急性冠脉综合征患者抵抗素和P-选择素的相关性研究
摘要
目的
研究急性冠脉综合征患者血浆抵抗素(Resistin)与P-选择素(P-selectin)的水平,分析二者的相关性,评价抵抗素和P-选择素在急性冠脉综合征发生发展中意义。
方法
选择经冠脉造影证实的102例急性冠脉综合征(acute coro-nary syndrome, ACS)患者,其中急性心肌梗死(acute myocardial infarction, AMI)50例,不稳定性心绞痛(unstable angina Pectoris, UAP)52例；拟诊冠心病冠脉造影正常的对照组(normal Control,NC)40例。酶联免疫吸附法(ELISA)测定血浆抵抗素和P-选择素水平,同时由我院检验中心统一检测血脂。
结果
1.急性冠脉综合征患者血浆抵抗素明显高于对照组[(4.09±0.78)ng/ml比(3.17±0.35)ng/ml p<0.05],其中急性心肌梗死组明显高于不稳定心绞痛组[(4.49±0.76)ng/ml比(3.70±0.59)ng/ml p<0.05]。
2.急性冠脉综合征患者血浆P-选择素明显高于对照组[(129.97±6.72)ng／ml比(80.42±4.75)ng/ml p<0.05],其中急性心肌梗死组明显高于不稳定心绞痛组[(133.77±6.55)ng/ml比(126.31±4.56)ng／ml p<0.05]。
3.抵抗素与甘油三酯呈正相关(r=0.28 p<0.05),与高密度脂蛋白胆固醇呈负相关(r=-0.45 p<0.05)。
4.抵抗素与P-选择素呈正相关(r=0.43 p<0.05)。
结论
1.急性冠脉综合征组血浆抵抗素高于对照组,其中急性心肌梗死组较不稳定心绞痛组抵抗素水平明显增高,提示抵抗素在急性冠脉综合征的发生和发展过程起到重要作用。
2.急性冠脉综合征组血浆P-选择素水平显著高于对照组,提示急性冠脉综合征患者可能存在血管内皮细胞的功能障碍和血小板高活性状态。其中P-选择素在急性心肌梗死组明显高于不稳定心绞痛组,提示急性心肌梗死较不稳定心绞痛血小板活化程度更重。
3.抵抗素与甘油三酯呈正相关,与高密度脂蛋白胆固醇呈负相关,提示可能抵抗素通过引起血脂异常参与冠心病的发生发展。
4.急性冠脉综合征患者血浆抵抗素和P-选择素正相关,提示血浆抵抗素浓度增加伴随P-选择素水平上升,两者可能共同在急性冠脉综合征的发生发展中发挥作用。
Objective
To investigate the changes of plasma resistin and P-selectin levels and study on the corelationship between resistin level and P-selectin level in patients with acute coronary syndrome(ACS). Methods
102 patients with ACS were proved by coronary angiograph, including 50 acute myocardial infarction(AMI) cases and 52 unstable angina Pectoris(UAP)cases,40 patients with dubious coronary heart disease (CHD) but proved by coronary angiograph to be normal were selected as control cases. The method of ELISA was used to determine the plasma resistin and P-selectin levels. total cholesterol (TC), triglycerides(TG) were investigated by enzyme reagent method, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) were investigated by direct method in the unified test center of the second hospital of Shanxi medical university.
Results
1.The plasma resistin level in ACS group was significantly higher than that in control group[(4.09±0.78)ng/ml vs (3.17±0.35)ng/ml P<0.05J and the plasma resistin level in AMI group was significantly higher than that in UAP group[(4.49±0.76)ng/ml vs (3.70±0.59)ng/ml P＜0.05].
2.The plasma P-selectin level in ACS patients was significantly higher than that in control group [(129.97±6.72)ng/ml vs (80.42±4.75)ng/ml P＜0.05] and the plasma P-selectin level in AMI group was significantly higher than that in UAP group[(133.77±6.55)ng/ml vs (126.31±4.56)ng/ml P<0.05].
3.The plasma resistin level was positively correlated with TG(r=0.28 P<0.05),negatively correlated with HDL(r=-0.45 P<0.05).
4.The plasma resistin level was positively correlated with P-selectin(r=0.43 P<0.05).
Conclusion
LACS patients have increased plasma resistin levels. plasma resistin levels was significantly higher in AMI group than in UAP group.suggesting that resistin in the occurrence and development of ACS has played an important role.
