利用血管内超声评价急性冠脉综合征与内皮素的相关性
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摘要
【目的】:
探讨内皮素(ET)与急性冠脉综合征(ACS)、易损斑块的发生发展及冠脉重构、狭窄程度的关系。
【资料和方法】:
对2007年1月至2008年4月间在昆明医学院第一附属医院住院的15例急性冠脉综合征(ACS)患者和15例稳定性心绞痛(SAP)患者行IVUS检查,对所检查的罪犯病变血管进行定性、定量检测,测量和计算靶血管的血管面积、管腔面积、斑块面积、斑块负荷、偏心指数及重构指数,识别出易损斑块,同时用放射免疫法检测两组患者血浆ET水平并进行比较分析。
【结果】:
1.ACS组和SAP组患者血浆ET水平均高于正常值,且两组患者血浆ET水平比较有显著性差异(P=0.001,P＜0.05),ACS组患者血浆ET水平明显高于SAP组患者。
2.稳定性斑块组和易损斑块组患者血浆ET水平比较有显著性差异(P=0.001,P＜0.05),易损斑块组患者血浆ET水平明显高于稳定性斑块组患者。
3.正性重构组与负性重构组患者比较有显著性差异(P=0.000,P＜0.05),正性重构组患者血浆ET水平明显高于负性重构组患者;正性重构组与无重构组患者比较无显著性差异(P=0.053,P＞0.05);无重构组与负性重构组患者比较无显著性差异(P=0.100,P＞0.05)。
4.偏心斑块组患者和向心斑块组患者血浆ET水平比较有显著性差异(P=0.001,P＜0.05),偏心斑块组患者血浆ET水平明显高于向心斑块组患者血浆ET水平。
5.不同组的冠脉病变支数及狭窄程度与血浆ET水平比较均无显著性差异(P＞0.05)。
【结论】:
1.ET水平在ACS患者中高于SAP患者和正常人。
2.ET水平在易损斑块组患者中高于稳定斑块组患者。
3.ET水平在正性重构组患者中高于负性重构组患者。
4.ET水平与冠脉病变支数、狭窄程度可能无明显相关。
[objective]: Discussion on the relationships between endothelin and the development of acute coronary syndrome(ACS)、vulnerable plaque, and then the relationships between endothelin and coronary remodeling、degree of coronary artery stenosis were also explored.
[Material and Methods]: IVUS was used to examine the coronary lesions in15 cases of acute coronary syndrome (ACS) patients and 15 cases of stable angina pectoris (SAP) patients who remittal to the First Affiliated Hospital of Kunming Medical College from January 2007 to April 2008. We measured the coronary lesions with IVUS to evaluate quality and quantity respectivly in order to identify vulnerable plaque. And then the external elastic membrane area、lumen area、plaque area、and plaque load were all measured and calculated. And the eccentric index and remodeling index of the target vessel were also calculated. In the mean time, we also detected blood plasma ET levels by radioimmunoassay in the two groups of patients. Meanwhile, comparison analysis between them was performed.
[Results]: (1). The ACS group patients and the SAP patients had higher blood plasma ET level than the normal, and the blood plasma ET levels in the ACS group patients were significantly higher than the SAP group patients(P<0.05). (2). Comparison on blood plasma ET levels between the stable plaque group and vulnerable plaque group, we found that the blood plasma ET levels in the vulnerable plaque group were significantly higher than the stable plaque group(P<0.05). (3). There were significant differences between the positive remodeling group and the negative remodeling group (P<0.05), the blood plasma ET levels in the positive remodeling group were significantly higher than the negative remodeling group. (4).
The blood plasma ET levels in the eccentric plaque group patients were significantly higher than the endocentric plaque group. (5) .There were not any significant difference between the blood plasma ET levels and coronary lesions count and the different degree of stenosis.
[Conclusion]: The blood plasma ET levels in the ACS group patients werehigher than the SAP group and the normal. Meanwhile, the blood plasma ET levels in the vulnerable plaque group patients were higher than the stable plaque group, and the positive remodeling group patients were higher than the negative remodeling group.
