治思路与方法探析[J].中国中医药信息杂志,2003,10(10):48.
[4]李宝同,张庆宏,石磊.中医药治疗冠心病研究进展[J].长春中医药大学学报,2007,23(1)：75-76.
[5]李芳,樊相军.胸痹诱发因素与辩证分型的调查分析[J].人民军医,2001,44(8):484-486.
[6]吴辉,于扬文,吴伟.116例冠心病患者中医证候及病因分析[J].江苏中医,2004,25(10)：30.
[7]杨利,邓铁涛.“冠心三论”[J].湖南中医药导报,2004,10(6)：8-10.
[8]吴以岭.从络病学说论治冠心病心绞痛[J].中国中医基础医学杂志,2001,7(4)：71
[9]1980年全国冠心病辨证论治研究座谈会.冠心病中医辨证试行标准[S].中医杂志,1980,(8)：46.
[10]陈贵延,薛赛琴.最新国内外疾病诊疗标准[S].北京：学苑出版社,1992.209-212, 678.
[11]中西医结合心血管学会.冠心病的中医辨证标准[S].中西医结合杂志,1991,11(5)：257.
[12]卫生部.中药新药治疗胸痹心痛的临床研究指导原则[S].1993.41
[13]郑筱萸.中药新药临床研究指导原则[S].北京：中国医药科技出版社,2002.
[14]王永炎.中医内科学[M].上海：上海科学技术出版社,1997.
[15]郭志华.冠心病心绞痛2432例中医辨证分型综合统计分析[J].湖南中医杂志,1998,14(2)：7.
[16]衷敬柏,董绍英,王阶,王永炎.2689例冠心病心绞痛证候要素的文献统计分析.[J]中国中医药信息杂志,2006,13(5):100-101.
[17]王阶,邢雁伟,姚魁武,李军.冠心病心绞痛中医证候要素研究及临床应用[J].湖北中医学院学报,2009,11(3):3-5.
[18]王晓才,林谦,王晓宝,农一兵.胸痹中医证候影响因素的回归分析.[J]北京中医,2007,26(4):218-220.
[19]文川,程伟.206例冠心病心绞痛患者问诊资料与中医辨证关系的探讨[J].湖北中医杂志,2002,(10)：3.
[20]王阶,李军,姚魁武,衷敬柏.冠心病心绞痛证候要素和冠脉病变的Logistic回归分析[J].辽宁中医杂志,2007,34(9):1209-1211.
[21]吴旸,金刚,崔杰,彭建军,任文林.冠心病中医证候特点的回归分析[J].中医药学报,2008,36(4):4-6.
[22]王永霞,胡宇才,朱明军,高传玉.冠心病心绞痛中医证候分布相关性研究[J].世界中西医结合杂志,2008,3(12):714-719.
[23]张敏州,邹旭,李新梅.胸痹心痛证冠状动脉造影100例临床分析[J].浙江中西医结合杂志,2001,11(8)：472-475.
[24]褚福永,王阶,姚魁武,李志忠.冠心病不稳定型心绞痛中医辨证分型与血脂及冠脉造影结果的相关性研究.[J]北京中医药2009,28(12)：918-921.
[25]邹旭,邓铁涛.冠状动脉成型术后再狭窄的中医证候初探[J].广州中医药大学学报,2001,18(4)：293.
[26]马晓昌,尹太英,陈可冀.冠心病中医辨证分型与冠状动脉造影所见相关性比较研究[J].中国中西医结合杂志,2001,21(9)：654-656.
[27]李佃贵,李俊峡,李振彬.冠心病患者病变程度与中医证型的关系[J].中国中医药信息杂志,2001,8(12)：57-58.
[28]张惠贞,张鸿文,贺莉清.心律失常与胸痹心痛证型关系的探讨[J].河南中医学刊,1996,11(4)：39-41.
[29]赵亚莉,杨幼新.冠心病心电图与中医辨证分型的关系[J].江苏中医,2001,22(9):20-
[30]陈伯钧,张文清,张敏州.冠心病中医分型与心律失常及心功能关系分析[J].现代中西医结合杂志,2000,9(19):1857-1858.
[31]张宁宁.气滞血瘀、气虚血瘀心绞痛患者心率变异性与心肌缺血指数相关性探讨[J].山东中医药大学学报,2003,27(2)：123.
[32]王阶,何庆勇,施展,刑雁伟.冠心病证候要素组合与心功能及血脂的相关性[J].中西医结合学报,2008,6(9)：897-901.
[33]周英.心血管病表现心虚证患者左心室舒张功能观察[J].中国中西医结合杂志,1995,15(1)：13.
[34]王硕仁,赵明镜,吕希滢.冠心病心气虚证与左心室功能及心肌缺血相关性的临床研究[J].中国中西医结合杂志,1998,18(8)：457-460.
[35]王阶,何庆勇,施展,邢雁伟,李霁,房玉涛,汤艳莉.冠心病证候要素组合与心功能及血脂的相关性.[J]中西医结合学报,2008,6(9):897-901.