2.ACS patients have increased plasma P-selectin levels, suggesting that endothelial cell dysfunction and platelet high activity state. P-selectin in AMI group was significantly higher than UAP group which indicates that AMI patients may have heavier degree of platelet activation than that in UAP patients.
3.plasma resistin levels was positively correlated with TG，and HDL were negatively correlated, suggesting that the resistin involved in CHD by causing the development of dyslipidemia.
4.plasma resistin levels in patients with ACS was positively correlated with P-selectin, suggesting that plasma resistin levels increased with P-selectin levels in patients with ACS, both common may play a role in the occurrence and development of ACS.
研究急性冠脉综合征患者血浆抵抗素(Resistin)与P-选择素(P-selectin)的水平,分析二者的相关性,评价抵抗素和P-选择素在急性冠脉综合征发生发展中意义。
方法
选择经冠脉造影证实的102例急性冠脉综合征(acute coro-nary syndrome, ACS)患者,其中急性心肌梗死(acute myocardial infarction, AMI)50例,不稳定性心绞痛(unstable angina Pectoris, UAP)52例；拟诊冠心病冠脉造影正常的对照组(normal Control,NC)40例。酶联免疫吸附法(ELISA)测定血浆抵抗素和P-选择素水平,同时由我院检验中心统一检测血脂。
结果
1.急性冠脉综合征患者血浆抵抗素明显高于对照组[(4.09±0.78)ng/ml比(3.17±0.35)ng/ml p<0.05],其中急性心肌梗死组明显高于不稳定心绞痛组[(4.49±0.76)ng/ml比(3.70±0.59)ng/ml p<0.05]。
2.急性冠脉综合征患者血浆P-选择素明显高于对照组[(129.97±6.72)ng／ml比(80.42±4.75)ng/ml p<0.05],其中急性心肌梗死组明显高于不稳定心绞痛组[(133.77±6.55)ng/ml比(126.31±4.56)ng／ml p<0.05]。
3.抵抗素与甘油三酯呈正相关(r=0.28 p<0.05),与高密度脂蛋白胆固醇呈负相关(r=-0.45 p<0.05)。
4.抵抗素与P-选择素呈正相关(r=0.43 p<0.05)。
结论
1.急性冠脉综合征组血浆抵抗素高于对照组,其中急性心肌梗死组较不稳定心绞痛组抵抗素水平明显增高,提示抵抗素在急性冠脉综合征的发生和发展过程起到重要作用。
2.急性冠脉综合征组血浆P-选择素水平显著高于对照组,提示急性冠脉综合征患者可能存在血管内皮细胞的功能障碍和血小板高活性状态。其中P-选择素在急性心肌梗死组明显高于不稳定心绞痛组,提示急性心肌梗死较不稳定心绞痛血小板活化程度更重。
3.抵抗素与甘油三酯呈正相关,与高密度脂蛋白胆固醇呈负相关,提示可能抵抗素通过引起血脂异常参与冠心病的发生发展。
4.急性冠脉综合征患者血浆抵抗素和P-选择素正相关,提示血浆抵抗素浓度增加伴随P-选择素水平上升,两者可能共同在急性冠脉综合征的发生发展中发挥作用。
Objective
To investigate the changes of plasma resistin and P-selectin levels and study on the corelationship between resistin level and P-selectin level in patients with acute coronary syndrome(ACS). Methods
102 patients with ACS were proved by coronary angiograph, including 50 acute myocardial infarction(AMI) cases and 52 unstable angina Pectoris(UAP)cases,40 patients with dubious coronary heart disease (CHD) but proved by coronary angiograph to be normal were selected as control cases. The method of ELISA was used to determine the plasma resistin and P-selectin levels. total cholesterol (TC), triglycerides(TG) were investigated by enzyme reagent method, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) were investigated by direct method in the unified test center of the second hospital of Shanxi medical university.
Results
1.The plasma resistin level in ACS group was significantly higher than that in control group[(4.09±0.78)ng/ml vs (3.17±0.35)ng/ml P<0.05J and the plasma resistin level in AMI group was significantly higher than that in UAP group[(4.49±0.76)ng/ml vs (3.70±0.59)ng/ml P＜0.05].
