冠状动脉病变的血管内超声研究
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摘要
目的
以血管内超声(IVUS)为研究手段，在介入治疗前对急性冠状动脉综合征(包括急性心肌梗死和不稳定性心绞痛)患者和稳定性心绞痛患者的罪犯病变及近端、远端参考段进行观测，测量各部位的EEM面积、斑块面积、管腔面积，计算斑块负担、重塑指数，确定重塑方向(正性重塑，负性重塑，无重塑)，观察病变性质和特征，并分组进行对比研究，以探讨斑块大小、斑块性质、重塑方向和斑块的形态特征等在动脉粥样硬化发展与消退和急性冠状动脉综合征发生中的作用、与各种临床表现之间的关系和对临床治疗的指导意义。
研究对象与方法
1、在冠状动脉介入治疗前对73例冠心病患者进行血管内超声检查，男55例，女18例，年龄57.37±10.59岁(范围：23～73岁)。根据临床表现将入选病人分为三组：包括急性心肌梗死(AMI)组，共27例；不稳定型心绞痛(UAP)组，共22例；稳定型心绞痛(SAP)组，共24例。急性冠状动脉综合征(ACS)组共49例，为急性心肌梗死患者27例+不稳定型心绞痛患者22例。收集病人的临床资料，测定血糖、血清磷酸肌酸激酶(CK)、血清磷酸肌酸激酶同功酶(CKMB)、血清胆固醇(TC)、高密度脂蛋白胆固醇(HDL)、低密度脂蛋白胆固醇(LDL)、极低密度脂蛋白胆固醇(VLDL)、血清甘油三酯(TG)、载脂蛋白A1(APOA1)、载脂蛋白B(APOB)、脂蛋白a(Lpa)水平。血清胆固醇水平＞5.7mmol／l为高胆固醇血症，血清甘油三酯水平＞1.69mmol／l为高甘油三酯血症。稳定性心绞痛定义为6周内心绞痛频率、持续时间和强度无改变，不稳定性心绞痛定义为新发生的严重心绞痛、加重的心绞痛和休息时心绞痛，急性心肌梗死为3周内发生的心肌梗死。
2、按Judkins法将造影导管分别送到左、右冠状动脉开口，依次行选择性左冠状动脉和右冠状动脉造影，并同步电影记录造影影像，供以后测量分
户
天津医科人学博_卜学位论文
析。常规多体位投照，根据多个投照体位中显示狭窄最严重的造影图像，协
助确定罪犯病变。
3、使用Boston Seientifie Ceivis血管内超声仪，采用3.2Fr 30 MHz超声
导管，应用标准的冠状动脉内介入导管操作技术。在肝素抗凝和冠状动脉内
注射硝酸甘油200陀后，将血管内超声导管通过导引钢丝越过靶病变，放至
靶病变远端，采用自动回撤装置，以lmm/秒的恒定速度自动回撤至病变近
端，并连续录像。再结合手动方式，将IVUS探头放至罪犯病变处，对罪犯
病变及其附近血管段进行反复观测，并将WUS探头固定于罪犯病变处，注
射造影剂，观察造影剂与斑块的关系，观测有无造影剂进入到斑块内。通过
手工描记外膜和内膜的内边缘测量外弹力膜(EEM)面积和管腔面积，斑块
面积为EEM面积减去管腔面积，斑块负担为斑块面积除以EEM面积。对患
者的罪犯病变及近端、远端参考段进行IVUS检查，测量各部位的EEM面积、
管腔面积，计算斑块面积、斑块负担、重塑指数，确定重塑方向，观察病变
性质和特点，并在各组间进行对比研究。
4、IVUS图像分析
①、各项定量指标的测量及定义
(l)、EEM面积:是指血管外弹力膜的横断面积，是手工描记外膜内边
缘，通过计算机自动边缘测量系统测得的。
(2)、管腔面积:是指血管腔的横断面积，是手工描记内膜的内边缘，通
过计算机自动边缘测量系统测得的。
③、斑块面积:为EEM面积减去管腔面积。
(4)、斑块负担(pl叫ue bUrden):为斑块面积+EEM面积X 1 00%。
(5)、罪犯病变:为病变处有最小的管腔直径(MLD)，由冠状动脉造影
协助确定。
(6)、近端参考段:为罪犯病变近端含有最少量斑块且没有分支的部位。
(7)、远端参考段:为罪犯病变远端含有最少量斑块且没有分支的部位。
(8)、动脉重塑计算:重塑指数为病变部位EEM面积与近端参段EEM面
天津医科大学博卜学位论文
积之比，重塑指数>l .05为正性重塑;重塑指数<0.95为负性重塑;重塑指数
在0.95与1.05之间为无重塑。
②、斑块性质的测定:斑块性质是通过目侧病变斑块成分而定的。
(1)、软斑块和硬斑块:软斑块的回声比血管壁外膜的回声弱，硬斑块与
血管壁外膜的回声一致或比血管壁外膜的回声强。软斑块定义为斑块内密度
低于外膜密度的成分占整个斑块的75%或以上，否则为硬斑块。
(2)、钙化斑块:钙化斑块的回声比血管壁外膜的回声强，其后方伴有声
影。浅表钙化:钙化分布在靠近病变的管腔与内膜交界侧，趴离管腔较近，
管腔与钙化之间看不到斑块。深部钙化:钙化分布在斑块的深层，靠近中层
与外膜交界侧，距离外膜较近。
墓
(3)、偏心斑块:斑块的最厚处与最薄处的厚度比值大于2:1。
(4)、破裂斑块:斑块内有腔洞，表面有撕裂的纤维帽，以注射造影剂时
可见造影剂通过撕裂的纤维帽进入斑块内的腔洞确认。
5、统计学分析
应用SPSS10.0软件进行统计学检验与处理，计量资料川均数士标准差(x
士s)表示。i{，量资料两组间比较采用非配对的t检验:计晕资料多组介lJ比较
采用方差分析(。ne一way ANovA法);计数资料组间比较采川卜力一检验(xZ
检验)。P<0.05为有统计学显著性差异。
结果
1、ACS、AMI、UAP和SAP四组?