探讨内皮素(ET)与急性冠脉综合征(ACS)、易损斑块的发生发展及冠脉重构、狭窄程度的关系。
【资料和方法】:
对2007年1月至2008年4月间在昆明医学院第一附属医院住院的15例急性冠脉综合征(ACS)患者和15例稳定性心绞痛(SAP)患者行IVUS检查,对所检查的罪犯病变血管进行定性、定量检测,测量和计算靶血管的血管面积、管腔面积、斑块面积、斑块负荷、偏心指数及重构指数,识别出易损斑块,同时用放射免疫法检测两组患者血浆ET水平并进行比较分析。
【结果】:
1.ACS组和SAP组患者血浆ET水平均高于正常值,且两组患者血浆ET水平比较有显著性差异(P=0.001,P＜0.05),ACS组患者血浆ET水平明显高于SAP组患者。
2.稳定性斑块组和易损斑块组患者血浆ET水平比较有显著性差异(P=0.001,P＜0.05),易损斑块组患者血浆ET水平明显高于稳定性斑块组患者。
3.正性重构组与负性重构组患者比较有显著性差异(P=0.000,P＜0.05),正性重构组患者血浆ET水平明显高于负性重构组患者;正性重构组与无重构组患者比较无显著性差异(P=0.053,P＞0.05);无重构组与负性重构组患者比较无显著性差异(P=0.100,P＞0.05)。
4.偏心斑块组患者和向心斑块组患者血浆ET水平比较有显著性差异(P=0.001,P＜0.05),偏心斑块组患者血浆ET水平明显高于向心斑块组患者血浆ET水平。
5.不同组的冠脉病变支数及狭窄程度与血浆ET水平比较均无显著性差异(P＞0.05)。
【结论】:
1.ET水平在ACS患者中高于SAP患者和正常人。
2.ET水平在易损斑块组患者中高于稳定斑块组患者。
3.ET水平在正性重构组患者中高于负性重构组患者。
4.ET水平与冠脉病变支数、狭窄程度可能无明显相关。
[objective]: Discussion on the relationships between endothelin and the development of acute coronary syndrome(ACS)、vulnerable plaque, and then the relationships between endothelin and coronary remodeling、degree of coronary artery stenosis were also explored.
[Material and Methods]: IVUS was used to examine the coronary lesions in15 cases of acute coronary syndrome (ACS) patients and 15 cases of stable angina pectoris (SAP) patients who remittal to the First Affiliated Hospital of Kunming Medical College from January 2007 to April 2008. We measured the coronary lesions with IVUS to evaluate quality and quantity respectivly in order to identify vulnerable plaque. And then the external elastic membrane area、lumen area、plaque area、and plaque load were all measured and calculated. And the eccentric index and remodeling index of the target vessel were also calculated. In the mean time, we also detected blood plasma ET levels by radioimmunoassay in the two groups of patients. Meanwhile, comparison analysis between them was performed.
[Results]: (1). The ACS group patients and the SAP patients had higher blood plasma ET level than the normal, and the blood plasma ET levels in the ACS group patients were significantly higher than the SAP group patients(P<0.05). (2). Comparison on blood plasma ET levels between the stable plaque group and vulnerable plaque group, we found that the blood plasma ET levels in the vulnerable plaque group were significantly higher than the stable plaque group(P<0.05). (3). There were significant differences between the positive remodeling group and the negative remodeling group (P<0.05), the blood plasma ET levels in the positive remodeling group were significantly higher than the negative remodeling group. (4).
The blood plasma ET levels in the eccentric plaque group patients were significantly higher than the endocentric plaque group. (5) .There were not any significant difference between the blood plasma ET levels and coronary lesions count and the different degree of stenosis.
[Conclusion]: The blood plasma ET levels in the ACS group patients werehigher than the SAP group and the normal. Meanwhile, the blood plasma ET levels in the vulnerable plaque group patients were higher than the stable plaque group, and the positive remodeling group patients were higher than the negative remodeling group.
