血管内超声评价冠状动脉粥样硬化
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摘要
背景和研究目的：血管内超声(IVUS)可以提供高分辩率的冠状动脉管腔和斑块的横截面图像，可以提供冠状动脉斑块和管壁的详细信息(包括斑块的体积、成分、钙化情况，是否稳定，有无破裂，血管壁体积和形态等)，因此成为研究冠状动脉粥样硬化的有力工具。近来，IVUS研究揭示出胆固醇水平、他汀类药物治疗、心血管危险因素等与冠状动脉斑块进展的关系，同时也有多项有关冠状动脉重构、不稳定斑块和斑块破裂的IVUS研究。本研究的目的为：1．评价他汀类药物对轻度胆固醇升高冠心病患者冠状动脉粥样硬化斑块的影响。2．探讨稳定型心绞痛(SAP)、不稳定型心绞痛(UAP)和急性心肌梗死(AMI)患者冠状动脉罪犯病变的钙化类型。3．探讨冠状动脉支架置入后斑块的重新分布对支架边缘的影响及此影响是否与所置入支架的长度有关。研究方法：1．将LDL-C2．6～3．．6 mmol／L患者分为三组：一组为冠心病患者49例，接受他汀类药物治疗组(他汀组)23例；不接受他汀类药物治疗组(非他汀组)26例。二组为冠心病患者57例，＞65岁组(Ⅰ组，30例)和≤65岁组(Ⅱ组，27例)，均接受他汀类药物治疗。三组为合并2型糖尿病的稳定性心绞痛患者78例，接受他汀类药物治疗组(他汀组)40例；不接受他汀类药物治疗组(非他汀组)38例。每位患者选取1处狭窄50％～70％的病变为靶病变。入院时和12个月后分别行冠状动脉造影(CAG)和靶病变的IVUS，比较治疗前后斑块体积、管腔体积和血管体积。
2．选取于经皮冠状动脉介入治疗(PCI)前行罪犯病变IVUS检查的SAP、UAP和AMI患者201例，IVUS分析部位是包括管腔横截面积最小的区域在内的10 mm的罪犯血管段。测量罪犯病变钙化的弧度和长度，钙化的弧度(°)乘以钙化的长度(mm)即为弧面积(AA)。比较SAP、UAP和AMI患者冠状动脉罪犯病变的AA。3．47例行PCI的SAP和UAP患者，冠状动脉内共置入支架70枚，根据支架的长度分为两组，支架长度≤18mm和＞18mm组。于支架置入前后的支架远端边缘(支架远端5mm)、支架和支架近端边缘(支架近端5mm)进行IVUS图像分析，测量冠状动脉横截面上的管腔面积(LA)、血管面积(VA)和管腔体积(LV)、血管体积(VV)、管壁体积(WV)、支架两端移动斑块体积并进行比较。研究结果：1．一组中，他汀组12个月后，LDL-C由(3．44±O．42)mmol／L降至(2．31±0．19)mmol／L，较入院时下降32．8％；非他汀组12个月后较入院时基本无变化。血管体积、管腔体积和斑块体积在入院时2组差异无统计学意义。12个月后，非他汀组斑块体积显著增加，由(82．1±14．5)mm~3增加至(95．9±20．5)mm~3(P＜0．05)；血管体积无明显变化，管腔体积缩小，由(55．1±7．8)mm~3减少至(44．6±6．6)mm~3(P＜0．05)。他汀组12个月后的斑块体积、血管体积和管腔体积均无明显变化。二组中，Ⅰ组和Ⅱ组患者12个月后LDL-C平均降至2．39 mmol／L和2．23mmol／L，较基线下降32．1％和33．2％。两组患者血管、管腔和斑块体积在治疗前无显著差异。治疗12个月后，Ⅰ组血管、管腔和斑块体积无显著变化，Ⅱ组血管体积无变化；管腔体积由(68．8+14．4)mm~3增加至(83．6+22．5)mm~3(P＜0．05)，斑块体积由(80．1+18．6)mm~3缩小至(69．9+21．7)mm~3(P＜0．05)。钙化斑块比例Ⅰ组明显高于Ⅱ组(56．7％vs 25．9％，P＜0．05)。三组中，他汀组12个月后，平均LDL-C由(3．52±0．56)mmol／L降至(2．41±0．33)mmol／L(P＜0．05)，较入组时下降3 1．5％；非他汀组平均LDL-C较入组时差异无统计学意义[(3．50±0．49)rnmol／L比(3．55±0．70)mmol／L，P＞0．05]。血管体积、管腔体积和斑块体积在入组时两组差异无统计学意义。与入组时比较，12个月后非他汀组斑块体积显著增加19．7％[(76．1±13．0)mm~3比(95．0±21．9)mm~3，P＜0．05]，血管体积差异无统计学意义，管腔体积由(65．0±10．9)mm~3减少至(45．4±6．6)mm~3，P＜0．05。他汀组的斑块体积增加10．1％[(79．5±15．2)mm~3比(87．5±17．9)mm~3，P＜0．05]、血管体积增加7．0％[(148．2±40．9)mm~3比(158．5±53．1)mm~3，P＞0．05]、管腔体积无明显变化。非他汀组治疗前后RI差异无统计学意义(0．93±0．08比0．92±0．09，P＞0．05)，而在他汀组RI由0．91±0．08增加至0．95±0．10(P＜0．05)。2．AMI患者罪犯病变中钙化的数量明显大于SAP和UAP患者，SAP和UAP患者罪犯病变中钙化的数量基本相同(AMI2．21±1．98，SAP 1．15±1．01，UAP 1．20±1．15，AMI vs SAP或UAP；p＜0．0005)。SAP和UAP、AMI患者罪犯病变每个钙化的平均AA显著不同，SAP患者大于UAP和AMI患者，UAP和AMI患者没有区别(SAP 788．6±767．0°mm，UAP 136．6±189．3°·mm，AMI 148．4±217．1°·mm，SAP vs UAP或AMI；p＜0．0005)。每例患者罪犯病变总AA，SAP患者最大，AMI患者次之，UAP患者最小(SAP 903．3±1018．8°mm，AMI 301．1±401．5°mm，UAP 163．9±279．6°·mm，SAP vs UAP或AMI；p＜0．0005，AMI vs UAP；p＜0．01)。3．在支架长度≤18mm组支架近远端分别检测到91％和93％斑块移位(P＞0．05)，在支架长度＞18mm组支架近远端分别检测到80％和91％的斑块移位(P＜0．05)。支架置入后支架长度≤18mm组支架近远端和支架长度＞18mm组支架近端边缘，LV缩小、VV无变化、WV明显增加，即由于斑块的移位造成支架置入后即刻以上部位有明显的管腔缩小，但是支架长度＞18mm组支架远端边缘情况不同，LV和VV反而增加，WV有所增加，即在支架长度＞18mm组支架远端边缘斑块的移位并没有造成支架置入即刻管腔的缩小。研究结论：1．他汀类药物可以阻止LDLC轻度升高的冠心病患者冠状动脉斑块的进展。他汀类药物可以阻止LDL-C轻度升高的老年冠心病患者冠状动脉斑块的进展，但效果较≤65岁患者差。他汀类药物可以延缓LDL-C轻度升高合并糖尿病的冠心病患者冠状动脉斑块的进展，且可使病变部位血管体积增大、负性重构减轻，甚至可以使部分冠状动脉重构类型发生变化。2．SAP、AMI和UAP患者的罪犯病变分别有最大、较大和最小的钙化负荷。SAP患者有大而少的钙化、AMI患者有小而多的钙化、UAP患者有少而小的钙化。3．长、短支架置入后对支架近远端边缘斑块的移位和管腔的影响不同，短支架近远端和长支架近端边缘在支架置入后有斑块的移入和管腔的缩小，而长支架远端边缘虽有斑块的移入但无管腔的缩小。
Background and Objective:Intravascular ultrasound (IVUS) is useful methodto evaluate coronary atherosclerosis and it can provide more details of atheroscleroticplaques and the wall of vascula.Recently,IVUS studies showed the relationship ofthe level of cholesterol,treatment of statins,cardiovascular risk factors and progressof atherosclerotic plaques,and there were also some studies to evaluate theremodeling of coronary arteries,the stability and rupture of atherosclerotic plaquewith IVUS.The projective of our study is 1.To evaluate the effects of statins onatherosclerotic plaque of coronary heart disease with mild elevation of LDL-C.2.Toquantify the different patterns of coronary calcification of patients with stable anginapectoris (SAP),unstable angina pectoris (UAP) and acute myocardial infaction (AMI).3.To evaluate the association between poststenting atherosclerotic plaqueredistribution/lumen reduction