[36]袁肇凯,田松,黄献平,胡志希,孙贵香,陈清华,莫莉,简维雄.冠心病痰瘀证候血脂指标的Meta分析。[J]云南中医学院学报,2008,31(5):1-8.
[37]金志刚,周端,顾仁樱.冠心病血瘀证与血清脂蛋白(a)含量的临床观察.河南中医药学刊,1995,10(3)：28
[38]孙锡印,杨妻琳.冠心病气滞血瘀与气虚血瘀证型间血载脂蛋白的异同及辨治影响[J].江苏中医,1997,18(6)：40.
[39]李俊,李小敏,刘映峰.冠心病冠状动脉造影结果与中医证型及血脂、脂蛋白关系的研究[J].中国中医急症,2000,9(3)：123-125.
[40]何剑平,李小敏,张瞥.冠心病中医辨证与血脂脂蛋白关系的探析[J].辽宁中医杂志,1998,25(11)：505-507.
[41]熊尚全,许少锋,郭云庚.冠心病本虚标实辨证与脂蛋白(a)关系的初步研究[J].福建中医学院学报,1998,8(1)：1-3.
[42]詹萍,施卿卿,郭云庚.不稳定心绞痛中医分型与胰岛素抵抗的关系[J].福建中医药,2001,3(2)：3.
[43]李俊,王天伟,严夏.冠心病不稳定型心绞痛中医证候与C反应蛋白和基质金属蛋白酶-9关系的研究[J].辽宁中医药大学学报,2008,10(2)：102-103.
[44]杨徐杭,汶医宁,魏敏慧.冠心病中医辨证与血清C反应蛋白的相关性研究[J].中医药学刊,2004,22(9)：1649.
[45]卢玉俊,石磊.冠心病中医证型与血浆同型半胱氨酸水平相关性的研究[J].浙江中医药大学学报,2009,33(1)：103-104.
[46]林凯旋,安辉,廖灿铭.冠心病血瘀证与同型半胱氨酸的相关性研究[J].中医研究,2007,20(2)：32-33.
[47]方建伟,黄源鹏,林求诚.冠心病中医证型与血浆ET、TXA2-PGI2的关系[J].实用中医药杂志,2005,21(9)：519.
[48]黄献平.心病气血辨证瘀血清锌铜铁钙含量的关系[J].辽宁中医杂志,1997,24(4)：149.
[49]江帆.左归饮加减治疗心肾阳虚型胸痹心痛50例[J].吉林中药,2006,3(3):271.
[50]刘亚光.现代自然科学与中医理论[M].福州：福建科学技术出版社,1983:247.
[51]王霭平.从肺论治胸痹心痛的临床观察[J].上海针灸杂志,2004,4(4):251.
[52]王中平.以活血化瘀法治疗冠心病心绞痛[J].中华实用中西医杂志,2002,2(15)：501.
[53]张跃林.中医活血化瘀法治疗冠心病心绞痛84例观察,中国医学杂志,2007,5(11):19-20.
[54]胥春梅.中医药治疗冠心病心绞痛30例[J].现代中医药,2003(2):28-29.
[55]贺敬波,黄绵清,张勤.加减暖肝煎胶囊治疗不稳定型心绞痛的临床研究及理论探讨[J].中国中医基础医学杂志,2003,9(9):55-56.
[56]刘慎柏.温心通脉方配合西药治疗不稳定性心绞痛60例临床观察[J].湖南中医药导报,2003,9(6)：22-23.
[57]张华伟.络脉舒通颗粒对不稳定型心绞痛疗效的临床观察[J].临床军医杂志,2004,32(6):8-9.
[58]洪永敦,黄衍寿,陈宇鹏,吴辉.清热化痰活血法治疗冠心病不稳定性心绞痛临床研究[J].辽宁中医杂志,2005,32(7)：625-627.
[59]彭桂阳.加减参脉汤治疗冠心病心绞痛60例总结[J].湖南中医杂志,2004,20(4)：14-15.
[60]李浩,崔玲,崔天红.益心通脉颗粒剂治疗阳癖心痛的临床研究[J].中国中医药信息,1999,6(10)：45-47.
[61]藕二祥.益气滋阴、活血通络法对不稳定性心绞痛血小板活化功能的影响[J].江苏中医药,2006,27(9)：24-25.
[62]叶建芳,刘文胜.健脾化痰活血法治疗不稳定性心绞痛50例疗效观察[J].新中医,2005,39(7)：36-37.
[63]唐其柱.补阳还五汤对不稳定心绞痛患者血小板功能和纤溶活性的影响[J].中国中西医结合杂志,1997,17(9)：523-525.
[64]姚槐芳.益气活血汤治疗不稳定性心绞痛32例[J].临床中老年保健,2001,4(3):174-175.
[65]金力华.补虚扶正法治疗冠心病心绞痛医案50例[J].山西中医,2003,19(1)：3132.
[66]欧阳智新,欧阳博文.补肾固本对治疗冠心病的作用[J].中国中医药信息杂志,2002,9(4)：7-8.
[67]张晓梅,张幼筠,梁来军.调肝舒心冲剂治疗冠心病心绞痛的临床疗效及实验研究[J].实用中西医结合杂志,1997,11(4):294-295.