引文
[1].Mielniczuk LM,Pfeffer MA,Lewis E F,et al.Estimated glomerular filtration rate,Inflammation,and cardiovascular events after an acute coronary syndrome[J].Am Heart,2008,155(4):725-731.
[2].Shah PK.Pathophysiology of coronary thrombosis role of plaque rupture and plaque erosion[J].Progress in Cardiovascular,2007,64(5):857-868.
[3].Yanagisawa M,Kurihara H,Kimura S,et al.A novel potent vasoconstrictor peptide produced by vascular endothelail cells[J].Nature,1988,332:411-415.
[4].Artigou J Y,Salloum J,Carayon A,et al.Variations in plasma endothelin concentrations during coronary spasm[J].Eur Heart,1993,14:780-784.
[5].Rioufol G,Finet G,Ginon G,et al.Multiple atherosclerotic plaque in acute coronary syndrome:a three-vessel intravascular ultrasound study[J].Circulation,2007,115(3)3453-52.
[6].Scherder D,Man F D,Herregods M C,et al.Intravascular ultrasound versus angiography for measurement of luminal diameters in normal and diseased coronary arteries[J].Am Heart,1994,127(2):243.
[7].Novakovic M,Boulauger C M,Luscher T F,et al.Effects of aggregation platelets on the release of endothelin from intact procine coronary artery[J].Circulation,1991,84:6276-29.
[8].Ray S G,Qiu S,et al.Circulating endothelin in acute ischemic syndromes[J].Br Heart,1992,67:388.
[9].Stewart D J,Kubac G,Costello K B,et al.Increased plasma endothelin-1 in the early hours of acute myocardial infarction[J].Am Coll Cardiol,2007,48(1):38-43.
[10].马中富,汪宗芳,马虹等.不同类型冠心病患者血浆内皮素变化的Meta 分析[J].中国危重病急救医学,2000,11:677-680.
[11].Taylor A J,Bobik A,Richards M,et al.Myocardial endothelin-1 release and indices of inflammation during angioplasty for acute myocardial infarction and stable coronary artery disease[J].Am Heart,2004,148(2):1012-1016.
[12].扎拥,贾国良,张正顺等.内皮素与冠心病患者冠状动脉病变的相关性研究[J].Chin Heart J,2001,13(5):383-387.
[13].Falk E,Shah P,Fuster V,et al.Coronary plaque disruption[J].Circulation,1995,92:657-671.
[14].Kaur S,Frishman W H,Singh I,et al.Endothelin as a therapeutic target in the treatment of cardiovascular disease[J].Heart Dis,2001,3(3):1761-88.
[15]. Traupe T, Ortmann J, Munter K, et al. Endothelial therapy of atherosclerosis and its risk factors [J]. Curr Vasc Pharmacol,2003,1(2): 111-121.
[16]. Shah PK. Mechanisms of plaque vulnerability and rupture[J]. Am Coll Cardiol, 2006,46(4): 15-22.
[17]. Rich S, Mclaughlin V V. Endothelin and receptor blockers in cardiovascular disease[J]. Circulation,2007, 115:784-790.
[18]. Kasuya T, Takuwa Y, Yanagisawa M, et al. Endothelin induces vasoconstrictor through two functionally distant pathways in porcine coronary contribution of phosphoinostide turnover[j]. Biochem Biophys Res Commum,1989, 111:1049.
[19]. Siegfried M R, Nihikibe M, Widimsky J, et al. Direct positive inotropic and vasoconstrictor effects of endothelin[J].Heart Vessels, 1990,5:146.
[20]. Bacon C R, Carry N R, Avenport AP, et al. Distribution of endothelin receptors in atherosclerotic human coronary artery[J].Cardiovas Pharmacol,2006,58: 1058-1062.
[21]. Naghvi M, Libby P. Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies [J].Part I. Circulation,2003,108(10):1664-1672.
[22]. Felton C V, Crook D, Davies M J. et al. Relation of plaque lipid composition and morphology to the stability of human aortic plaque[J]. Arterioscler Thromb Vasc Biol, 1997,17:1337-1345.