Objective
We studied the culprit lesions,proximal and distal reference segments in patients with acute coronary syndromes(included acute myocardial infarctions and unstable angina pectoris) and in patients with stable angina pectoris before interventional therapy,measured the external elastic membrane cross-sectional area and lumen cross-sectional area,and calculated the plaque area, plaque burden, remodeling index and the direction of remodeling of each site, and compared the characteristics of each group to investigate the morphological and remodeling characteristics of coronary lesions in vivo with intravascular ultrasound, and to explore the relationship between plaque size,arterial remodeling ,lesion characteristics and clinical presentations.
Methods
1 73 cases of patients with coronary artery disease were studied using intravascular ultrasound before coronary intervention,55 cases were male, 18 cases were female,aged as 57.37+ 10.59 years(ranged 23 to 73 years).The patients were divided into three groups according to the clinical presentations:including the group of acute myocardial infarction, 27 cases; the group of unstable angina pectoris,22 cases; the group of stable angina pectoris,24 cases. The lesion site and a proximal reference site were analyzed .The external elastic membrane cross-sectional area and lumen cross-sectional area were measured,and the plaque area, plaque burden, remodeling index were calculated , and the direction of remodeling were determined. The characteristics of each group were compared.
2 The selective coronary angiographys were performed according to the
Judkins method,multiple projection views were taken.
3 All IVUS studies were performed before any intervention and after the intracoronary administration of nitroglycerin 200 ug using a commercially available system (Boston Scientific Corp Ceivis ). The IVUS catheter was advanced distally to the lesion, and retrograde imaging was performed back to the proximally to the lesion (motorized pullback speed of 1 mm/s). The external elastic membrane and minimum lumen cross-sectional area (the minimum lumen area site) of the lesion sites and the proximal and distal reference sites were identified and measured. Plaque area was external elastic membrane cross-sectional area minus lumen cross-sectional area, plaque burden was plaque area divided by the external elastic membrane cross-sectional area.
4 The calculation of remodeling index: The remodeling index was lesion external elastic membrane area divided by the proximal reference external elastic membrane cross-sectional area. We defined positive remodeling as a remodeling index of >1.05,negative remodeling as a remodeling index of <0.95, and neutral remodeling as a remodeling index between 0.95 and 1.05.
5 The characterization of plaque: The characterization of plaque was qualitatively analysed according to the plaque composition. Hypoechoic plaque was less bright than the adventitia. Hyperechoic, noncalcified plaque was as bright or brighter than the adventitia without shadowing. Hyperechoic, calcified plaque was as bright or brighter than the adventitia with shadowing. Hypoechoic lesion within a plaque was >75% of the plaque , the plaque was considered "soft",otherwise, the plaque was considered "hard".
Results
1 There was no significantly differences among plaque area in ACS AMI UAP and SAPgroups.The plaque burden was significantly greater at culprit lesions in patients with acute coronary syndromes than in patients with stable
angina pectoris
2 The remodeling index was significantly greater in patients with acute coronary syndromes than in patients with stable angina pectoris(0.97 + 0.23 versus 0.79+0.13; P=0.003).The distribution of remodeling index in these two groups was different, Positive remodeling was more frequent in patients with acute coronary syndromes than in patients with stable angina pectoris (34.69% versus 4.17%,P=0.038), whereas negative remodeling was more frequent in stable angina pectoris (91.67% versus 46.94 % ,P=0.000).