at the stent edge and stent length.Methods:1.Coronary heart disease patients with mild elevation of LDL-C were divided into threegroups:Gourp one,Forty-nine coronary heart disease patients were divided into twosub-groups,statins group and non-statins group.Group two,Fifty-seven coronaryheart disease patients were divided into two sub-groups,＞65 years old group and≤65 years old group.Group three,Seventy-eight patients with stable angina pecterisand type 2 diabetes mellitus were divided into two sub-group,statins group andnon-statins group.One 50%-70% stenosis plaque was selected as target plaque ineach patient.Coronary artery angiography (CAG) and target plaque intravascularultrasound (IVUS) were performed on admission and after 12 months later tocompare the plaque volume,lumen volume and vascular volume.2.We selected 201patients with SAP,UAP,or AMI who underwent IVUS imaging of a de novo nativeatherosclerotic lesion considered to be the culprit lesion before percutaneous coronaryintervention.The culprit lesion site for analysis was the 10-mm-long segmentincluding the smallest lumen cross-sectional area.The arc of each calcium deposit ineach image was measured with a protractor centered on the lumen and the length ofeach calcium deposit was calculated with the number of images containing thecalcium deposit minus 1,then multiplying 0.5 mm (the images were 0.5 mm apart). Finally,the AA was calculated by arc (degree) multiplying length (mm).3.Seventystents were implanted to 47 patients with stable or unstable angina and 33 stents were＜18 mm and 37 stents were＞18 mm.IVUS analysis was performed on proximalstent edge,stent area and distal stent edge.Lumen area (LA) and vascular area (VA)were measured and lumen volume (LV) and vascular volume (VV) were calculatedon the three segments.Vascular wall volume (WV) was calculated as VV—LV,volume of plaque redistribution=poststenting WV—prestenting WV.Results:1.Ingroup one,12 months later,LDL-C levels decreased by 32.8% from (3.44±0.42)mmol/L to (2.31±0.19) mmol/L in statins group and unchanged in non-statins group.These were no significant difference in vascular volume,lumen volume and plaquevolume between the two groups on admission.In non-statins group,plaque volumeincreased from (82.1±14.5) mm~3 to (95.9±20.5) mm~3(p＜0.05),lumen volumedecreased from (55.1±7.8) mm~3 to (44.6±6.6) mm~3(p＜0.05) and vascular volumeunchanged.All the indexes showed no changes after 12-months thearapy in statinsgroup.In group two,after 12 months,LDL-C in＞65 years old group and≤65years old group LDL-C decreased to 2.39 mmol/L and 2.23 mmol/L,i.e.,decreasedby 32.1% and 33.2% of the baseline values respectively.In＞65 years old group,plaque volume,lumen volume and vascular volume were unchanged,while in≤65years old group,the plaque volume decreased from (80.1±18.6) mm~3 to (69.9±21.7)mm~3 (P＜0.05),the lumen volume increased from (68.8±14.4) mm~3 to (83.6±22.5)mm~3 (P＜0.05),and the vascular volume was unchanged.There were more calcificplaques in＞65 years old group than in≤65 years old group.In group three,after12 months,LDL-C decreased 31.5% in statin group and remained unchanged innon-statin group.After 12 months,plaque volume was significantly increased [(76.1±13.0) mm~3 vs.(95.0±21.9) mm~3,P＜0.05],lumen volume was significantlydecreased [(65.0±10.9) mm~3 vs.(45.4±6.6) mm~3,P＜0.05] and vascular volumeremained unchanged in non-statins group;plaque volume was also significantlyincreased [(79.5±15.2) mm~3 vs.