[23]. Loree H M, Kamm R D, Stringfellow R G, et al. Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels[J].Circ Res,2004,151:1921-1925.
[24]. Ward MR, Pasterkamp G, Yeung AC, et al. Arterial remodeling:mechanisms and clinical implications[J]. Circulation,2000,102:1986-1991.
[25]. Imoto K, Hiro T, Fujii T, et al. Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging[J].Vasc Res,2007,56(8):1007-1015.
[26]. Hasdai D, Holmes D R, Nakaki T, et al. Mechanical pressure and stretch release endothelin-1 from human atherosclerotic coronary arteries in vivo[J]. Circulation,1997,95(2):357-362.
[27]. Nakaki T, Nakagama M, Yamamoto, et al. Endothelin mediated stimulation of DNA synthesis in vascular smooth muscle[J]. Biochem Biophy Res Commun, 1989, 158:880-883.
[28]. Camsari A, Pekdemit H, Cieek D, et al. Endothelin-1 and nitric oxide concentrations and their response to exercise in patients with slow coronary flow[J].Clin Patho. 2006,59:232-239.
[29]. LermanA, Cannon CR, Higano SH, et al. Coronary vascular remodeling in association with endothelial dysfunction [J]. Am J Cardiol, 1998,81: 1105-1109.
[30]. Britten MB, Zeiher AM, Schachinger V. Effects of cardiovascular risk factors on coronary artery remodeling in patients with mild atherosclerosis [J]. Coron Artery Dis, 2003,24: 415-422.
[31]. Lerman A, Edwards BS, Hallett JW, et al. Circulation and tissue endothelin immunoreactivity in advanced atherosclerosis[JJ. N Engl J Med, 1991, 325(10):997-1001.
[32]. Lanza GA, Bencardino G, Sestito A, et al. Association of endothelin-1 with transient myocardial ischemia in patients with unstable angina pectoris[J]. Am J Cardiol, 2005, 95(4):492-494.
[1].Glagov S, Weisenberg E, Zarins CK, et al. Compensatory enlargement of human atherosclerotic coronary arteries[J ]. N Engl J Med, 1987, 316: 1371-1375.
[2].Fussel RT, Kranenberg E, Kiausch U, et al.Vascular remodeling in atherosclerotic coronary arteries is affected by plaque composition [J]. Coron Artery Dis, 2001,12: 91-97.
[3].Hasegawa T, Ehara S, Kataoka T, et al. Acute myocardial infarction: clinical characteristics and plaque morphology between expansive remodeling and constrictiveremodeling by intravascular ultrasound J]. AmHeart J, 2006,151 (2):332-337.
[4].Mcleod AL, Newby DE, Northridge DB, et al. Influence of differential vascular remodeling on coronary vasomotor response [J]. Cardiovasc Res,2003, 59: 520-526.
[5].Ward MR, Pasterkamp G, Yeung AC, et al. Arterial remodeling: mechanisms and clinical implications [J]. Circulation, 2000,102: 1986-1991.
[6].Rudic RD, Shesely EG, Maeda N, etal. Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling[J]. J Clin Invest, 1998,101: 317-336.
[7].Britten MB, Zeiher AM, Schachinger V. Effects of cardiovascular risk factors on coronary artery remodeling in patients with mild atherosclerosis [J]. Coron Artery dis, 2003,24: 415-422.
[8].LermanA, Cannon CR, Higano SH, et al. Coronary vascular remodeling in association with endothelial dysfunction [J]. Am J Cardiol, 1998,81: 51-59.
[9].Tronc F, Wassef M, Esposito B, et al. Role of NO in flow-induced remodeling of the rabbit common carotid artery [J]. Arterioscler Thromb Vasc Biol, 1996, 16:561-562.
[10].Daniel RR, Mariarosaria B, Darid F, et al. Temporal events underlying arterial remodeling after chronic flow reduction in mice: correlation of structural changes with a deficit in basal nitric oxide synthesis [J].Circulation, 2000, 86:101-106.