3 The remodeling
以血管内超声(IVUS)为研究手段，在介入治疗前对急性冠状动脉综合征(包括急性心肌梗死和不稳定性心绞痛)患者和稳定性心绞痛患者的罪犯病变及近端、远端参考段进行观测，测量各部位的EEM面积、斑块面积、管腔面积，计算斑块负担、重塑指数，确定重塑方向(正性重塑，负性重塑，无重塑)，观察病变性质和特征，并分组进行对比研究，以探讨斑块大小、斑块性质、重塑方向和斑块的形态特征等在动脉粥样硬化发展与消退和急性冠状动脉综合征发生中的作用、与各种临床表现之间的关系和对临床治疗的指导意义。
研究对象与方法
1、在冠状动脉介入治疗前对73例冠心病患者进行血管内超声检查，男55例，女18例，年龄57.37±10.59岁(范围：23～73岁)。根据临床表现将入选病人分为三组：包括急性心肌梗死(AMI)组，共27例；不稳定型心绞痛(UAP)组，共22例；稳定型心绞痛(SAP)组，共24例。急性冠状动脉综合征(ACS)组共49例，为急性心肌梗死患者27例+不稳定型心绞痛患者22例。收集病人的临床资料，测定血糖、血清磷酸肌酸激酶(CK)、血清磷酸肌酸激酶同功酶(CKMB)、血清胆固醇(TC)、高密度脂蛋白胆固醇(HDL)、低密度脂蛋白胆固醇(LDL)、极低密度脂蛋白胆固醇(VLDL)、血清甘油三酯(TG)、载脂蛋白A1(APOA1)、载脂蛋白B(APOB)、脂蛋白a(Lpa)水平。血清胆固醇水平＞5.7mmol／l为高胆固醇血症，血清甘油三酯水平＞1.69mmol／l为高甘油三酯血症。稳定性心绞痛定义为6周内心绞痛频率、持续时间和强度无改变，不稳定性心绞痛定义为新发生的严重心绞痛、加重的心绞痛和休息时心绞痛，急性心肌梗死为3周内发生的心肌梗死。
2、按Judkins法将造影导管分别送到左、右冠状动脉开口，依次行选择性左冠状动脉和右冠状动脉造影，并同步电影记录造影影像，供以后测量分
户
天津医科人学博_卜学位论文
析。常规多体位投照，根据多个投照体位中显示狭窄最严重的造影图像，协
助确定罪犯病变。
3、使用Boston Seientifie Ceivis血管内超声仪，采用3.2Fr 30 MHz超声
导管，应用标准的冠状动脉内介入导管操作技术。在肝素抗凝和冠状动脉内
注射硝酸甘油200陀后，将血管内超声导管通过导引钢丝越过靶病变，放至
靶病变远端，采用自动回撤装置，以lmm/秒的恒定速度自动回撤至病变近
端，并连续录像。再结合手动方式，将IVUS探头放至罪犯病变处，对罪犯
病变及其附近血管段进行反复观测，并将WUS探头固定于罪犯病变处，注
射造影剂，观察造影剂与斑块的关系，观测有无造影剂进入到斑块内。通过
手工描记外膜和内膜的内边缘测量外弹力膜(EEM)面积和管腔面积，斑块
面积为EEM面积减去管腔面积，斑块负担为斑块面积除以EEM面积。对患
者的罪犯病变及近端、远端参考段进行IVUS检查，测量各部位的EEM面积、
管腔面积，计算斑块面积、斑块负担、重塑指数，确定重塑方向，观察病变
性质和特点，并在各组间进行对比研究。
4、IVUS图像分析
①、各项定量指标的测量及定义
(l)、EEM面积:是指血管外弹力膜的横断面积，是手工描记外膜内边
缘，通过计算机自动边缘测量系统测得的。
(2)、管腔面积:是指血管腔的横断面积，是手工描记内膜的内边缘，通
过计算机自动边缘测量系统测得的。
③、斑块面积:为EEM面积减去管腔面积。
(4)、斑块负担(pl叫ue bUrden):为斑块面积+EEM面积X 1 00%。
(5)、罪犯病变:为病变处有最小的管腔直径(MLD)，由冠状动脉造影
协助确定。
(6)、近端参考段:为罪犯病变近端含有最少量斑块且没有分支的部位。
(7)、远端参考段:为罪犯病变远端含有最少量斑块且没有分支的部位。
(8)、动脉重塑计算:重塑指数为病变部位EEM面积与近端参段EEM面
天津医科大学博卜学位论文
积之比，重塑指数>l .05为正性重塑;重塑指数<0.95为负性重塑;重塑指数
在0.95与1.05之间为无重塑。
②、斑块性质的测定:斑块性质是通过目侧病变斑块成分而定的。
(1)、软斑块和硬斑块:软斑块的回声比血管壁外膜的回声弱，硬斑块与
血管壁外膜的回声一致或比血管壁外膜的回声强。软斑块定义为斑块内密度
低于外膜密度的成分占整个斑块的75%或以上，否则为硬斑块。
(2)、钙化斑块:钙化斑块的回声比血管壁外膜的回声强，其后方伴有声
影。浅表钙化:钙化分布在靠近病变的管腔与内膜交界侧，趴离管腔较近，
管腔与钙化之间看不到斑块。深部钙化:钙化分布在斑块的深层，靠近中层
与外膜交界侧，距离外膜较近。
墓
(3)、偏心斑块:斑块的最厚处与最薄处的厚度比值大于2:1。
(4)、破裂斑块:斑块内有腔洞，表面有撕裂的纤维帽，以注射造影剂时
可见造影剂通过撕裂的纤维帽进入斑块内的腔洞确认。
5、统计学分析
应用SPSS10.0软件进行统计学检验与处理，计量资料川均数士标准差(x
士s)表示。i{，量资料两组间比较采用非配对的t检验:计晕资料多组介lJ比较
采用方差分析(。ne一way ANovA法);计数资料组间比较采川卜力一检验(xZ
检验)。P<0.05为有统计学显著性差异。
结果
1、ACS、AMI、UAP和SAP四组?