[68]杨丁友,段学忠.舒心益脉胶囊对冠心病不稳定性心绞痛患者血小板活化功能的影响[J].中国实验方剂学杂志,2001,7(4)：50-51.
[69]刘海波,高润霖.C反应蛋白与冠心病患者冠状动脉斑块形态的关系[J].中国循环杂志,2002,17(2)：130-133.
[70]王显刚,张文高.益气活血解毒法对不稳定性心绞痛患者血管内皮保护与抑制血小板活化作用[J].山东生物医学工程,2002,21(1):24-26.
[71]吴同和.清热解毒法对不稳定性心绞痛患者C反应蛋白的影响[J].吉林中医药,2006,26(11)：43-44.
[1]R idker PM. Clinical app lication of C-reactive p roteinfor cardiovascular disease detection and p revention[J]. Circulation,2003,107 (3):363-369.
[2]R idker PM,Morrow D,M PH. H igh sensitivity C-reaction p rotein and cardiovascular risk:rational forscreening and p rimary p revention [J]. Am J Cardiol,2003,92 (Supp 1): 17-22.
[3]ZairisMN,M anousak is SJ, StefanidisA S. C-reactive p rotein and rap idly p rogressive coronary artery disease is there any relation? [J]. Clin Card iol,2003,26 (2):85-90.
[4]Eren E, Yilmaz N, Pence S. D iagnostic value ofC-reactive p rote in patients with angiograph ically documented coronary heart disease [J]. Acta Med ica,2002,45 (4): 155-160.
[5]Ridker P M, Buring J F, Shih J. Prospcctive study of C-reactive protein and the risk of future cardiovascularevente among apparently healthy women[J]. Circulation,1998,98: 731-733.
[6]Balbay Y, Tikiz H, Baptiste RJ. Circulating interleukin-1 beta, interleukin-6, tumornecrosis factor-alpha, and soluble ICAM-1 in patients with chronic stable angina and myocardial infarction. Angiology,2001,52 (2):109-114.
[7]Dinarello CA. Modalities for reducing interleukin-1 activity in disease.Immunol Today,1993,14(6):260-264.
[8]Ikesa U, Ikwda M, Ohara T. Interleukin-6stimulates the growth of vascular smooth muscle cells in thePDGF2dependen manner[J]. Am J Phydiol,1991,260:1713.
[9]CruIickshanka M, Oldroyd K, Cobbe S, et al.Serum interleukin-6 in suspected myocardial infarction[J].Lancet,1994,343:974.
[10]陈绍宇.急性心肌梗死患者血清TNF. IL-6和sIL-2水平的变化[J].临床心血管病杂志,1999,15(9):4251.
[11]Masashi S, Kenj IU, Masako H. Effect ofmagnesium sulfate pretreatment and dignificance of matrixmetal loproteinase-1 and interleukin-6 levels in coronaryreperfusion therapy for patients with acute myocardialinfarction[J]. Angiol, 1999,50:573.
[12]Paul M, Ridker N R, Meir J S. Plasmaconcentration of interleukin-6 and the risk of futuremyocardial infarction among apparently healthy men [J].Circulation,2000,18 (5):17671
[13]Ridker P M, Hennekens C H, BuringJ E. C-reactive protein and other markers of inflammation in theprediction of cardiovascular disease in women[J]. N Eng J Med, 2000,342:836-843.
[14]Yamashita H, Shlimada K, Seki E. Concentrations of interleukins, interferon, and C-reactiveprotein in stable and unstable angina pectoris [J]. Am JArdiol,2003, 91:133-136.
[15]李艳,杨超,黄从新.白细胞介素6基因2174G/C和2634C/G多态性与冠心病的相关性研究[J].中华检验医学杂志,2005,28(4):369-372.
[16]Lyon H, Lange C, Lake S. IL-10 gene polymorphisms are associatedwith asthma phenotypes in children. Genet Epidemiol,2004,26(2):155-165.
[17]Henke PK,DeBrunye LA, Strieter RM. Viral IL-10 gene transferdecreases inflammation and cell adhesion molecule expression in a rat model of venous thrombosis.J Immunol,2000,164(4):2131-2141.
[18]Morise Z, Eppihimer M, Granger DN. Effects of lipopolysaccharideon endothelial cell adhesion molecule expression ininterleukin-10 deficient mice. Inflammation,1999, 23(2):99-110.
[19]Uyemura K, Demer LL,Castle SC. Cross-regulatory roles of interleukin(IL)-12 and IL-10 in atherosclerosis. J Clin Invest,1996,97(9):2130-2138.
[20]Mallat Z, Henry P, Fressonnet R. Increased plasma concentrations of interleukin-18 in acute coronary syndromes. Heart,2002,88 (5):467-469.
[21]Gupta S, Pablo AM, Jiang X. IFN-gamma potentiates atherosclerosisin Apo E knockout mice. J Clin Invest,1997,99(11):2752-2761.
[22]Blankenberg S, Tiret L, Bickel C. Interleukin-18 is a strong predictor of cardiovascular death in stable and unstable angina. Circulation,2002,106 (1):24-30.