[11].Tsuruda T, Kato J, Matsui E, et al. Adrenomedullin alleviates not only neointimal formation but also peri vascular hyperplasia following arterial injury in rats[J]. EurJ Pharmacol, 2005, 508 (13): 12-14.
[12].Lau AK, Leichtweis SB, Hume P, et al. Probucol promotes functional reendothelialization in balloon-injured rabbit aortas[J], Circulation, 2003,107: 31-36.
[13].Lusis AJ. Atherosclerosis[J]. Nature,2000,407:32-41.
[14]. Fujii K,Carlier SG. Minta GS, et al. Association of plaque characterization by intravascular ultrasound virtual histology and arterial remodeling[J].Am J Cardiol,2005,96(11):76-83.
[15]. Biasucci LM, Liuzzo G, Grillo RL, et al. Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability [J]. 1999,99:558-560.
[16]. Pasterkamp G, Galis ZS, Kleijn DP. Expansive arterial remodeling: Location [J ].Arterioscler Thromb VascBiol, 2004, 24: 506-507.
[17]. Pasterkamp G, Fitzgerald PF, de-Kleijn DP. Atherosclerotic expansive remodeled plaques: a wolf in sheep's clothing[J]. J Vasc Res,2002,39: 514-523.
[18]. Imoto K, Hiro T, Fujii T, et al.Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging [J]. J Vasc Res, 2007,56(8): 1507-1515.
[19]. Galis ZS, Khatri JJ. Matrix metallop roteinases in vascular remodeling and athrogenesis: the good, the bad, and the ugly[J]. Circ Res, 2002,90: 512-516.
[20]. Dangas G, Mintz GS, Mehran R,et al. Preintervention arterial remodeling as an independent predictor of target-lesion revascularization after nonstent coronary intervention : 777 lesions with intravascular ultrasound imaging [J].Circulation,1999, 99: 93-104.
[21]. Gyongyosi M, Yang P, Hassan A, et al.Intravascular ultrasound predictors of major adverse cardiac events in patients with unstable angina[J]. Clin Cardiol, 2000,23:75-79.
[22].Tardif Jc.Atherosclerosis imaging[J].Can J Cardiol,2005,21(12): 1035-1039.
[23]. Smits PC, Bos L, Quarles Van Ufford MA,et al. Shinkage of human coronary arteries is an important determinant of the novo atherosclerotic luminal stenosis:an in vivo intravascular ultrasound study [J] .heart, 1998,79:1431 -1437.
[24]. Rioufol G, Finet G, Ginon I,et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study [J].circulation, 2002,106:48-58.
[25]. Schoenhagen P, Tuzcu EM, Apperson-Hansen C,et al. Determinants of arterial wall remodeling during lipid-lowering therapy:serial intravascular ultrasound observations from the reversal of atherosclerosis with aggressive lipid lowering therapy(REVERSAL)trial[J]. Circulation, 2006,113(24):26-39.
[26]. Hong MK, Mintiz GS, Lee CW.et al. Comparison of coronary plaque rupture between stable angia and acute myocardial infarction:a three-vessel intravascular ultrasound study in 235 patients[J].Circulation,2004,110:281-283.
[27]. Wexberg P, Gyongyosi M, Sperker W.et al. Per-existing arterial remodeling is associated with in-hospital and late adverse cardiac events after coronary interventions in patients with stable angina pectoris[J]. Am Coll Cardiol,2000,36:1860 -1869.
[28]. Sousa JE, Costa MA, Sousa AG, et al. Two-year angiographic and intravascular ultrasound follow-up after implantation of sirolimus-eluting stents in human coronary arteries[J].2003,107(3):813-814.
[29]. Mintz Ds, Kovach JA.Pichard AD, et al.Geometric remodeling is the predominant mechanism of clinical restenosis after coronary angioplasty. Am Coll Cardiol,1994,138:923-926.
[30]. Clark DJ, Lessio S, O'Donoghue M,Tsalamandris C,et al. Mechanisms and predictors of carotid artery stent restenosis: a serial intravascular ultrasound study[J]. Am Coll Cardiol, 2006,47(12):902-906.