(87.5±17.9) mm~3,P＜0.05] while lumen volumeand vascular volume remained unchanged in statin group.Remodeling index (RI)remained unchanged in non-statin group but significantly increased in statin group (0.91±0.08 vs.0.95±0.10,P＜0.05) after 12 months.2.The average number ofcalcium deposits in the culprit lesions of patients with AMI was significantly largerthan patients with SAP or UAP and the number of calcium deposits of patients withSAP or UAP was almost same (AMI 2.21±1.98,SAP 1.15±1.01,UAP 1.20±1.15,AMI vs SAP or UAP;P＜0.0005).The average AA per calcium deposit wassignificantly different in culprit lesions of patients with SAP and UAP or AMI,thecalcium deposits were bigger in SAP than in UAP or AMI,and there were nodifferent between UAP and AMI (SAP 788.6±767.0 degree x mm,UAP 136.6±189.3degree x mm,AMI 148.4±217.1 degree x mm,SAP vs UAP or AMI;P＜0.0005).Thetotal AA of culprit lesions per patient was greatest in patients with SAP,less inpatients with AMI,and least in patients with UAP (SAP 903.3±1018.8 degree x mm,AMI 301.1±401.5 degree x mm,UAP 163.9±279.6 degree x mm,SAP vs UAP orAMI;P＜0.0005,AMI vs UAP;P＜0.01).3.Compared to prestenting,poststentingLV significantly decreased,VV remained unchanged and WV significantly increasedat proximal and distal edge of≤18 mm group and at proximal edge of＞18 mmgroup,suggesting reduced lumen due to plaque distribution.At distal edge of＞18mm group,poststenting LV,VV and WV all equally significantly increased thereforethe lumen was not effected by plaque distribution.Couclusion:1.Statins therapy canprevent the development of atherosclerotic plaque of coronary artery of coronaryheart disease patients with mild elevation of LDL-C.Statin therapy can halt thedevelopment of atherosclerotic plaque of coronary artery in old coronary heartdisease patients with mild elevation of LDL-C,but the same therapy can make theplaque regress in≤65 years old group regress.Chronic statin therapy could retardthe coronary atherosclerotic progression in patients with stable angina pectoris andtype 2 diabetes with mild elevated LDL-C.2.The culprit lesions of patients with SAP,AMI,or UAP have greatest,less,or least calcification burden,respectively.Theculprit lesions of patients with SAP have bigger and fewer calcium deposits,patientswith AMI have smaller and more numerous calcium deposits,and patients with UAPhave smaller and fewer calcium deposits.3.The poststenting lumen changes due to plaque redistribution were associated with stent length,lumen reduced at proximaland distal edge of short stents and proximal edge of long stents but not at distal edgeof long stents.
2．选取于经皮冠状动脉介入治疗(PCI)前行罪犯病变IVUS检查的SAP、UAP和AMI患者201例，IVUS分析部位是包括管腔横截面积最小的区域在内的10 mm的罪犯血管段。测量罪犯病变钙化的弧度和长度，钙化的弧度(°)乘以钙化的长度(mm)即为弧面积(AA)。比较SAP、UAP和AMI患者冠状动脉罪犯病变的AA。3．47例行PCI的SAP和UAP患者，冠状动脉内共置入支架70枚，根据支架的长度分为两组，支架长度≤18mm和＞18mm组。于支架置入前后的支架远端边缘(支架远端5mm)、支架和支架近端边缘(支架近端5mm)进行IVUS图像分析，测量冠状动脉横截面上的管腔面积(LA)、血管面积(VA)和管腔体积(LV)、血管体积(VV)、管壁体积(WV)、支架两端移动斑块体积并进行比较。研究结果：1．一组中，他汀组12个月后，LDL-C由(3．44±O．42)mmol／L降至(2．31±0．19)mmol／L，较入院时下降32．8％；非他汀组12个月后较入院时基本无变化。血管体积、管腔体积和斑块体积在入院时2组差异无统计学意义。12个月后，非他汀组斑块体积显著增加，由(82．1±14．5)mm~3增加至(95．9±20．5)mm~3(P＜0．05)；血管体积无明显变化，管腔体积缩小，由(55．1±7．8)mm~3减少至(44．6±6．6)mm~3(P＜0．05)。他汀组12个月后的斑块体积、血管体积和管腔体积均无明显变化。二组中，Ⅰ组和Ⅱ组患者12个月后LDL-C平均降至2．39 mmol／L和2．23mmol／L，较基线下降32．1％和33．2％。两组患者血管、管腔和斑块体积在治疗前无显著差异。治疗12个月后，Ⅰ组血管、管腔和斑块体积无显著变化，Ⅱ组血管体积无变化；管腔体积由(68．8+14．4)mm~3增加至(83．6+22．5)mm~3(P＜0．05)，斑块体积由(80．1+18．6)mm~3缩小至(69．9+21．7)mm~3(P＜0．05)。钙化斑块比例Ⅰ组明显高于Ⅱ组(56．7％vs 25．9％，P＜0．05)。三组中，他汀组12个月后，平均LDL-C由(3．52±0．56)mmol／L降至(2．41±0．33)mmol／L(P＜0．05)，较入组时下降3 1．5％；非他汀组平均LDL-C较入组时差异无统计学意义[(3．50±0．49)rnmol／L比(3．55±0．70)mmol／L，P＞0．05]。血管体积、管腔体积和斑块体积在入组时两组差异无统计学意义。与入组时比较，12个月后非他汀组斑块体积显著增加19．7％[(76．1±13．0)mm~3比(95．0±21．9)mm~3，P＜0．05]，血管体积差异无统计学意义，管腔体积由(65．0±10．9)mm~3减少至(45．4±6．6)mm~3，P＜0．05。他汀组的斑块体积增加10．1％[(79．5±15．2)mm~3比(87．5±17．9)mm~3，P＜0．05]、血管体积增加7．0％[(148．2±40．9)mm~3比(158．5±53．1)mm~3，P＞0．05]、管腔体积无明显变化。非他汀组治疗前后RI差异无统计学意义(0．93±0．08比0．92±0．09，P＞0．05)，而在他汀组RI由0．91±0．08增加至0．95±0．10(P＜0．05)。2．AMI患者罪犯病变中钙化的数量明显大于SAP和UAP患者，SAP和UAP患者罪犯病变中钙化的数量基本相同(AMI2．21±1．98，SAP 1．15±1．01，UAP 1．20±1．15，AMI vs SAP或UAP；p＜0．0005)。SAP和UAP、AMI患者罪犯病变每个钙化的平均AA显著不同，SAP患者大于UAP和AMI患者，UAP和AMI患者没有区别(SAP 788．6±767．0°mm，UAP 136．6±189．3°·mm，AMI 148．4±217．1°·mm，SAP vs UAP或AMI；p＜0．0005)。每例患者罪犯病变总AA，SAP患者最大，AMI患者次之，UAP患者最小(SAP 903．3±1018．8°mm，AMI 301．1±401．5°mm，UAP 163．9±279．6°·mm，SAP vs UAP或AMI；p＜0．0005，AMI vs UAP；p＜0．01)。3．在支架长度≤18mm组支架近远端分别检测到91％和93％斑块移位(P＞0．05)，在支架长度＞18mm组支架近远端分别检测到80％和91％的斑块移位(P＜0．05)。支架置入后支架长度≤18mm组支架近远端和支架长度＞18mm组支架近端边缘，LV缩小、VV无变化、WV明显增加，即由于斑块的移位造成支架置入后即刻以上部位有明显的管腔缩小，但是支架长度＞18mm组支架远端边缘情况不同，LV和VV反而增加，WV有所增加，即在支架长度＞18mm组支架远端边缘斑块的移位并没有造成支架置入即刻管腔的缩小。研究结论：1．他汀类药物可以阻止LDLC轻度升高的冠心病患者冠状动脉斑块的进展。他汀类药物可以阻止LDL-C轻度升高的老年冠心病患者冠状动脉斑块的进展，但效果较≤65岁患者差。他汀类药物可以延缓LDL-C轻度升高合并糖尿病的冠心病患者冠状动脉斑块的进展，且可使病变部位血管体积增大、负性重构减轻，甚至可以使部分冠状动脉重构类型发生变化。2．SAP、AMI和UAP患者的罪犯病变分别有最大、较大和最小的钙化负荷。SAP患者有大而少的钙化、AMI患者有小而多的钙化、UAP患者有少而小的钙化。3．长、短支架置入后对支架近远端边缘斑块的移位和管腔的影响不同，短支架近远端和长支架近端边缘在支架置入后有斑块的移入和管腔的缩小，而长支架远端边缘虽有斑块的移入但无管腔的缩小。