[23]Elhage R, Jawien J, Rudling M. Reduced atherosclerosis in interleukin-18 deficient apolipoprotein E knock2out mice. Cardiovasc Res,2003,59 (1):234-240.
[24]Ridker PM, Rifai N, Pfeffer MA. Long-term effects of pravastatinon plasma concentration of C-reactive protein:TheCholesteroland Recurrent Events (CARE) Investigators [J].Circulation,1999,100(3):230-235.
[25]Ridker PM,Cushman M,Stampfer MJ. Inflammation,aspirin,andrisks of cardiovascular disease in apparently healthy men [J]. NEng JMed,1997,336(14): 973-979.
[26]Meek R L, Urieli2Shoval S,Benditt E P. Expression ofapolipoprotein serum amyloid A mRNA inhumanatherosclerotic lesions and cultured vascular cells:implica-tions for serum amyloid A function. Proc Natl Acad SciUSA,1994,91:3186-3190.
[27]Johnson B D, Kip K E, Marroquin O C. Serumamyloid A as a predictor of coronary artery disease and car-diovascular outcome in women:the National Heart, Lung,and Blood Institute-Sponsored Women's Ischemia Syn-drome Evaluation (WISE). Circulation,2004,109:726-732.
[28]Coetzee G A, Strachan A F,van-der-Westhuyzen D R. Serum amyloid A-containing human high density lipoprotein 3:density,size and apolipoprotein composition.J Biol Chem,1986,261:9644-9651.
[29]丁云秋.心脑血管疾病多重危险因素控制会议概述.中华内科志,2000,39(12):858-859.
[30]Artl A, Marsche G, Lestavel S. Role of serum amy-loid A during metabolism of acute-phase HDL bymacrophages. Arterioscler Thromb Vasc Biol,2000,20:763-772.
[31]Migita K, Kawabe Y, Tominaga M. Serum amyloid Aprotein induces production of matrix metalloproteinases by human synovial fibroblasts. Lab Invest,1998,78:535-539.
[32]Daughterty A, Dunn JL, Rateri DL. Myeloperoxidase,a catalyst for lipoprotein oxidation, is expressed in human atheroscletoticlesions.J Clin Invest,1994,94 (1):437.
[33]Zhang R, Brennum ML, Fu X. Associa2tion between myeloperoxidase levels and riskof coronary artery disease. JAMA,2001,286(17): 2136-142.
[34]Nikpoor B, Turecki G, Fournier C. Afunctional myeloperoxidase polymorphic vari2ant is asscociated with coronary artery diseasein Frencn2Canadians. Am Heart J, 2001,142(2):336-339.
[35]Bekesi G, Magyar Z, Kakuss R. Changes in the myeloperoxidase activity of hu2man neutrophinic granulocytes and the amountof enzyme deriving from them under the effectof estrogenl. Orv Hetil,1999,140 (29):324-344.
[37]PostonR N, Haskard D O, Coucher J R. Expression of intercellularad-hesion molecule-1 in atherosclerotic plaques[J]. Am J Patho,1992,140:889-896.
[38]MaliK I, DanesH J, WhincuP P. Solubleadhesion molecules and prediction of coronary heart disease:a prospective study and meta-analysis [J].Lancet,2001,358:971-975.
[39]Blankenberg S, Rupprecht H J, Bickel C. Circulating cell adhesion molecules and death in patients with coronary artery disease [J]. Circulation,2001,104(12) 1336-1342.
[40]Haim M, Tanne D, Boyko V. Solubleintercellular adhesion molecule-1 and long-term risk of acutcoronary events in patients with chronic coronary heartdisease[J]. J Am Coll Cardiol,2002,39(7):1133-1138.
[41]Giesen PL, U Rauch, B Bohrmann. Blood-brone tissue factor:another view of thrombosis[J].Proc Natl Acad Sci USA,1999,96:2311-2315.
[42]Berg K. A new serum type system in men—the lipop rotein system [J].Acta PatholMicrobiol Scand,1963,59:369-382.
[43]Darvies MJ. Reactive oxygen species, metalloproteinases, and plaquesta-bility[J]. Circulation,1998,97(24):2382-2383.
[44]Ritchie ME. Nuclear factor-KB is selectively and markedly activated in humans with unstable angina pectoris[J]. Circulation,1998,98 (17):1707-1713.
[45]陈在嘉,高润霖.脂蛋白(α)与动脉粥样硬化[J].冠心病,2003,5(2)：133-135.
[46]Boerwinkle E, Leffert CC, L in J. Apolipop rotein(a) gene accounts for greater than 90% of the variation in p lasma lipop rotein (a) concentrations[J]. J Clin Invest,1992, 90 (1):52-60.
[47]Dahlen G H. Lipoprotein (a) in cardiovascular disease.Atherosclerosis,1994,108:111-120.
[48]Dahlen CH. Lp (a) lipop rotein in cardiovascular disease [J]. Athero-sclerosis,2001, 108:111.
[49]Mary S,Ayrs S,Humphris S. Lipoprotein(a) as predictor of myocardial infarction in middle-aged men. [J]Am J Med,2001,110(1):22-27.