Objective
We studied the culprit lesions,proximal and distal reference segments in patients with acute coronary syndromes(included acute myocardial infarctions and unstable angina pectoris) and in patients with stable angina pectoris before interventional therapy,measured the external elastic membrane cross-sectional area and lumen cross-sectional area,and calculated the plaque area, plaque burden, remodeling index and the direction of remodeling of each site, and compared the characteristics of each group to investigate the morphological and remodeling characteristics of coronary lesions in vivo with intravascular ultrasound, and to explore the relationship between plaque size,arterial remodeling ,lesion characteristics and clinical presentations.
Methods
1 73 cases of patients with coronary artery disease were studied using intravascular ultrasound before coronary intervention,55 cases were male, 18 cases were female,aged as 57.37+ 10.59 years(ranged 23 to 73 years).The patients were divided into three groups according to the clinical presentations:including the group of acute myocardial infarction, 27 cases; the group of unstable angina pectoris,22 cases; the group of stable angina pectoris,24 cases. The lesion site and a proximal reference site were analyzed .The external elastic membrane cross-sectional area and lumen cross-sectional area were measured,and the plaque area, plaque burden, remodeling index were calculated , and the direction of remodeling were determined. The characteristics of each group were compared.
2 The selective coronary angiographys were performed according to the
Judkins method,multiple projection views were taken.
3 All IVUS studies were performed before any intervention and after the intracoronary administration of nitroglycerin 200 ug using a commercially available system (Boston Scientific Corp Ceivis ). The IVUS catheter was advanced distally to the lesion, and retrograde imaging was performed back to the proximally to the lesion (motorized pullback speed of 1 mm/s). The external elastic membrane and minimum lumen cross-sectional area (the minimum lumen area site) of the lesion sites and the proximal and distal reference sites were identified and measured. Plaque area was external elastic membrane cross-sectional area minus lumen cross-sectional area, plaque burden was plaque area divided by the external elastic membrane cross-sectional area.
4 The calculation of remodeling index: The remodeling index was lesion external elastic membrane area divided by the proximal reference external elastic membrane cross-sectional area. We defined positive remodeling as a remodeling index of >1.05,negative remodeling as a remodeling index of <0.95, and neutral remodeling as a remodeling index between 0.95 and 1.05.
5 The characterization of plaque: The characterization of plaque was qualitatively analysed according to the plaque composition. Hypoechoic plaque was less bright than the adventitia. Hyperechoic, noncalcified plaque was as bright or brighter than the adventitia without shadowing. Hyperechoic, calcified plaque was as bright or brighter than the adventitia with shadowing. Hypoechoic lesion within a plaque was >75% of the plaque , the plaque was considered "soft",otherwise, the plaque was considered "hard".
Results
1 There was no significantly differences among plaque area in ACS AMI UAP and SAPgroups.The plaque burden was significantly greater at culprit lesions in patients with acute coronary syndromes than in patients with stable
angina pectoris
2 The remodeling index was significantly greater in patients with acute coronary syndromes than in patients with stable angina pectoris(0.97 + 0.23 versus 0.79+0.13; P=0.003).The distribution of remodeling index in these two groups was different, Positive remodeling was more frequent in patients with acute coronary syndromes than in patients with stable angina pectoris (34.69% versus 4.17%,P=0.038), whereas negative remodeling was more frequent in stable angina pectoris (91.67% versus 46.94 % ,P=0.000).
3 The remodeling
引文
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3. Nissen SE, Grines CL, Gurley JC, et al. Application of a new phased-array ultrasound imaging catheter in the assessment of vascular dimensions: in vivo comparison to cineangiography. Circulation. 1990;81:660-666.
4. Tobis JM, Mallery J, Mahon D, et al. Intravascular ultrasound imaging of human coronary arteries in vivo: analysis of tissue characterizations with comparison to in vitro histological specimens. Circulation. 1991 ;83:913-926.
5. Nissen SE, Gurley JC, Grines CL, et al. Intravascular ultrasound assessment of lumen size and wall morphology in normal subjects and patients with coronary artery disease. Circulation. 1991 ;84:1087-1099.
6. Isner JM, Kishel J, Kent KM. Accuracy of angiographic determination of left main coronary arterial narrowing. Circulation. 1981 ;63:1056-1061.
7. Steven EN, Paul Y. Intravascular Ultrasound:Novel Pathophysioiogical Insights and Current Clinical Applications.Circulation. 2001; 103:604-616.
8. Nissen SE, Gurley JC. Application of intravascular ultrasound to detection and quantitation of coronary atherosclerosis. Int J Card Imaging 1991 ;6:165-77.
9. Fuster V, Badimon L,Badimon JJ,et al.The pathogenesis of coronary artery disease and the acute coronary syndromes.N Engl J Med 1987;316:1371-1373
10. Qiao JH,Fishbein MC.The severity of coronary atherosclerosis at site of plaque rupture with occlusive thrombosis.J Am Coll Cardiol
1991;17:1138-1142.
11. Fishbein MC,Siegel RJ.How big are coronary atherosclerotic plaques that rupture?Circulation 1996;94:2662-2666.
12. Mann JM,Davies MJ.Assessment of the severity of coronary artery disease at postmortem examination.Are the measurements clinically valid?Br Heart J 1995;74:528-530.