2.The plasma P-selectin level in ACS patients was significantly higher than that in control group [(129.97±6.72)ng/ml vs (80.42±4.75)ng/ml P＜0.05] and the plasma P-selectin level in AMI group was significantly higher than that in UAP group[(133.77±6.55)ng/ml vs (126.31±4.56)ng/ml P<0.05].
3.The plasma resistin level was positively correlated with TG(r=0.28 P<0.05),negatively correlated with HDL(r=-0.45 P<0.05).
4.The plasma resistin level was positively correlated with P-selectin(r=0.43 P<0.05).
Conclusion
LACS patients have increased plasma resistin levels. plasma resistin levels was significantly higher in AMI group than in UAP group.suggesting that resistin in the occurrence and development of ACS has played an important role.
2.ACS patients have increased plasma P-selectin levels, suggesting that endothelial cell dysfunction and platelet high activity state. P-selectin in AMI group was significantly higher than UAP group which indicates that AMI patients may have heavier degree of platelet activation than that in UAP patients.
3.plasma resistin levels was positively correlated with TG，and HDL were negatively correlated, suggesting that the resistin involved in CHD by causing the development of dyslipidemia.
4.plasma resistin levels in patients with ACS was positively correlated with P-selectin, suggesting that plasma resistin levels increased with P-selectin levels in patients with ACS, both common may play a role in the occurrence and development of ACS.
引文
[1]陆在英,钟南山等。冠状动脉粥样硬化性心脏病。7版内科学,北京：人民卫生出版社,2007,7：274-300
[2]BertrandM E, SimoonsM I, Fox KAA, et al. Management of acute coronary syndromes: acute coronary syndromes without persistent ST segment elevation; recommendations of the Task Force of the European Society of Cardiology [J]. Eur Heart J,2000,21:1406-1432.
[3]Libby P. Current concepts of the pathogenesis of the acute coronary syndromes[J] Circulation,2001,104:365-372
[4]RossiML, Marziliano N, Merlini PA, et al. Diferentquantitative apoptotic traits in coronary atherosclerodc plaques from patients with stable angina pectoris and acute co ronary syndromes [J].Circulation,2004,110:1767-1773.
[5]Herman MP, Sukhova GK,Libby P, et al. Expression of neutrophil collagenase(matrixmetallo proteinase-8) in human atheroma:A novel collagenolytic pathway suggested by transcriptional profiling[J]. Circulation,2001,104:1899-1904.
[6]Kol A, L ichtman AH, Finberg RW, et al. Cutting edge:Heat-shock protein(HSP) 60 activates the innate immune response:CD14 is an essential receptor for HSP60 activation of mononuclear cells[J]. J Immunol,2000,164:13-17.
[7]Yan JC,W u ZG, Huang Z, et al. Clinical implications of increased expression of CD40L in patients with acute coronary syndromes [J]. Chinese M edical Journal,2002,115 (4):491-493.
[8]黄体钢.不稳定型心绞痛的病理生理机制和血清标志物水平变化的临床意义[M].黄体钢,丛洪良,张承宗,主编.心脏病学高级教程.沈阳：辽宁科学技术出版社,2003.84-94.
[9]Rasche H. Haemostasis and thrombosis:an overview [J]. Eur Heart J,2001,3 (Supp 1 Q):Q3.
[10]Badimon I, Vilahur G, Sanchez S, et al. Atheromatous plaque formation and thrombogenesis:formation, risk factors and therapeutic approaches[J]. Eur Heart J,2001,3 (Suppl Ⅰ):116.
[11]Filippone L and Farina GA.Acute coronary syndrome,a practical review for primary care physicians.Primary Care Updates for OB/GYNS,2003;10:224-230.
[12]Steppan CM, Bailey ST, Bhat S, et al. The hormone resistine links obesity to dliabetes. Nature,2001,409(6818):307-312
[13]Steppan CM, Lazar M A.et al. Resistin and obesity associated insulin resistiance Trends Endoerinol Metab,2002,13:18-23
[14]Fain JN, Cheema PS, Bahouth SW, et al. [J]. Biochem Biophys Res Commun,2003, 300(3):674-678.
[15]Mu H, Ohashi R, Yan S, et al. Adipokine resistin promotes in vitro angiogenesis of human endothelial cells. Cardiovasc Res,2006,70:146-157.