Background and Objective:Intravascular ultrasound (IVUS) is useful methodto evaluate coronary atherosclerosis and it can provide more details of atheroscleroticplaques and the wall of vascula.Recently,IVUS studies showed the relationship ofthe level of cholesterol,treatment of statins,cardiovascular risk factors and progressof atherosclerotic plaques,and there were also some studies to evaluate theremodeling of coronary arteries,the stability and rupture of atherosclerotic plaquewith IVUS.The projective of our study is 1.To evaluate the effects of statins onatherosclerotic plaque of coronary heart disease with mild elevation of LDL-C.2.Toquantify the different patterns of coronary calcification of patients with stable anginapectoris (SAP),unstable angina pectoris (UAP) and acute myocardial infaction (AMI).3.To evaluate the association between poststenting atherosclerotic plaqueredistribution/lumen reduction at the stent edge and stent length.Methods:1.Coronary heart disease patients with mild elevation of LDL-C were divided into threegroups:Gourp one,Forty-nine coronary heart disease patients were divided into twosub-groups,statins group and non-statins group.Group two,Fifty-seven coronaryheart disease patients were divided into two sub-groups,＞65 years old group and≤65 years old group.Group three,Seventy-eight patients with stable angina pecterisand type 2 diabetes mellitus were divided into two sub-group,statins group andnon-statins group.One 50%-70% stenosis plaque was selected as target plaque ineach patient.Coronary artery angiography (CAG) and target plaque intravascularultrasound (IVUS) were performed on admission and after 12 months later tocompare the plaque volume,lumen volume and vascular volume.2.We selected 201patients with SAP,UAP,or AMI who underwent IVUS imaging of a de novo nativeatherosclerotic lesion considered to be the culprit lesion before percutaneous coronaryintervention.The culprit lesion site for analysis was the 10-mm-long segmentincluding the smallest lumen cross-sectional area.The arc of each calcium deposit ineach image was measured with a protractor centered on the lumen and the length ofeach calcium deposit was calculated with the number of images containing thecalcium deposit minus 1,then multiplying 0.5 mm (the images were 0.5 mm apart). Finally,the AA was calculated by arc (degree) multiplying length (mm).3.Seventystents were implanted to 47 patients with stable or unstable angina and 33 stents were＜18 mm and 37 stents were＞18 mm.IVUS analysis was performed on proximalstent edge,stent area and distal stent edge.Lumen area (LA) and vascular area (VA)were measured and lumen volume (LV) and vascular volume (VV) were calculatedon the three segments.Vascular wall volume (WV) was calculated as VV—LV,volume of plaque redistribution=poststenting WV—prestenting WV.Results:1.Ingroup one,12 months later,LDL-C levels decreased by 32.8% from (3.44±0.42)mmol/L to (2.31±0.19) mmol/L in statins group and unchanged in non-statins group.These were no significant difference in vascular volume,lumen volume and plaquevolume between the two groups on admission.In non-statins group,plaque volumeincreased from (82.1±14.5) mm~3 to (95.9±20.5) mm~3(p＜0.05),lumen volumedecreased from (55.1±7.8) mm~3 to (44.6±6.6) mm~3(p＜0.05) and vascular volumeunchanged.All the indexes showed no changes after 12-months thearapy in statinsgroup.In group two,after 12 months,LDL-C in＞65 years old group and≤65years old group LDL-C decreased to 2.39 