[31]. Kimura T, Kaburagi S.Tamura T.et al. Remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy. Circulation, 1997,96:475.
[2].Shah PK.Pathophysiology of coronary thrombosis role of plaque rupture and plaque erosion[J].Progress in Cardiovascular,2007,64(5):857-868.
[3].Yanagisawa M,Kurihara H,Kimura S,et al.A novel potent vasoconstrictor peptide produced by vascular endothelail cells[J].Nature,1988,332:411-415.
[4].Artigou J Y,Salloum J,Carayon A,et al.Variations in plasma endothelin concentrations during coronary spasm[J].Eur Heart,1993,14:780-784.
[5].Rioufol G,Finet G,Ginon G,et al.Multiple atherosclerotic plaque in acute coronary syndrome:a three-vessel intravascular ultrasound study[J].Circulation,2007,115(3)3453-52.
[6].Scherder D,Man F D,Herregods M C,et al.Intravascular ultrasound versus angiography for measurement of luminal diameters in normal and diseased coronary arteries[J].Am Heart,1994,127(2):243.
[7].Novakovic M,Boulauger C M,Luscher T F,et al.Effects of aggregation platelets on the release of endothelin from intact procine coronary artery[J].Circulation,1991,84:6276-29.
[8].Ray S G,Qiu S,et al.Circulating endothelin in acute ischemic syndromes[J].Br Heart,1992,67:388.
[9].Stewart D J,Kubac G,Costello K B,et al.Increased plasma endothelin-1 in the early hours of acute myocardial infarction[J].Am Coll Cardiol,2007,48(1):38-43.
[10].马中富,汪宗芳,马虹等.不同类型冠心病患者血浆内皮素变化的Meta 分析[J].中国危重病急救医学,2000,11:677-680.
[11].Taylor A J,Bobik A,Richards M,et al.Myocardial endothelin-1 release and indices of inflammation during angioplasty for acute myocardial infarction and stable coronary artery disease[J].Am Heart,2004,148(2):1012-1016.
[12].扎拥,贾国良,张正顺等.内皮素与冠心病患者冠状动脉病变的相关性研究[J].Chin Heart J,2001,13(5):383-387.
[13].Falk E,Shah P,Fuster V,et al.Coronary plaque disruption[J].Circulation,1995,92:657-671.
[14].Kaur S,Frishman W H,Singh I,et al.Endothelin as a therapeutic target in the treatment of cardiovascular disease[J].Heart Dis,2001,3(3):1761-88.
[15]. Traupe T, Ortmann J, Munter K, et al. Endothelial therapy of atherosclerosis and its risk factors [J]. Curr Vasc Pharmacol,2003,1(2): 111-121.
[16]. Shah PK. Mechanisms of plaque vulnerability and rupture[J]. Am Coll Cardiol, 2006,46(4): 15-22.
[17]. Rich S, Mclaughlin V V. Endothelin and receptor blockers in cardiovascular disease[J]. Circulation,2007, 115:784-790.
[18]. Kasuya T, Takuwa Y, Yanagisawa M, et al. Endothelin induces vasoconstrictor through two functionally distant pathways in porcine coronary contribution of phosphoinostide turnover[j]. Biochem Biophys Res Commum,1989, 111:1049.
[19]. Siegfried M R, Nihikibe M, Widimsky J, et al. Direct positive inotropic and vasoconstrictor effects of endothelin[J].Heart Vessels, 1990,5:146.
[20]. Bacon C R, Carry N R, Avenport AP, et al. Distribution of endothelin receptors in atherosclerotic human coronary artery[J].Cardiovas Pharmacol,2006,58: 1058-1062.
[21]. Naghvi M, Libby P. Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies [J].Part I. Circulation,2003,108(10):1664-1672.
[22]. Felton C V, Crook D, Davies M J. et al. Relation of plaque lipid composition and morphology to the stability of human aortic plaque[J]. Arterioscler Thromb Vasc Biol, 1997,17:1337-1345.
[23]. Loree H M, Kamm R D, Stringfellow R G, et al. Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels[J].Circ Res,2004,151:1921-1925.