[50]Von Eckardstein,Schulte H,Cullen P,oteet al.Lipoprotein(a) farther increase the risk of coronary events in men with high global cardiovascular risk.[J]Am Coll Cardiol,2001,37(2):434-439.
[51]刘毅,姜敏辉,高敏.c反应蛋白、心肌肌钙蛋白I对急性冠脉综合征的诊断价值[J].南通医学院学报,2003:23(4):419.
[52]戴秋艳,孙宝贵.脉压与冠心病患者左室肥厚的相关分析[J].中华国际医学杂志,2002:2(4)：301.
[53]盛富强.肌钙蛋白在诊断心肌损伤中的临床应用[J].郧阳医学院学报,2003:22(6):376.
[1]丁邦晗,马长生,张敏州.胸痹胸痛病人375例的冠脉病变程度及证型分析[J].中医药学刊,2004,22(6)：1096-1097.
[2]马晓昌,尹太英,陈可冀.冠心病中医辨证分型与冠状动脉造影所见相关性比较研究[J].中国中西医结合杂志,2001,21(9)：654-656.
[3]邢雁伟,王阶,衷敬柏,李海霞,高永红,何庆勇.采用聚类分析和对应相关方法研究1069例冠心病心绞痛证候应证组合规律[J],中华中医药杂志,2007,22(11):747-750.
[4]贾振华,王永军,吴以岭.基于熵的复杂系统分划方法与冠心病心绞痛证候要素提取及其分布规律[J].第二军医大学学报,2007,28(7):775-777.
[5]王阶,李军,姚魁武,等.冠心病心绞痛证候要素与应证组合研究[J].中医杂志,2007,48(10)：920-922.
[6]吴焕林,阮新民,杨小波.319例冠心病患者证候分布规律分析[J].中国中西医结合志,2007,27(6)：498-500.
[7]李江,赵水平.冠心病整体危险因素评估的方法及临床意义[J].中国循环杂志,2001：235-236.
[8]Taddei S, Virdis A, Mattei P. Unstable Angina/Myocardial Infarction/Atherosclerosis: Aging and Endothelial Function in Normotensive Subjects and Patients With Essential Hypertension. [Article]. Circulation April 1,1995,91(7):1981-1987.
[9]王小平.女性冠心病临床特征的分析.中国心血管杂志,2005,2:132-134.
[10]宋小虎,蔡学究,张德云.女性冠心病的发病特征及一级康复干预.中国临床康复,2005,19:154-155.
[11]Jensen J, Eriksson SV, Lindvall Bc. Women react with more myocardial ischemia and angina pectoris during elective percutaneous transluminal coronary angioplasty. [Miscellaneous Article]. Coronary ArteryDisease October 2000,11(7):527-535.
[12]Murphy NF, Simpson CR, MacIntyre K. Prevalence, incidence, primary care burden and medical treatment of angina in Scotland:age, sex and socioeconomic disparities:a population-based study. [Miscellaneous]. HeartAugust 2006,92(8):1047-1054.
[13]陈武,王邦宁,高世明.老中青年急性心肌梗塞的临床特点及相关因素分析[J].疾病控制杂志,2005,2:175-176.
[14]Gebara OCE, Mittleman MA, Sutherland P. Unstable Angina/Myocardial Infarction/Atherosclerosis:Association Between Increased Estrogen Status andIncreased Fibrinolytic Potential in the Framingham Offspring Study. [Article].Circulation April 1, 1995,91(7):1952-1958.
[15]Jousilahti P, Vartiainen E, Tuomilehto J. Sex, age, cardiovascular risk factors, and coronary heart disease:a prospective follow-up study of 14 786 middle-aged men and women in Finland. Circulation,1999,9:1165-1172.
[16]文川,程伟.206例冠心病心绞痛患者问诊资料与中医辨证关系的探讨[J].湖北中医杂志,2002,(10):3.
[17]赵慧辉,王伟,郭淑贞.冠心病不稳定性心绞痛血瘀证的蛋白质组学[J].中国动脉硬化杂志,2008,16(7):545-548.
[18]姚魁武,杨戈,王阶.高血压病血瘀证患者血液学指标判别分析[J].世界科学技术-中医药现代化基础研究,2006,8(5):30-42.
[19]丘瑞香,罗致强,朱雅宜,秦鉴。冠心病血瘀证血液理化特性与中医相关性研究[J].中医杂志,2002,43(5):378-379.
[20]丁邦晗,严夏,林晓忠,李松.血脂异常与胸痹心痛基本证型的相关性分析[J].辽宁中医杂志,2006,33(10):1261-1262.
[21]李松,丁邦晗,张敏州,蚁楷宏,陈伯钧,林晓忠,刘泽银.365例胸痹心痛患者证型血脂分析[J].广州中医药大学学报,2005,22(2):87-97.
[22]褚福永,王阶,姚魁武,李志忠.冠心病不稳定型心绞痛中医辨证分型与血脂及冠脉造影结果的相关性研究.[J]北京中医药2009,28(12):918-921.