[16]Subodh Verma, MD, PhD;Shu-Hong Li, MSc,Chao-Hung Wang,MD,et al. Resistin Promotes Endothelial Cell Activation Further Evidence of Adipokine-Endothelial Interaction. Circulation.2003,108:r24-r28
[17]Nicoletta Di Simone, Fiorella Di Nicuolo, et al. Resistin regulates human choriocarcinoma cell invasive behaviour and endothelial cell angiogenic processes. J. Endocrinol., Jun 2006; 189: 691-699.
[18]W Xu, L Yu, W Zhou, M Luo。 Resistin increases lipid accumulation and CD36 expression in human macrophages.Biochem Biophys Res Commun, December 15,2006; 351(2):376-82.
[19]Jung HS, Park KH, Cho YM, et al. Resistin is secreted from macrophages in atheromas and promotes atherosclerosis. Cardiovasc Res,2006,69:76-85.
[20]W u GX, L i FG, L i PX, et al. Detection of plasma alpha-granule membrane pro tein (GM P2140) using radio labeled monoclonal antibodies in thrombotic disease. Haemo stasis, 1993,23(2):
[21]周 同,董德长.细胞粘附分子研究进展.上海免疫学杂志,1995,15(1)：58
[22]Mulvihill N,Foley JB.Inflammation in acute coronary sydromes Heart,2002,87(3):201-4
[23]Burnett MS, Devaney JM, Adenika RJ, et al. Cross-sectional associations of resistin, coronary heart disease, and insulin resistance. JClin EndocrinolMetab,2006,91:64-68.
[24]Johnson RC, Chapman SM, Dong ZM, et al. Absence of P-selectin delays fatty streak from ation in mice. J Clin Invest,1997,99:10372-10401
[25]YIPH K,SUN CK,et al.Strong correlation between serum levels of imflammatory mediators and theinlistribution in frarct-related cornary artery [J].Cire J.2006.70(7):838-845
[26]Verma S, Li SH, Wang CH, et at. Resistin Promotes Endothelial Cell Activation:Further Evidence of Adipokine-Endothelial Interaction [J]. Circulation,2003,108(6):736-740.
[27]Kawanami D, Maemura K, Takeda N, et at. [J]. Biochem Biophys Res Commun, 2004,314(2):415-419
[28]Patel L,Buckels AC,Kinghom IJ, et al.Resistin is expressed in human macro-phages and directly regulated by PPAR gamma activators [J]. Biochem BioPhys Res,2003,300:472-6.
[29]Rossi ML, Marziliano N, Merlini PA, et al. Diferent quantitative apop-totic traits in coronary atherosclerodcplaques from patients with stable anginapectoris and acute coronary syndromes [J].Circulation,2004,110:1767-1773.
[30]Yip HK, Chang LT, Sun CK, et al. Platelet activity is a biomarker of cardiac necrosis and predictive of untoward clinical outcomes in patients with acute myocardial infarction undergoing primary coronary stenting[J]. Circ J,2006,70 : 31-36.
[31]Sato N,Kobayashi K,Inoguchi T,et al.Adenovirus-mediated high expression of resistin causes dyslipidemia in mice.Endocrinology,2002;146:273-379.
[32]Silswal N, Singh AK, Aruna B, et al-Human resistin stimulates the proinflammatory cytokines TNF-alpha and IL-12 in macrophages by NF-kappa B dependent pathwayBiochem BiophysRes Commun,2005,334(4):1092-1101.
[1]BertrandM E, SimoonsM I, Fox KAA, et al. M anagement of acute coronary syndromes: acute coronary syndromes without persistent ST segment elevation; recommendations of the Task Force of the European Society of Cardiology [J]. Eur Heart J,2000,21:1406-1432.
[2]Libby P. Current concepts of the pathogenesis of the acute coronary syndromes[J] Circulation,2001,104:365-372
[3]Reilly MP, Lehrke M, Wolfe ML, et al. Resistin is an inflammatory marker of atherosclerosis in humans [J]. Circulation,2005,111 (7):932-939.
[4]Burnett MS, Lee CW, Kinnaird TD, et al. The potential role of resistin in atherogenesis [J]. Atheroscler osis,2005,182(2):241-248.