[24]. Ward MR, Pasterkamp G, Yeung AC, et al. Arterial remodeling:mechanisms and clinical implications[J]. Circulation,2000,102:1986-1991.
[25]. Imoto K, Hiro T, Fujii T, et al. Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging[J].Vasc Res,2007,56(8):1007-1015.
[26]. Hasdai D, Holmes D R, Nakaki T, et al. Mechanical pressure and stretch release endothelin-1 from human atherosclerotic coronary arteries in vivo[J]. Circulation,1997,95(2):357-362.
[27]. Nakaki T, Nakagama M, Yamamoto, et al. Endothelin mediated stimulation of DNA synthesis in vascular smooth muscle[J]. Biochem Biophy Res Commun, 1989, 158:880-883.
[28]. Camsari A, Pekdemit H, Cieek D, et al. Endothelin-1 and nitric oxide concentrations and their response to exercise in patients with slow coronary flow[J].Clin Patho. 2006,59:232-239.
[29]. LermanA, Cannon CR, Higano SH, et al. Coronary vascular remodeling in association with endothelial dysfunction [J]. Am J Cardiol, 1998,81: 1105-1109.
[30]. Britten MB, Zeiher AM, Schachinger V. Effects of cardiovascular risk factors on coronary artery remodeling in patients with mild atherosclerosis [J]. Coron Artery Dis, 2003,24: 415-422.
[31]. Lerman A, Edwards BS, Hallett JW, et al. Circulation and tissue endothelin immunoreactivity in advanced atherosclerosis[JJ. N Engl J Med, 1991, 325(10):997-1001.
[32]. Lanza GA, Bencardino G, Sestito A, et al. Association of endothelin-1 with transient myocardial ischemia in patients with unstable angina pectoris[J]. Am J Cardiol, 2005, 95(4):492-494.
[1].Glagov S, Weisenberg E, Zarins CK, et al. Compensatory enlargement of human atherosclerotic coronary arteries[J ]. N Engl J Med, 1987, 316: 1371-1375.
[2].Fussel RT, Kranenberg E, Kiausch U, et al.Vascular remodeling in atherosclerotic coronary arteries is affected by plaque composition [J]. Coron Artery Dis, 2001,12: 91-97.
[3].Hasegawa T, Ehara S, Kataoka T, et al. Acute myocardial infarction: clinical characteristics and plaque morphology between expansive remodeling and constrictiveremodeling by intravascular ultrasound J]. AmHeart J, 2006,151 (2):332-337.
[4].Mcleod AL, Newby DE, Northridge DB, et al. Influence of differential vascular remodeling on coronary vasomotor response [J]. Cardiovasc Res,2003, 59: 520-526.
[5].Ward MR, Pasterkamp G, Yeung AC, et al. Arterial remodeling: mechanisms and clinical implications [J]. Circulation, 2000,102: 1986-1991.
[6].Rudic RD, Shesely EG, Maeda N, etal. Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling[J]. J Clin Invest, 1998,101: 317-336.
[7].Britten MB, Zeiher AM, Schachinger V. Effects of cardiovascular risk factors on coronary artery remodeling in patients with mild atherosclerosis [J]. Coron Artery dis, 2003,24: 415-422.
[8].LermanA, Cannon CR, Higano SH, et al. Coronary vascular remodeling in association with endothelial dysfunction [J]. Am J Cardiol, 1998,81: 51-59.
[9].Tronc F, Wassef M, Esposito B, et al. Role of NO in flow-induced remodeling of the rabbit common carotid artery [J]. Arterioscler Thromb Vasc Biol, 1996, 16:561-562.
[10].Daniel RR, Mariarosaria B, Darid F, et al. Temporal events underlying arterial remodeling after chronic flow reduction in mice: correlation of structural changes with a deficit in basal nitric oxide synthesis [J].Circulation, 2000, 86:101-106.
[11].Tsuruda T, Kato J, Matsui E, et al. Adrenomedullin alleviates not only neointimal formation but also peri vascular hyperplasia following arterial injury in rats[J]. EurJ Pharmacol, 2005, 508 (13): 12-14.