[23]袁肇凯,田松,黄献平,胡志希,孙贵香,陈清华,莫莉,简维雄.冠心病痰瘀证候血脂指标的Meta分析[J].云南中医学院学报,2008,31(5):1-8.
[24]王阶,何庆勇,施展,邢雁伟,李霁,房玉涛,汤艳莉.冠心病证候要素组合与心功能及血脂的相关性[J].中西医结合学报,2008,6(9):897-901.
[25]Schwertner HA, Jackson WQ Tolan G Association oflow serum concentration of bilirubin with increased risk ofcoronary artery disease. Clin Chem,1994,40(1):18-23.
[26]林燕,黄维义.氧化应激致动脉粥样硬化作用的研究进展[J].黑龙江医学,2004,28:517-520.
[27]Mayer M. Association of serum bilirubin concerntrationwith risk of coronary artery disease [J]. ClinChem,2000,46(11):1723-1727.
[28]黄维义,曹林生,贺立群.冠心病患者胆红素浓度变化及其对低密度脂蛋白氧化修饰水平的影响.中国实用内科杂志,2001,21:23-24.
[29]李熹娟.胆红素与冠心病相关性的研究进展[J].心血管病学进展,2005,26:646-649.
[30]Peytonkj, Reynasv, Chapmangb. Hemeoxygenasel derived carbon monoxideisanautocrineinhibitorofvascularSmooth musclecell growth[J]. Blood,2002,99: 444-448.
[31]Sharma HS, Das DK, Verdouw PD. Enhanced expressionand localization of heme oxygenase-1 during recovery phaseof porcine stunned myocardium. Mol Cell Biochem,1999,196(1-2):133-139.
[32]李静,张继东,刘同涛.血清胆红素与冠脉病变程度、血脂及冠心病中医证型关系[J].南京中医药大学学报,2006,22(2):77-79.
[33]Hillis GS, Dalsey WC, Terregino C A. Altered CD18 leukocyteintegrin expression and adhesive function in patients with acute coronarysyntrome. Heart,2001,85:702-704.
[34]Shah P K. Mechanisms of plaque nulnerability and rupture. J Am CollCardiol, 2003,41:S15-22.
[35]Avanzas P, Arroyo2Espliguero R, Cosin Sales J. Multiplecomplex stenoses,high neutrophil count and C-reactive protein levels inpatients with chronic stable angina. Atherosclerosis,2004,175:151-157.
[36]蓝景生,黄照河,潘兴寿.外周血白细胞分类计数与冠心病及其危险因素聚集性的关系[J].中国全科医学,2008,11.(10)：1844-1845.
[37]卫任龙,杨志健,贾恩志,王连生,朱铁兵,陈波,曹克将,马文珠.外周血白细胞计数与冠状动脉狭窄的相关性[J].中国介入心脏病学杂志,2005,13(4):241-243.
[38]洪永敦,黄衍寿,吴辉,陈宇鹏,李斐媛,莫鸿辉.冠心病中医证候与炎症因子关系的临床研究[J].2005,,22(2)：81-86.
[39]Wolfgang Volker, Borszewski A,Unruh V. Copperinduced in flammatory of rat corotid arteries mimic restenosis arterosclerosislikeneointima formation. Atherosclerosis,1997,130:29.
[40]Lowe G, Rumley A, Norrie J. Blood rheology,cardiovascular risk factors and cardiovascular disease:the west of Scotland coronary prevention study. Thromb Haemost,2000,84 (4):553.
[41]张一娜,崔璨,张亚清.老年心脑血管疾病、糖尿病血液流变学改变[J].中国微循环杂志,2002,6(3)：167.
[42]冯永钦,谢传英,张清平.心脑血管疾病血液流变学指标的分析[J].中国血液流变学杂志,2002,12(1):22.
[43]何静脉,谭笑江,李巍.血液黏度检验中几个参数意义的探讨[J].大连医科大学学报,2000,22(2)：139.
[44]沈琪琳.老年冠心病患者血液流变学及血细胞参数的观察.中国慢性病预防与控制,2000,8(6)：252.
[45]Carallo C, Pujia A, Irace C. Whole blood viscosity andhaematocrit are associated with internal carotid atherosclerosisin men. Coron Artery Dis,1998,9 (2-3):113.
[46]Baskurt OK, Edremitlioglu M,Temiz A, Effect of ervthrocvte deformabilitv on myocardial hematocrit gradient. Am J Physiol,1995,268(lpt2):H:260-264.
[47]Gustavsson CG, Pwrsson SU, Larsson H. Changed blood rheology in patients with idiopathic dilated cardiomyopathy. Angioogy 1994,45(2):107-111.
[48]Syoten OKA. Cardiovas cular haemorheology [M]. Cambridge University Press,1983.
[49]潘瑞彭,王鸿利主编.血液学及血液学检验[M].北京：人民卫生出版社,1990.
[50]翁维良,廖福龙,吴云鹏.血液流变学研究方法及其应用[M].北京：科学出版社,1989.96-99.
[51]Walport MJ, Schifferli JA, Walza. the change of immunologic function of erythrocyte in the patients with coronary heart disease[J]. Clin. Immunol. EXP,1998,56:536-542.