mmol/L and 2.23 mmol/L,i.e.,decreasedby 32.1% and 33.2% of the baseline values respectively.In＞65 years old group,plaque volume,lumen volume and vascular volume were unchanged,while in≤65years old group,the plaque volume decreased from (80.1±18.6) mm~3 to (69.9±21.7)mm~3 (P＜0.05),the lumen volume increased from (68.8±14.4) mm~3 to (83.6±22.5)mm~3 (P＜0.05),and the vascular volume was unchanged.There were more calcificplaques in＞65 years old group than in≤65 years old group.In group three,after12 months,LDL-C decreased 31.5% in statin group and remained unchanged innon-statin group.After 12 months,plaque volume was significantly increased [(76.1±13.0) mm~3 vs.(95.0±21.9) mm~3,P＜0.05],lumen volume was significantlydecreased [(65.0±10.9) mm~3 vs.(45.4±6.6) mm~3,P＜0.05] and vascular volumeremained unchanged in non-statins group;plaque volume was also significantlyincreased [(79.5±15.2) mm~3 vs.(87.5±17.9) mm~3,P＜0.05] while lumen volumeand vascular volume remained unchanged in statin group.Remodeling index (RI)remained unchanged in non-statin group but significantly increased in statin group (0.91±0.08 vs.0.95±0.10,P＜0.05) after 12 months.2.The average number ofcalcium deposits in the culprit lesions of patients with AMI was significantly largerthan patients with SAP or UAP and the number of calcium deposits of patients withSAP or UAP was almost same (AMI 2.21±1.98,SAP 1.15±1.01,UAP 1.20±1.15,AMI vs SAP or UAP;P＜0.0005).The average AA per calcium deposit wassignificantly different in culprit lesions of patients with SAP and UAP or AMI,thecalcium deposits were bigger in SAP than in UAP or AMI,and there were nodifferent between UAP and AMI (SAP 788.6±767.0 degree x mm,UAP 136.6±189.3degree x mm,AMI 148.4±217.1 degree x mm,SAP vs UAP or AMI;P＜0.0005).Thetotal AA of culprit lesions per patient was greatest in patients with SAP,less inpatients with AMI,and least in patients with UAP (SAP 903.3±1018.8 degree x mm,AMI 301.1±401.5 degree x mm,UAP 163.9±279.6 degree x mm,SAP vs UAP orAMI;P＜0.0005,AMI vs UAP;P＜0.01).3.Compared to prestenting,poststentingLV significantly decreased,VV remained unchanged and WV significantly increasedat proximal and distal edge of≤18 mm group and at proximal edge of＞18 mmgroup,suggesting reduced lumen due to plaque distribution.At distal edge of＞18mm group,poststenting LV,VV and WV all equally significantly increased thereforethe lumen was not effected by plaque distribution.Couclusion:1.Statins therapy canprevent the development of atherosclerotic plaque of coronary artery of coronaryheart disease patients with mild elevation of LDL-C.Statin therapy can halt thedevelopment of atherosclerotic plaque of coronary artery in old coronary heartdisease patients with mild elevation of LDL-C,but the same therapy can make theplaque regress in≤65 years old group regress.Chronic statin therapy could retardthe coronary atherosclerotic progression in patients with stable angina pectoris andtype 2 diabetes with mild elevated LDL-C.2.The culprit lesions of patients with SAP,AMI,or UAP have greatest,less,or least calcification burden,respectively.Theculprit lesions of patients with SAP have bigger and fewer calcium deposits,patientswith AMI have smaller and more numerous calcium deposits,and patients with UAPhave smaller and fewer calcium deposits.3.The poststenting lumen changes due to plaque redistribution were associated with stent length,lumen reduced at proximaland distal edge of short stents and proximal edge of long stents but not at distal edgeof long stents.
引文
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[27] Campbell CY, Rivera JJ, Blumenthal RS. Residual risk in statin-treated patients: future therapeutic options[J]. Curr Cardiol Rep, 2007;9(6):499-505.
[28] Roze S, Ferrieres J, Bruckert E, et al. Cost-effectiveness of raising HDL cholesterol by adding prolonged-release nicotinic acid to statin therapy in the secondary prevention setting:a French perspective[J]. Int J Clin Pract, 2007;61(11):1805-11.