13. von Birgelen C,Airiian SG,Mintz GS,et al.Variations of remodeling in response to left main atherosclerosis assessed with intravascular ultrasound in vivo.Am J Cardiol 1997;80:1408-1413.
14. Smits PC,Pasterkamp G, de Jaegere PPT, et al.Angioscopic complex lesions are predominantly compensatory enlarged:an angioscopic and intravascular ultrasound sdudy.Cardiovasc Res 1999;41:458-464.
15. Glagov S,Weisenberg E,Zarins CK,et al.Compensatory enlargement of human atherosclerotic coronary arteries.N Engl J Med 1987;316:1371-1375
16. McPherson DD,Sirna SJ,Hiratzka LF, et al.Coronary arterial remodeling studied by high-frequency epicardial echocardiography.J Am Coll Cardiol 1991; 17:79-86
17. Nishioka T, Luo H,Eigler NL,et al.Contribution of inadequate compensatory enlargement of human artery stenosis. J Am Coll Cardiol 1996;27:1571-1576
18. Mintz GS, Nissen SE, Anderson WD, et al. American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol 2001 ;37:1478-92.
19. Galbraith JE, Murphy ML, Desoyza N. Coronary angiogram interpretation: interobserver variability. JAMA. 1981 ;240:2053-2059.
20. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Am J Cardiol. 1979;44:39-44.
21. Topol EJ, Nissen SE. Our preoccupation with coronary luminology: the dissociation between clinical and angiographic findings in ischemic heart disease. Circulation. 1995;92:2333-2342.
22. Detre KM,Wright E,Murphy ML,et al.Observer agreement in evaluating coronary angiograms.Circulation 1975;52:979～986.
23. DeRouen TA,Murray JA,Owen W.Variability in the analysis of coronary arteriograms.Circulation 1997;55:324～328.
24. Fisher LD,Judkins MP, Lesperance J,et al.Reproducibility of coronary arteriographic reading in the Coronary Artery Surgery Study(CASS).Cathet Cardiovasc Diagn 1982;8:565～575.
25. Vlodaver Z,Frech R,Van Tassel RA,et al.Correlation of the antemortem coronary arteriogram and the postmortem specimen.Circulation 1973;47:162～169.
26. Grondin CM,Dyrda I,Pasternac A,et al.Discrepancies between cineangiographic and postmortem findings in patients with coronary artery disease and recent myocardial revascularization.Circulation 1974;49:703～708.
27. Arnett EN,Isner JM,Redwood DR,et al.Coronary artery narrowing in coronary artery disease:comparison of cineangiographic and necropcy findings.Ann Intern Med 1079;91:350～356.
28. Isner JM,Kishel J,Kent KM,et al.Accuracy of angiographic determination of left main coronary artery narrowing: angiographic-histologic correlative analysis in 28 patients.Circulation 1981 ;63: 1056～1064.
29. Dietz WA,Tobis JM,Isner JM.failure of angiography to accurately depict the extent of coronary artery narrowing in three fatal cases of percutaneous
transluminal coronary angioplasty.J Am Coll Cardiol 1992; 19:1261～1270.
30. Davies MJ,Thomas AC.Plaque fissuring:the cause of acute myocardial infarction,sudden ischemic death and crescendo angina.Br Heart J. 1985;53:363～373.
31. Qiao JH,Fishbein MC.The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thombosis.J Am Coll Cardiol. 1991 ;17:1138～1142.
32. Horie T, Sekiguchi M,Hirosawa K.Coronary thombosis in pathogenesis of acute myocardial infarction. Br Heart J. 1978;40:153～161.
33. Liebson PR,Klein LW.Intravascular ultrasound in coronary atherosclerosis:a new approach to clinical assessment.Am Heart J 1992; 123:1643～1660.
34. Di Mario C,The SH,Madretsma S,et al.Detection and characterization of vascular lesions by intravascular ultrasound:an in vitro study correlated with histology.J Am Soc Echocardiogr 1992;5:135～146.
35. Nakamura S,Colombo A,Gaglione A,et al.Intracoronary ultrasound observations during stent implantation.Circulation 1994;89:2026～2034.
36. Colombo A,Hall P, Nakamura S,et al. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation 1995;91: 1676～1688.
37. Ozaki Y, Keane D,Nobuyoshi M,et al.Coronary lumen at six-month follow-up of a new radiopaque Cordis tantalum stent using quantitative angiography and intracoronary ultrasound.Am J Cardiol 1995;76:1135～1143.
38. Topol EJ, Nissen SE. Our preoccupation with coronary luminology: the dissociation between clinical and angiographic findings in ischemic heart disease. Circulation. 1995;92:2333-2342.
39. Erbel R, Ge J, Bockisch A, et al. Value of intracoronary ultrasound and Doppler in the differentiation of angiographically normal coronary arteries: a
prospective study in patients with angina pectoris. Eur Heart J. 1996; 17:880-889.
40. Mintz GS, Painter JA, Pichard AD, et al. Atherosclerosis in angiographically "normal" coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J Am Coll Cardiol. 1995;25:1479-1485
41. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Am J Cardiol. 1979;44:39-44.
42. Lee DY, Eigler N, Luo H, et al. Effect of intracoronary ultrasound imaging on clinical decision making. Am Heart J. 1995;129:1084-1093.