[52]Kunapuli S P. ADP receptors:targetsfor developing antithrombotic agents [J].Curr Pharm,2003,9:2303-2316.
[53]Day CP. Br Heart J 1990,63:342.
[54]曹济民,王向东.急性心肌缺血时心室易颤期的变化趋势.中国应用生理学杂志,1992；8(1)：85
[55]陈良细.OT离散度评价心肌梗塞预后的临床意义.医学综述,1997;3(8):378
[1]Ross R. A therosclerosis an inflammatory disease [J].N Engl J Med,1999,340:115-126.
[2]Buffon A, Biasucci LM, Liuzzo G. Widespread coronary inflammationin unstable angina. NEngl J Med,2002,347(1):5-12.
[3]Mulvihill NT, Foley JB. Inflammation in acute coronary syndromes.Heart,2002,87(3):201-204.
[4]Rohde L E, Hennekens CH, Ridker P M. Survey of C-reactive protein and cardiovascular risk factor in apparently healthy men[J]. Am J Cardiol,1999,84:1018-1022.
[5]Ridker P M, Buring J F, Shih J. Prospcctive study of C-reactive protein and the risk of future cardiovascularevente among apparently healthy women[J]. Circulation,1998,98: 731-733.
[6]Liuzzo G, Biasucci L M, Gallimore L R. The prognostic value of C-reactive protein and serum amyloid A protein in seruere unstable angina[J]. N Engl J Med,1994,331:417-424.
[7]Anderson J L, Carlquist J F, Muhlestein J B. Evaluation of C-reactive protein, an inflammation and myocardialinfectins serology as risk factors for coronary artery disease and myocardial infarction[J]. J Am Coll Cardiol,1998,32:35-41.
[8]赵慧辉、王伟、郭淑贞.冠心病不稳定型心绞痛血瘀证的蛋白质组学[J].中国动脉硬化杂志,2008,16(7)：545-548.
[9]Coetzee G A, Strachan A F,van-der-Westhuyzen D R. Serum amyloid A-containing human high densitylipoprotein:density,size and apolipoprotein composition.J Biol Chem,1986,261:9644-9651.
[10]丁云秋.心脑血管疾病多重危险因素控制会议概述[J].中华内科志,2000,39(12)：858-859.
[11]Artl A, Marsche G, Lestavel S. Role of serum amy-loid A during metabolism of acute-phase HDL bymacrophages. Arterioscler Thromb Vasc Biol,2000,20:763-772.
[12]Migita K, Kawabe Y, Tominaga M. Serum amyloid Aprotein induces production of
matrix metalloproteinases by human synovial fibroblasts. Lab Invest,1998,78:535-539.
[13]Ridker PM, Morrow D, M PH. High sensitivity C-reaction protein and cardiovascular risk: rational forscreening and p rimary p revention [J]. Am J Card iol,2003,92 (Supp 1):17-22.
[14]Zwaka TP, Hombach V, Torzewski J. C-reactive Protein mediated low density lipoprotein uptake by macrophages:implicationsfor at herosclersis[J]. Circulation 2001,103:1194-1197.
[14]Nakagomi A, Freedman SB, Geczy CL. Interferon-gamma andlipopolysaccharide potentiate monocyte tissue factor inductionby C-reactive protein:relationship wit h age, sex,and hormonereplacement t reatment [J]. Circulation,2000,101:1784-1791.
[15]Bickel C, Rupprecht HJ, Blankenberg S. Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease[J].Am J Cardiol,2002,89(1):12-17.
[16]Woodward M, Low e G D, Rum ley A. Fibrinogen as a risk factor for coronary heart disease and mortality in middle-aged men and women-The Scottish heart Health Studu[J]Eur Heart J,1998,19(1):55-62.
[17]毛以林,李旭,彭素娟,罗昌国.冠心病血瘀证与高敏c反应蛋白相关性研究[J].中国中医药信息杂志,2007,17(6):26-27.
[18]商秀洋,石洁.冠心病中医辨证与血清高敏c反应蛋白的关系研究[J].现代中西医结合杂志,2008,17(6):818-819.
[19]托马斯.临床实验诊断学[M].第1版.上海：上海科学技术出版社,2004,575.
[20]Robins S J, Collins D, Wittes J T. Relation of gemfibrozil treatmenttreatmentand lipid levels with major coronary events:VA-HIT:a randomizedcontrolled trial[J]. JAMA, 2001,285:1585-1591.
[21]Von Fckardstein A, Hersberger M, Rohrer L. Current understandingof the metabolism and biological actions of HDL[J]. Curr Opin Clin NutrMetab Care,2005,8:147-152.
[22]Lee JM,Okumura MJ, Davis MM. Prevalence and determinants of insulin resistance among US adolescents:a population-bases study[J]. Diabetes Care,2006,29(11) 2427-2432.
[23]Nakagomi A, Freedman SB, Geczy CL. Interferon-gamma andlipopolysaccharide potentiate monocyte tissue factor inductionby C-reactive protein:relationship wit h age, sex,and hormonereplacement treatment [J]. Circulation,2001,103:1194-1197.