[29] Steven E, Stephen J, Ilke S, et al. Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis The ASTEROID Trial[J], JAMA, 2006, 295: 1556-1565.
[30] Jukema JW, Liem AH, Dunselman PH, et al. LDL-C/HDL-C ratio in subjects with cardiovascular disease and a low HDL-C: results of the RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) study. Curr Med Res Opin[J],2005;21(11):1865-74.
[31] Jones PH, Davidson MH, Stein EA, et al. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial) [J]. Am J Cardiol, 2003;92(2):152-60.
[32] Jensen LO, Thayssen P, Mintz GS, et al. Intravascular ultrasound assessment of remodelling and reference segment plaque burden in type-2 diabetic patients[J]. Eur Heart J, 2007,28:1759-1764.
[33] Schukro C, Syeda B, Yahya N, et al. Volumetric intravascular ultrasound imaging to illustrate the extent of coronary plaque burden in type 2 diabetic patients[J]. J Diabetes Complication,2007,21:381-386.
[34] Tauth J, Pinnow E, Sullebarger JT, et al. Predictors of coronary arterial remodeling patterns in patients with myocardial ischemia[J]. Am J Cardiol, 1997, 80:1352-1355.
[35] Nishioka T, Nagai T, Luo H, et al. Coronary remodeling of proximal and distal stenotic aterosclerotic plaque within the same artery by intravascular ultrasound study[J]. Am J Cardiol, 2001, 87:387-391.
[36] Burke AP, Weber DK, Kolodgie FD,et al. Pathophysiology of calcium deposition in coronary arteries[J]. Herz 2001;26:239-244.
[37] Ramakrishna G, Miller TD, Breen JF, et al. Relationship and prognostic value of coronary artery calcification by electron beam computed tomography to stress-induced ischemia by single photon emission computed tomography[J]. Am Heart J 2007; 153:807-814.
[38] Shisen J, Leung DY, Juergens CP. Gender and age differences in the prevalence of coronary artery calcification in 953 Chinese subjects[J]. Heart Lung Circ 2005; 14:69-73.
[39] Keelan PC, Bielak LF, Ashai K, Jamjoum LS, Denktas AE, Rumberger JA, Sheedy II PF,Peyser PA, Schwartz RS. Long-term prognostic value of coronary calcification detected by electron-beam computed tomography in patients undergoing coronary angiography[J].Circulation 2001;104:412-417.
[40] Arad Y, Spadaro LA, Goodman K, et al. Prediction of coronary events with electron beam computed tomography[J]. J am Coll Cardiol 2000;36:1253-1260.
[41] Raggi P, Callister TQ, Cooil B, et al. Identification of patients at increased risk of first unheralded acute myocardial infarction by electron-beam computed tomography[J].Circulation 2000;101:850-855.
[42] Konieczynska M, Tracz W, Pasowicz M, Przewlocki T. Use of coronary calcium score in the assessment of atherosclerotic lesions in coronary arteries[J]. Kardiol Pol 2006;64:1073-1079.
[43] de Feyter PJ, Ozaki Y, Baptista J, et al. Ischemia-related lesion characteristics in patients with stable or unstable angina. A study with intracoronary angioscopy and ultrasound[J].Circulation 1995;92:1408-1413.
[44] Beckman JA, Ganz J, Creager MA, et al. Relationship of clinical presentation and calcification of culprit coronary artery stenoses[J]. Arterioscler Thromb Vasc Biol 2001;21:1618-1622.
[45] Mintz GS, Pichard AD, Popma JJ, et al. Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study[J]. J Am Coll Cardiol 1997;29:268-274.
[46] Rasheed Q, Nair R, Sheehan H, Hodgson JM. Correlation of intracoronary ultrasound plaque characteristics in atherosclerotic coronary artery disease patients with clinical variables[J]. Am J Cardiol 1994;73:753-758.
[47] Ehara S, Kobayashi Y, Kataoka T, Yoshiyama M, et al. Quantification of coronary calcification by intravascular ultrasound[J]. Circ J 2007;71:530-535.
[48] Ehara S, Kobayashi Y, Yoshiyama M, et al. Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study[J]. Circulation 2004; 110:3424-3429.
[49] Fujii K, Carlier SG, Mintz GS, et al. Intravascular ultrasound study of patterns of calcium in ruptured coronary plaques[J]. Am J Cardiol 2005;96:352-357.
[50] Scott DS, Arora UK, Farb A, et al. Pathologic validation of a new method to quantify coronary calcific deposits in vivo using intravascular ultrasound[J]. Am J Cardiol 2000;85:37-40.
[51] Vengrenyuk Y, Carlier S, Xanthos S, et al. A hypothesis for vulnerable plaque rupture due to stress-induced debonding around cellular microcalcification in thin fibrous caps[J].Proc Natl Acad Sci USA 2006; 103:14678-14683.
[52] Huang H, Virmani R, Younis H, et al. The impact of calcification on the biomechanical stability of atherosclerotic plaques[J]. Circulation 2001; 103:1051 -1056.
[53] Mintz GS, Pichard AD, Kent KM, et al. Axial plaque redistribution as a mechanism of percutaneous transluminal coronary angioplasty[J]. Am J Cardiol, 1996, 77: 427-430.
[54] Honda Y, Yock CA, Hermiller JB, et al. Longitudinal redisfribution of plaque is an important mechanism for lumen expansion in stenting. J Am Coll Cardiol, 1997, 29 (suppl A): 281 A.
[55] Maehara A, Takagi A, Okura H, et al. Longitudinal plaque redistribution during stent expansion[J]. Am J Cardiol, 2000, 86: 1069-1072.
[56] Algowhary M, Matsumura A, Hashimoto Y, et al. Poststenting axial redistribution of atherosclerotic plaque into the reference segments and lumen reduction at the stent edge[J]. Int Heart J, 2006, 47: 159-171.