43. Mintz GS, Pichard AD, Kovach JA, et al. Impact of preintervention intravascular ultrasound imaging on transcatheter treatment strategies in coronary artery disease. Am J Cardiol. 1994;73:423-430
44. Shoenhagen P, Ziada K, Kapadia SR, et al. Extent and direction of arterial remodeling in stable versus unstable coronary syndromes: an intravascular ultrasound study. Circulation. 2000; 101:598-603.
45. Ge J,Chirillo F, Schwedtmann J,et al.Screening of ruptured plaques in patients with coronary artery disease by intravascular ultrasound.Heart. 1999;81:621～627.
46. von Birgelen C,Klinkhart W, Mintz GS,et al.Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel:an intravascular ultrasound study in vivo.J Am Coll Cardiol 2001 ;37:1864-1870.
47. Mintz GS, Popma JJ, Pichard AD, et al. Patterns of calcification in coronary artery disease. A statistical analysis of intravascular ultrasound and coronary angiography in 1155 lesions. Circulation. 1995 Apr 1 ;91 (7): 1959-65.
48. Fuchs S, Stabile E, Mintz GS,et al. Intravascular ultrasound findings in patients with acute coronary syndromes with and without elevated troponin Ⅰ
level,Am J Cardiol. 2002 May 1 ;89(9): 1111-3.
49. Duissaillant GR, Mintz GS, Pichard AD, et al. Intravascular ultrasound identification of calcified intraluminal lesions misdiagnosed as thrombi by coronary angiography.Am Heart J. 1996 Sep; 132(3):687-9.
50. Hodgson JM, Reddy KG, Suneja R, et al. Intracoronary ultrasound imaging: correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty. J Am Coll Cardiol. 1993;21:35-44.
51. Kimura T, Kaburagi S, Tamura T, et al. Remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy. Circulation. 1997;96:475-483.
52. Kearney P, Erbel R, Rupprecht HJ, et al. Differences in the morphology of unstable and stable coronary lesions and their impact on the mechanisms of angioplasty: an in vivo study with intravascular ultrasound. Eur Heart J. 1996;17:721-730.
53. Bocksch W, Schartl M, Beckmann S, et al. Intravascular ultrasound imaging in patients with acute myocardial infarction. Eur Heart J. 1995;16(Suppl J):46-52.
54. Siegel RJ, Ariani M, Fishbein MC, et al. Histopathoiogic validation of angioscopy and intravascular ultrasound. Circulation. 1991 ;84:109-117
55. Davies MJ,Thomas AC.Plaque fissuring-the cause of acute myocardial infarction,sudden ischemic death,and crescendo angina.Br Heart J 1985;53:363-373.
56. Davies MJ,Bland MJ,Hangartner WR,et al.Factors influencing the presence or absence of acute coronary thrombi in sudden ischemic death.Eur Heart J 1989; 10:203-208.
57. Falk E.Why do plaques rupture?Circulation 1992;86(suppl):30-42.
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59. Giroud D,Li JM,Urban P, et al.Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis prior to angiography.Am J Cardiol. 1992;69:729～732.
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61. Little WC,Constantinescu M,Applegate RJ,et al.Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to -moderate coronary artery disease?Circulation 1988;78:1157～1166.
62. Davies MJ,Thomas AC.Plaque fissuring the cause of acute myocardial infarction,sudden ischaemic death,and crescendo angina.Br Heart J.1985;53:363～373.
63. Falk E.Why do plaques rupture?Circulation, 1992;86(suppl):30～42.
64. Hermiller JB, Tenaglia AN, Kisslo KB, Phillips HR, Bashore TM, Stack RS, Davidson CJ. In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol 1993;71:665-8.
65. Hermiller JB,Tenaglia AN,Kisslo KB,et al.In vivo validation of compensatory enlargement of atherosclerotic coronary arteries.Am J Cardiol 1993;71:665～668.
66. Losorda DW, Rosenfieled K,Kaufman J,et al.Focal compensatory enlargement of human arteries in response to progressive atherosclerosis:in vivo documentation using intravasculer ultrasound.Circulation 1994;89:2570～2577.)
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73. Schoenhagen P, Ziada KM, Vince DG, Nissen SE, Tuzcu EM. Arterial remodeling and coronary artery diseasethe concept of "dilated" versus "obstructive" coronary atherosclerosis. J Am Coll Cardiol 2001;38:297-306.
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75. Mintz GS,Kent KM,Pichard AD,et al.Contribution of inadequate arterial remodeling to the development of focal coronary artery stenoses:an intravasculer ultrasound study.Circulation 1997;95:1791-1798.
76. Topol EJ, Nissen SE. Our preoccupation with coronary luminology. The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation 1995;92:2333-42.
77. Nissen SE, Yock P. Intravascular ultrasoundnovel diagnostic insights and current clinical applications. Circulation 2001; 103:604-16.
78. Smits PC,Pasterkamp G, de Jaegere PPT, et al.Angioscopic complex lesions are predominantly compensatory enlarged.Cardiovasc Res 1999;41:458-464
79. Schoenhagen P, Ziada KM,Kapadia SR,et al.Extent and direction of arterial remodeling in stable and unstable coronary syndromes.Circulation 2000; 101:598-603
80. Schoenhagen P, Ziada KM, Kapadia SR, Nissen SE, Tuzcu EM. Extent and direction of arterial remodeling in stable versus unstable coronary syndromesan intravascular ultrasound study. Circulation 2000;101:598-603.