[5]乔小芝、杨云梅等,Resistin与急性冠脉综合征、稳定性心绞痛相关性研究.浙江预
防医学2007,19(9)：14-19
[6]Steppan CM, Bailey ST, Bhat S, et al. The hormone resistine links obesity to dliabetes. Nature,2001,409(6818):307-312
[7]Steppan CM,Brown EJ,Wright CM,et al. A family of tissue-specific resistin-like molecules[J].Proc Natl Acad Sci USA,2001,98 (2):502-526
[8]Steppan CM, Lazar M A.et al. Resistin and obesity-associated insulin resistiance Trends Endoerinol Metab,2002,13:18 - 23
[9]Ghosh S, Singh AK, Aruna B, et al. The genomic organization of mouse resistin reveals major differences from the human resistin:functional implications[J].Gene,2003,305 (1):27-34.。
[10]Patel L,Buckels AC,Kinghom IJ, et al.Resistin is expressed in human macro-phages and directly regulated by PPAR gamma activators [J]. Biochem BioPhys Res,2003,300:472-6.
[11]Rossi ML, Marziliano N, Merlini PA, et al. Diferent quantitative apop-totic traits in coronary atherosclerodcplaques from patients with stable anginapectoris and acute coronary syndromes [J].Circulation,2004,110:1767-1773.
[12]Subodh Verma, MD, PhD;Shu-Hong Li, MSc,Chao-Hung Wang,MD,et al. Resistin Promotes Endothelial Cell Activation Further Evidence of Adipokine-Endothelial Interaction. Circulation.2003,108:r24-r28
[13]Kougias P,Chai H, et al.Adipocyte-derived cytokine resistin causes endothelia-1 dysfunction of porcine coronary arteries. J Vasc Surg.2005,41(4):691-8
[14]Mu H, Ohashi R, Yan S, etal, Resistin promotes endothelial cell activation further evidence of adpokine-endothethelial interaction, Circulation,2003,108:736-740
[15]Fasshauer M,Klein J,Neumann S,et al.Tumor necrosis factor-a is a negative regulator of resistin gene expression and secretion in 3T3-L1 adipocytes[J].Bio-chem Biophys Res Commun.2001,288:1027-1031
[16]Anne Kunnari, Olavi Ukkola,et al.High Plasma Resistin Level Is Associated with Enhanced Highly Sensitive C-Reactive Protein and Leukocytes [J] Clinical Endocrinology & Metabolism Vol.91, No.72755-2760
[17]Nicoletta Di Simone, Fiorella Di Nicuolo, Maurizio Sanguinetti, Roberta Castellani, Marco D'Asta, Leonardo Caforio, and Alessandro Caruso J. Endocrinol., Jun 2006; 189:691-699
[18]Sung HS,Park KH,Cho YM,et al.Resistin is secreted from macrophages in atheromas and promotes atherosclerosis.Cardiovasc Res,2006;69:76-85
[19]Rothwell SE, Richards AM, Pemberton CJ, et al-Resistin worsens cardiac ischaemia-reperfusion injury-Biochem Biophys Res Commun,2006,349(1):400-407.
[2]BertrandM E, SimoonsM I, Fox KAA, et al. Management of acute coronary syndromes: acute coronary syndromes without persistent ST segment elevation; recommendations of the Task Force of the European Society of Cardiology [J]. Eur Heart J,2000,21:1406-1432.
[3]Libby P. Current concepts of the pathogenesis of the acute coronary syndromes[J] Circulation,2001,104:365-372
[4]RossiML, Marziliano N, Merlini PA, et al. Diferentquantitative apoptotic traits in coronary atherosclerodc plaques from patients with stable angina pectoris and acute co ronary syndromes [J].Circulation,2004,110:1767-1773.
[5]Herman MP, Sukhova GK,Libby P, et al. Expression of neutrophil collagenase(matrixmetallo proteinase-8) in human atheroma:A novel collagenolytic pathway suggested by transcriptional profiling[J]. Circulation,2001,104:1899-1904.
[6]Kol A, L ichtman AH, Finberg RW, et al. Cutting edge:Heat-shock protein(HSP) 60 activates the innate immune response:CD14 is an essential receptor for HSP60 activation of mononuclear cells[J]. J Immunol,2000,164:13-17.
[7]Yan JC,W u ZG, Huang Z, et al. Clinical implications of increased expression of CD40L in patients with acute coronary syndromes [J]. Chinese M edical Journal,2002,115 (4):491-493.