[57] Takimura CK, Lemos PA, Perin MA, et al. Angiographic geometric predictors of myocardial infarction are not associated with ultrasonographic markers of plaque vulnerability[J]. Arq Bras Cardiol, 2006, 87: 99-105.
[58] Fernando A, Rafael M. Therapeutic implications of in-stent restenosis located at the stent edge[J]. European Heart Journal, 2004, 25: 1829-1835.
[59] Ahmed JM, Mintz GS, Weissman NJ, et al. Mechanism of lumen enlargement during intracoronary stent implantation: an intravascular ultrasound study[J]. Circulation, 2000, 102:7-10.
[60] Dudek D, Legutko J, Kaluza GL, et al. Intravascular ultrasonic evaluation of the magnitude of stent expansion and the mechanisms of lumen enlargement after direct stenting and after conventional stenting with balloon predilatation[J]. Am J Cardiol, 2002, 90: 639-641.
[61] Finet G, Weissman NJ, Mintz GS, et al. Comparison of luminal enlargement by direct coronary stenting versus predilation coronary stenting by three-dimensional volumetric intravascular ultrasound analysis[J]. Am J Cardiol, 2001, 88:1179-1182.
[62] Albertal M, Abizaid A, Munoz JS, et al. A novel mechanism explaining early lumen loss following balloon angioplasty for the treatment of in-stent restenosis[J]. Am J Cardiol, 2005,95:751-754.
[1] Von Birgelen C, Hartmann M, Mintz GS, et al. Relation between progression and regression of atherosclerotic left main coronary artery disease and serum cholesterol levels as assessed with serial long-term (≥12 months) follow-up intravascular ultrasound[J]. Circulation, 2003,108:2757-2762.
[2] Nissen SE, Tuzcu EM, Schoenhagen P, et al. Effect of intensive compared with moderate lipid-lowing therapy on progression of coronary atherosclerosis: a randomized controlled trial (REVERSAL) [J]. JAMA, 2004,291: 1071-1080.
[3] Yamada T, Azuma A, Sasaki S, et al. Randomized evaluation of atorvastatin in patients with coronary heart disease: a serial intravascular ultrasound study[J]. Circ J, 2007, 71:1845-1850.
[4] Okkels Jensen L, Thayssen P, Pederson KE, et al. Regression of coronary atherosclerosis by simvastatin: a serial intravascular ultrasound study[J]. Circulation, 2004,110: 265-270.
[5] Konig A, Kilian E, Rieber J, et al. Assessment of early atherosclerosis in de novo heart transplant recipients: analysis with intravascular ultrasound-derived radiofrequency analysis[J]. J Heart Lung Transplant, 2008, 27: 26-30.
[6] Kavamoto T, Okura H, Koyama Y, et al. The relationship between coronary plaque characteristics and small embolic particles during coronary stent implantation[J]. J Am Coll Cardiol, 2007, 50: 1635-1640.
[7] Von Birgelen C, Hartmann M, Mintz GS, et al. Relationship between cardiovascular risk as predicted by established risk scores versus plaque progression as measured by serial intravascular ultrasound in left main coronary arteries[J]. Circulation, 2004, 110: 1579-1585.
[8] Von Birgelen C, Hartmann M, Mintz GS, et al. Spectrum of remodeling behavior observed with serial long-term (>/=12 months) follow-up intravascular ultrasound studies in left main coronary arteries[J]. Am J Cardiol, 2004, 93: 1107-1113.
[9] Shiran A, Mintz GS, Leiboff B, et al. Serial volumetric intravascular ultrasound assessment of arterial remodeling in left main coronary artery disease[J]. Am J Cardiol, 1999, 83:1427-1432.
[10] Schartl M, Bocksch W, Fateh-Moghadam S, on behalf of the GAIN-Study group. Effects of lipid-lowing on coronary artery remodeling[J]. Coron Artery Dis, 2004,15: 45-51.
[11] Sipahi I, Tuzcu EM, Moon KW, et al. Do the extent and direction of arterial remodelling predict subsequent progression of coronary atherosclerosis? A serial intravascular ultrasound study[J]. Heart, 2008, 94: 623-627.
[12] Kume T, Okura H, Kawamoto T, et al. Relationship between coronary remodeling and plaque characterization in patients without clinical evidence of coronary artery disease[J].Atherosclerosis, 2008, 197: 799-805.
[13] GyOngyOsi M, Yang P, Hassan A, et al. Arterial remodeling of native human coronary arteries in patients with unstable angina pectoris: a prospective intravascular ultrasound study[J]. Heart, 1999, 82: 68-74.
[14] 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: 804-808.
[15] Mintz GS, Pichard AD, Kent KM, et al. Axial plaque redistribution as a mechanism of percutaneous transluminal coronary angioplasty[J]. Am J Cardiol, 1996, 77: 427-430.
[16] Honda Y, Yock CA, Hermiller JB, et al. Longitudinal redistribution of plaque is an important mechanism for lumen expansion in stenting[J]. J Am Coll Cardiol, 1997, 29 (suppl A) :281A.
[17] Maehara A, Takagi A, Okura H, et al. Longitudinal plaque redistribution during stent expansion[J]. Am J Cardiol, 2000, 86: 1069-1072.
[18] Algowhary M, Matsumura A, Hashimoto Y, et al. Poststenting axial redistribution of atherosclerotic plaque into the reference segments and lumen reduction at the stent edge[J].Int Heart J, 2006, 47: 159-171.
[19] The Long-Term Intervention with Pravastatin in Ischaemic Disease(LIPID) Study Group.Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels[J]. N Engl J Med, 1998, 339:1349-1357.
[20] Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: A randomised placebo-controlled trial[J]. Lancet, 2002, 360: 7-22.