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intravascular ultrasound study. J Am Coll Cardiol 1996;27:1571-6.
86. Mintz GS, Kent KM, Pichard AD, et al. Contribution of inadequate arterial remodeling to the development of focal coronary artery stenoses. An intravascular ultrasound study. Circulation 1997;95:1791-8.
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111. Falk E.Unstable angina with fatal outcome:dynamic coronary thrombosis leading to infarction and/or sudden death:autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion.Circulation 1985;71:699-708.
112. 75. Davies M.J., Thomas A.. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N Engl J Med 1984;310:1137-40.
113. Farb A., Burke A.P., Tang A.L., et al. Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. Circulation 1996;93:1354-63.
114. Montenegro MR,Eggen DA.Tomography of atherosclerosis in the coronary arteries.Lab Invest 1968; 18:586-593.
2. Hodgson JM, Graham SP, Savakus AD, et al. Clinical percutaneous imaging of coronary anatomy using an over-the-wire ultrasound catheter system, Int J Card Imaging. 1989;4:187-193.
3. Nissen SE, Grines CL, Gurley JC, et al. Application of a new phased-array ultrasound imaging catheter in the assessment of vascular dimensions: in vivo comparison to cineangiography. Circulation. 1990;81:660-666.
4. Tobis JM, Mallery J, Mahon D, et al. Intravascular ultrasound imaging of human coronary arteries in vivo: analysis of tissue characterizations with comparison to in vitro histological specimens. Circulation. 1991 ;83:913-926.
5. Nissen SE, Gurley JC, Grines CL, et al. Intravascular ultrasound assessment of lumen size and wall morphology in normal subjects and patients with coronary artery disease. Circulation. 1991 ;84:1087-1099.
6. Isner JM, Kishel J, Kent KM. Accuracy of angiographic determination of left main coronary arterial narrowing. Circulation. 1981 ;63:1056-1061.
7. Steven EN, Paul Y. Intravascular Ultrasound:Novel Pathophysioiogical Insights and Current Clinical Applications.Circulation. 2001; 103:604-616.
8. Nissen SE, Gurley JC. Application of intravascular ultrasound to detection and quantitation of coronary atherosclerosis. Int J Card Imaging 1991 ;6:165-77.
9. Fuster V, Badimon L,Badimon JJ,et al.The pathogenesis of coronary artery disease and the acute coronary syndromes.N Engl J Med 1987;316:1371-1373
10. Qiao JH,Fishbein MC.The severity of coronary atherosclerosis at site of plaque rupture with occlusive thrombosis.J Am Coll Cardiol
1991;17:1138-1142.
11. Fishbein MC,Siegel RJ.How big are coronary atherosclerotic plaques that rupture?Circulation 1996;94:2662-2666.
12. Mann JM,Davies MJ.Assessment of the severity of coronary artery disease at postmortem examination.Are the measurements clinically valid?Br Heart J 1995;74:528-530.
13. von Birgelen C,Airiian SG,Mintz GS,et al.Variations of remodeling in response to left main atherosclerosis assessed with intravascular ultrasound in vivo.Am J Cardiol 1997;80:1408-1413.
14. Smits PC,Pasterkamp G, de Jaegere PPT, et al.Angioscopic complex lesions are predominantly compensatory enlarged:an angioscopic and intravascular ultrasound sdudy.Cardiovasc Res 1999;41:458-464.
15. Glagov S,Weisenberg E,Zarins CK,et al.Compensatory enlargement of human atherosclerotic coronary arteries.N Engl J Med 1987;316:1371-1375
16. McPherson DD,Sirna SJ,Hiratzka LF, et al.Coronary arterial remodeling studied by high-frequency epicardial echocardiography.J Am Coll Cardiol 1991; 17:79-86
17. Nishioka T, Luo H,Eigler NL,et al.Contribution of inadequate compensatory enlargement of human artery stenosis. J Am Coll Cardiol 1996;27:1571-1576
18. Mintz GS, Nissen SE, Anderson WD, et al. American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol 2001 ;37:1478-92.
19. Galbraith JE, Murphy ML, Desoyza N. Coronary angiogram interpretation: interobserver variability. JAMA. 1981 ;240:2053-2059.
20. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Am J Cardiol. 1979;44:39-44.
21. Topol EJ, Nissen SE. Our preoccupation with coronary luminology: the dissociation between clinical and angiographic findings in ischemic heart disease. Circulation. 1995;92:2333-2342.
22. Detre KM,Wright E,Murphy ML,et al.Observer agreement in evaluating coronary angiograms.Circulation 1975;52:979～986.
23. DeRouen TA,Murray JA,Owen W.Variability in the analysis of coronary arteriograms.Circulation 1997;55:324～328.
24. Fisher LD,Judkins MP, Lesperance J,et al.Reproducibility of coronary arteriographic reading in the Coronary Artery Surgery Study(CASS).Cathet Cardiovasc Diagn 1982;8:565～575.