[8]黄体钢.不稳定型心绞痛的病理生理机制和血清标志物水平变化的临床意义[M].黄体钢,丛洪良,张承宗,主编.心脏病学高级教程.沈阳：辽宁科学技术出版社,2003.84-94.
[9]Rasche H. Haemostasis and thrombosis:an overview [J]. Eur Heart J,2001,3 (Supp 1 Q):Q3.
[10]Badimon I, Vilahur G, Sanchez S, et al. Atheromatous plaque formation and thrombogenesis:formation, risk factors and therapeutic approaches[J]. Eur Heart J,2001,3 (Suppl Ⅰ):116.
[11]Filippone L and Farina GA.Acute coronary syndrome,a practical review for primary care physicians.Primary Care Updates for OB/GYNS,2003;10:224-230.
[12]Steppan CM, Bailey ST, Bhat S, et al. The hormone resistine links obesity to dliabetes. Nature,2001,409(6818):307-312
[13]Steppan CM, Lazar M A.et al. Resistin and obesity associated insulin resistiance Trends Endoerinol Metab,2002,13:18-23
[14]Fain JN, Cheema PS, Bahouth SW, et al. [J]. Biochem Biophys Res Commun,2003, 300(3):674-678.
[15]Mu H, Ohashi R, Yan S, et al. Adipokine resistin promotes in vitro angiogenesis of human endothelial cells. Cardiovasc Res,2006,70:146-157.
[16]Subodh Verma, MD, PhD;Shu-Hong Li, MSc,Chao-Hung Wang,MD,et al. Resistin Promotes Endothelial Cell Activation Further Evidence of Adipokine-Endothelial Interaction. Circulation.2003,108:r24-r28
[17]Nicoletta Di Simone, Fiorella Di Nicuolo, et al. Resistin regulates human choriocarcinoma cell invasive behaviour and endothelial cell angiogenic processes. J. Endocrinol., Jun 2006; 189: 691-699.
[18]W Xu, L Yu, W Zhou, M Luo。 Resistin increases lipid accumulation and CD36 expression in human macrophages.Biochem Biophys Res Commun, December 15,2006; 351(2):376-82.
[19]Jung HS, Park KH, Cho YM, et al. Resistin is secreted from macrophages in atheromas and promotes atherosclerosis. Cardiovasc Res,2006,69:76-85.
[20]W u GX, L i FG, L i PX, et al. Detection of plasma alpha-granule membrane pro tein (GM P2140) using radio labeled monoclonal antibodies in thrombotic disease. Haemo stasis, 1993,23(2):
[21]周 同,董德长.细胞粘附分子研究进展.上海免疫学杂志,1995,15(1)：58
[22]Mulvihill N,Foley JB.Inflammation in acute coronary sydromes Heart,2002,87(3):201-4
[23]Burnett MS, Devaney JM, Adenika RJ, et al. Cross-sectional associations of resistin, coronary heart disease, and insulin resistance. JClin EndocrinolMetab,2006,91:64-68.
[24]Johnson RC, Chapman SM, Dong ZM, et al. Absence of P-selectin delays fatty streak from ation in mice. J Clin Invest,1997,99:10372-10401
[25]YIPH K,SUN CK,et al.Strong correlation between serum levels of imflammatory mediators and theinlistribution in frarct-related cornary artery [J].Cire J.2006.70(7):838-845
[26]Verma S, Li SH, Wang CH, et at. Resistin Promotes Endothelial Cell Activation:Further Evidence of Adipokine-Endothelial Interaction [J]. Circulation,2003,108(6):736-740.
[27]Kawanami D, Maemura K, Takeda N, et at. [J]. Biochem Biophys Res Commun, 2004,314(2):415-419
[28]Patel L,Buckels AC,Kinghom IJ, et al.Resistin is expressed in human macro-phages and directly regulated by PPAR gamma activators [J]. Biochem BioPhys Res,2003,300:472-6.
[29]Rossi ML, Marziliano N, Merlini PA, et al. Diferent quantitative apop-totic traits in coronary atherosclerodcplaques from patients with stable anginapectoris and acute coronary syndromes [J].Circulation,2004,110:1767-1773.
[30]Yip HK, Chang LT, Sun CK, et al. Platelet activity is a biomarker of cardiac necrosis and predictive of untoward clinical outcomes in patients with acute myocardial infarction undergoing primary coronary stenting[J]. Circ J,2006,70 : 31-36.
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