[24]Masashi S, Kenj IU, Masako H. Effect ofmagnesium sulfate pretreatment and dignificance of matrixmetal loproteinase-1 and interleukin-6 levels in coronaryreperfusion therapy for patients with acute myocardialinfarction[J]. Angiol 1999,50：573.
[25]洪永敦,黄衍寿,吴辉,陈宇鹏.冠心病中医证候与炎症因子关系的临床研究[J].广州中医药大学学报,2005,22(2):81-86.
[26]Ridker PM, Rifai N, Pfeffer M, et al. Elevation oftumor necrosis factor-alpha and increased risk of recurrentcoronary events after myocardial infarction [J].Circulation, 2000,101:2149-2153.
[27]毛以林,谭光波,袁肇凯,黄献平.高敏C反应蛋白和可溶性细胞间黏附分子-1与冠心病血瘀证的相关性研究[J].新中医,2007,39(3):25-26.
[28]朱青霞.冠心病中医证型与血清可溶性细胞间黏附分子的相关性研究[J].中国中医基础医学杂志,2007,13(11):842-843.
[39]Hao Y, Qiu Q Y, W J. Effect of astragaius polysaccharin(APS) on ymphocyte-endothelium adhesion and the moiecular mechanism [J]. Immunnol Ji：免疫学学杂志),2000,16(3):206-209.
[30]Peng Q,Wei Z, Lau BH. Pycnogenol inhibits tumor necrosis factor-alphainduced nuclear factor kappa B activation and adhesion molecule expressionin human vascular endothelial cells[J]. Cell Mol Life scj,2000,57 (5):834-41.
[31]Nakagomi A, Freedman SB, Geczy CL. Interferon-gamma andlipopolysaccharide potentiate monocyte tissue factor inductionby C-reactive protein:relationship wit h age, sex,and hormonereplacement t reatment [J]. Circulation,2000,101:1784-1791.
[32]Yasojima K, Schwab C, Mcgeer EG. Generation of C-reactive Protein and complment component s in at herosclerotic plaques[J]. Am J Pat hol,2001,158:1039-1049.
[33]柏正平,谭光波,卜献春,孙春林.冠心病中医辨证分型与细胞黏附分子的关系[J].中西医结合心脑血管病杂志,2006,4(2)：108-109.
[34]杨徐杭,汶医宁,党琳,魏敏慧.冠心病中医辨证与E-选择素、细胞间黏附分子-1的关系的研究[J].四川中医,2008,26(1)：61-62.
[35]丁邦晗,严夏,林晓忠,李松.血脂异常与胸痹心痛基本证型的相关性分析[J].辽宁中医杂志,2006,33(10)：1261-1262.
[36]Simonini A, Moscuci M, Muller DW. IL-8 is an angiogenicfactor in human coronary atheretonry tissue. Circulation,2000,101:1519-1526.
[37]Hearse DJ. Myocardial protection during ischemia and reperfusion.Mol Cell Biochem, 1998,186:177-184.
[38]Giesen PL, U Rauch, B Bohrmann. Blood-brone tissue factor:another view of thrombosis[J]. Proc Natl Acad Sci USA,1999,96:2311-2315.
[39]Lee SH, Wolf PL, Eseudero R. Early expression of angiogenesisfactors in acute myocardial ischemia and infarction. N Engl J Med,2000,342:626-633.
[40]Ritchie ME. Nuclear factor-κB is selectively and markedly activated in humans with unstable angina pectoris[J]. Circulation,1998,98 (17):1707-1713.
[41]Darvies MJ. Reactive oxygen species, metalloproteinases, and plaquesta-bility[J]. Circulation,1998,97(24):2382-2383.
[42]Wilson SH, Best PJ, Edwards WD. Nuclear factor-kappa-B immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectovis. Atheroscl-rosis,2002,160:147-53
[43]Calabresi L,Villa B,Omobom L. Soluble cellular adhesion molecules are increased in patients with low HDL-cholesterol [J]. Atherosclerosis,2000,151(1):216-226.
[44]Park SH, Park JH, Kang JS. Involvement of transcrip tion factors in p lasmaHDL protection against TNF-alpha induced vascular cell adhesion molecule-lexp ression[J]. IntB iochem CellB iol,2003,35 (2):168-182.
[45]James AL, David AM, Marc SS.Association Between Plasma Levels of Monocyte Chemoattractant Protein-1 and Long-Term Clinical Outcomes in Patients With Acute Coronary Syndromes [J]. Circulation,2003,107:690-695.
[46]Masamichi K, Kensuke E,Shiro K.Role of Monocyte Chemoattractant Protein-1 in Cardiovascular Remodeling Induced by Chronic Blockade of Nitric Oxide Synthesis[J].Circulation;2000,102:2243-2248.
[47]Peng Q,Wei Z, Lau BH. Pycnogenol inhibits tumor necrosis factor-alphainduced nuclear factor kappa B activation and adhesion molecule expressionin human vascular endothelial cells[J]. Cell Mol Life scj,2000,57 (5):834-41.
[48]Darvies MJ. Reactive oxygen species, metalloproteinases, and plaquesta-bility[J]. Circulation,1998,97(24):2382-2383.