25. Vlodaver Z,Frech R,Van Tassel RA,et al.Correlation of the antemortem coronary arteriogram and the postmortem specimen.Circulation 1973;47:162～169.
26. Grondin CM,Dyrda I,Pasternac A,et al.Discrepancies between cineangiographic and postmortem findings in patients with coronary artery disease and recent myocardial revascularization.Circulation 1974;49:703～708.
27. Arnett EN,Isner JM,Redwood DR,et al.Coronary artery narrowing in coronary artery disease:comparison of cineangiographic and necropcy findings.Ann Intern Med 1079;91:350～356.
28. Isner JM,Kishel J,Kent KM,et al.Accuracy of angiographic determination of left main coronary artery narrowing: angiographic-histologic correlative analysis in 28 patients.Circulation 1981 ;63: 1056～1064.
29. Dietz WA,Tobis JM,Isner JM.failure of angiography to accurately depict the extent of coronary artery narrowing in three fatal cases of percutaneous
transluminal coronary angioplasty.J Am Coll Cardiol 1992; 19:1261～1270.
30. Davies MJ,Thomas AC.Plaque fissuring:the cause of acute myocardial infarction,sudden ischemic death and crescendo angina.Br Heart J. 1985;53:363～373.
31. Qiao JH,Fishbein MC.The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thombosis.J Am Coll Cardiol. 1991 ;17:1138～1142.
32. Horie T, Sekiguchi M,Hirosawa K.Coronary thombosis in pathogenesis of acute myocardial infarction. Br Heart J. 1978;40:153～161.
33. Liebson PR,Klein LW.Intravascular ultrasound in coronary atherosclerosis:a new approach to clinical assessment.Am Heart J 1992; 123:1643～1660.
34. Di Mario C,The SH,Madretsma S,et al.Detection and characterization of vascular lesions by intravascular ultrasound:an in vitro study correlated with histology.J Am Soc Echocardiogr 1992;5:135～146.
35. Nakamura S,Colombo A,Gaglione A,et al.Intracoronary ultrasound observations during stent implantation.Circulation 1994;89:2026～2034.
36. Colombo A,Hall P, Nakamura S,et al. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation 1995;91: 1676～1688.
37. Ozaki Y, Keane D,Nobuyoshi M,et al.Coronary lumen at six-month follow-up of a new radiopaque Cordis tantalum stent using quantitative angiography and intracoronary ultrasound.Am J Cardiol 1995;76:1135～1143.
38. Topol EJ, Nissen SE. Our preoccupation with coronary luminology: the dissociation between clinical and angiographic findings in ischemic heart disease. Circulation. 1995;92:2333-2342.
39. Erbel R, Ge J, Bockisch A, et al. Value of intracoronary ultrasound and Doppler in the differentiation of angiographically normal coronary arteries: a
prospective study in patients with angina pectoris. Eur Heart J. 1996; 17:880-889.
40. Mintz GS, Painter JA, Pichard AD, et al. Atherosclerosis in angiographically "normal" coronary artery reference segments: an intravascular ultrasound study with clinical correlations. J Am Coll Cardiol. 1995;25:1479-1485
41. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Am J Cardiol. 1979;44:39-44.
42. Lee DY, Eigler N, Luo H, et al. Effect of intracoronary ultrasound imaging on clinical decision making. Am Heart J. 1995;129:1084-1093.
43. Mintz GS, Pichard AD, Kovach JA, et al. Impact of preintervention intravascular ultrasound imaging on transcatheter treatment strategies in coronary artery disease. Am J Cardiol. 1994;73:423-430
44. Shoenhagen P, Ziada K, Kapadia SR, et al. Extent and direction of arterial remodeling in stable versus unstable coronary syndromes: an intravascular ultrasound study. Circulation. 2000; 101:598-603.
45. Ge J,Chirillo F, Schwedtmann J,et al.Screening of ruptured plaques in patients with coronary artery disease by intravascular ultrasound.Heart. 1999;81:621～627.
46. von Birgelen C,Klinkhart W, Mintz GS,et al.Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel:an intravascular ultrasound study in vivo.J Am Coll Cardiol 2001 ;37:1864-1870.
47. Mintz GS, Popma JJ, Pichard AD, et al. Patterns of calcification in coronary artery disease. A statistical analysis of intravascular ultrasound and coronary angiography in 1155 lesions. Circulation. 1995 Apr 1 ;91 (7): 1959-65.
48. Fuchs S, Stabile E, Mintz GS,et al. Intravascular ultrasound findings in patients with acute coronary syndromes with and without elevated troponin Ⅰ
level,Am J Cardiol. 2002 May 1 ;89(9): 1111-3.
49. Duissaillant GR, Mintz GS, Pichard AD, et al. Intravascular ultrasound identification of calcified intraluminal lesions misdiagnosed as thrombi by coronary angiography.Am Heart J. 1996 Sep; 132(3):687-9.
50. Hodgson JM, Reddy KG, Suneja R, et al. Intracoronary ultrasound imaging: correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty. J Am Coll Cardiol. 1993;21:35-44.
51. Kimura T, Kaburagi S, Tamura T, et al. Remodeling of human coronary arteries undergoing coronary angioplasty or atherectomy. Circulation. 1997;96:475-483.
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