[12].Lau AK, Leichtweis SB, Hume P, et al. Probucol promotes functional reendothelialization in balloon-injured rabbit aortas[J], Circulation, 2003,107: 31-36.
[13].Lusis AJ. Atherosclerosis[J]. Nature,2000,407:32-41.
[14]. Fujii K,Carlier SG. Minta GS, et al. Association of plaque characterization by intravascular ultrasound virtual histology and arterial remodeling[J].Am J Cardiol,2005,96(11):76-83.
[15]. Biasucci LM, Liuzzo G, Grillo RL, et al. Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability [J]. 1999,99:558-560.
[16]. Pasterkamp G, Galis ZS, Kleijn DP. Expansive arterial remodeling: Location [J ].Arterioscler Thromb VascBiol, 2004, 24: 506-507.
[17]. Pasterkamp G, Fitzgerald PF, de-Kleijn DP. Atherosclerotic expansive remodeled plaques: a wolf in sheep's clothing[J]. J Vasc Res,2002,39: 514-523.
[18]. Imoto K, Hiro T, Fujii T, et al.Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging [J]. J Vasc Res, 2007,56(8): 1507-1515.
[19]. Galis ZS, Khatri JJ. Matrix metallop roteinases in vascular remodeling and athrogenesis: the good, the bad, and the ugly[J]. Circ Res, 2002,90: 512-516.
[20]. Dangas G, Mintz GS, Mehran R,et al. Preintervention arterial remodeling as an independent predictor of target-lesion revascularization after nonstent coronary intervention : 777 lesions with intravascular ultrasound imaging [J].Circulation,1999, 99: 93-104.
[21]. Gyongyosi M, Yang P, Hassan A, et al.Intravascular ultrasound predictors of major adverse cardiac events in patients with unstable angina[J]. Clin Cardiol, 2000,23:75-79.
[22].Tardif Jc.Atherosclerosis imaging[J].Can J Cardiol,2005,21(12): 1035-1039.
[23]. Smits PC, Bos L, Quarles Van Ufford MA,et al. Shinkage of human coronary arteries is an important determinant of the novo atherosclerotic luminal stenosis:an in vivo intravascular ultrasound study [J] .heart, 1998,79:1431 -1437.
[24]. Rioufol G, Finet G, Ginon I,et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study [J].circulation, 2002,106:48-58.
[25]. Schoenhagen P, Tuzcu EM, Apperson-Hansen C,et al. Determinants of arterial wall remodeling during lipid-lowering therapy:serial intravascular ultrasound observations from the reversal of atherosclerosis with aggressive lipid lowering therapy(REVERSAL)trial[J]. Circulation, 2006,113(24):26-39.
[26]. Hong MK, Mintiz GS, Lee CW.et al. Comparison of coronary plaque rupture between stable angia and acute myocardial infarction:a three-vessel intravascular ultrasound study in 235 patients[J].Circulation,2004,110:281-283.
[27]. Wexberg P, Gyongyosi M, Sperker W.et al. Per-existing arterial remodeling is associated with in-hospital and late adverse cardiac events after coronary interventions in patients with stable angina pectoris[J]. Am Coll Cardiol,2000,36:1860 -1869.
[28]. Sousa JE, Costa MA, Sousa AG, et al. Two-year angiographic and intravascular ultrasound follow-up after implantation of sirolimus-eluting stents in human coronary arteries[J].2003,107(3):813-814.
[29]. Mintz Ds, Kovach JA.Pichard AD, et al.Geometric remodeling is the predominant mechanism of clinical restenosis after coronary angioplasty. Am Coll Cardiol,1994,138:923-926.
[30]. Clark DJ, Lessio S, O'Donoghue M,Tsalamandris C,et al. Mechanisms and predictors of carotid artery stent restenosis: a serial intravascular ultrasound study[J]. Am Coll Cardiol, 2006,47(12):902-906.
[31]. Kimura T, Kaburagi S.Tamura T.et al. Remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy. Circulation, 1997,96:475.