[21] Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia: West of Scotland Coronary Prevention Study Group[J]. N Engl J Med, 1995, 333: 1301- 1307.
[22] Sacks FM, Tonkin AM, Shepherd J, et al for the Prospective Pravastatin Pooling Project Investigators Group. Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: The Prospective Pravastatin Pooling Project[J]. Circulation, 2000,102: 1893-1900.
[23] Cannon CP, Braunwald E, McCabe CH, et al for the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes[J]. N Engl J Med,2004,350: 1495-1504.
[24] Takashi Y, Akihiro A, Susumu S, et al. Randomized Evaluation of Atorvastatin in Patients With Coronary Heart Disease A Serial Intravascular Ultrasound Study[J]. Circ J, 2007, 71:1845-1850.
[25] Nissen SE, Tuzcu EM, Schoenhagen P, et al; REVERSAL Investigators. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis:A randomized controlled trial[J]. JAMA, 2004, 291:1071-1080.
[26] Nissen SE, Nicholls SJ, Sipahi I, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: The ASTEROID trial[J]. JAMA, 2006, 295:1556-1565.
[27] Campbell CY, Rivera JJ, Blumenthal RS. Residual risk in statin-treated patients: future therapeutic options[J]. Curr Cardiol Rep, 2007;9(6):499-505.
[28] Roze S, Ferrieres J, Bruckert E, et al. Cost-effectiveness of raising HDL cholesterol by adding prolonged-release nicotinic acid to statin therapy in the secondary prevention setting: a French perspective[J]. Int J Clin Pract, 2007;61(11):1805-11.
[29] Steven E, Stephen J, Ilke S, et al. Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis The ASTEROID Trial[J], JAMA, 2006, 295:1556-1565.
[30] Jukema JW, Liem AH, Dunselman PH, et al. LDL-C/HDL-C ratio in subjects with cardiovascular disease and a low HDL-C: results of the RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) study. Curr Med Res Opin[J],2005;21(11): 1865-74.
[31] Jones PH, Davidson MH, Stein EA, et al. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial) [J]. Am J Cardiol, 2003;92(2):152-60.
[32] Jensen LO, Thayssen P, Mintz GS, et al. Intravascular ultrasound assessment of remodelling and reference segment plaque burden in type-2 diabetic patients[J]. Eur Heart J, 2007,28:1759-1764.
[33] Schukro C, Syeda B, Yahya N, et al. Volumetric intravascular ultrasound imaging to illustrate the extent of coronary plaque burden in type 2 diabetic patients[J]. J Diabetes Complication,2007,21:381-386.
[34] Tauth J, Pinnow E, Sullebarger JT, et al. Predictors of coronary arterial remodeling patterns in patients with myocardial ischemia[J]. Am J Cardiol, 1997, 80:1352-1355.
[35] Nishioka T, Nagai T, Luo H, et al. Coronary remodeling of proximal and distal stenotic aterosclerotic plaque within the same artery by intravascular ultrasound study[J]. Am J Cardiol, 2001, 87:387-391.
[36] Burke AP, Weber DK, Kolodgie FD,et al. Pathophysiology of calcium deposition in coronary arteries[J]. Herz 2001;26:239-244.
[37] Ramakrishna G, Miller TD, Breen JF, et al. Relationship and prognostic value of coronary artery calcification by electron beam computed tomography to stress-induced ischemia by single photon emission computed tomography[J]. Am Heart J 2007; 153:807-814.
[38] Shisen J, Leung DY, Juergens CP. Gender and age differences in the prevalence of coronary artery calcification in 953 Chinese subjects[J]. Heart Lung Circ 2005;14:69-73.
[39] Keelan PC, Bielak LF, Ashai K, Jamjoum LS, Denktas AE, Rumberger JA, Sheedy II PF,Peyser PA, Schwartz RS. Long-term prognostic value of coronary calcification detected by electron-beam computed tomography in patients undergoing coronary angiography[J].Circulation 2001;104:412-417.
[40] Arad Y, Spadaro LA, Goodman K, et al. Prediction of coronary events with electron beam computed tomography[J]. J am Coll Cardiol 2000;36:1253-1260.
[41] Raggi P, Callister TQ, Cooil B, et al. Identification of patients at increased risk of first unheralded acute myocardial infarction by electron-beam computed tomography[J].Circulation 2000; 101:850-855.
[42] Konieczynska M, Tracz W, Pasowicz M, Przewlocki T. Use of coronary calcium score in the assessment of atherosclerotic lesions in coronary arteries[J]. Kardiol Pol 2006;64:1073-1079.
[43] de Feyter PJ, Ozaki Y, Baptista J, et al. Ischemia-related lesion characteristics in patients with stable or unstable angina. A study with intracoronary angioscopy and ultrasound[J].Circulation 1995;92:1408-1413.
[44] Beckman JA, Ganz J, Creager MA, et al. Relationship of clinical presentation and calcification of culprit coronary artery stenoses[J]. Arterioscler Thromb Vasc Biol 2001;21:1618-1622.
[45] Mintz GS, Pichard AD, Popma JJ, et al. Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study[J]. J Am Coll Cardiol 1997;29:268-274.
[46] Rasheed Q, Nair R, Sheehan H, Hodgson JM. Correlation of intracoronary ultrasound plaque characteristics in atherosclerotic coronary artery disease patients with clinical variables[J]. Am J Cardiol 1994;73:753-758.
[47] Ehara S, Kobayashi Y, Kataoka T, Yoshiyama M, et al. Quantification of coronary calcification by intravascular ultrasound[J]. Circ J 2007;71:530-535.
[48] Ehara S, Kobayashi Y, Yoshiyama M, et al. Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study[J]. Circulation2004;110:3424-3429.
[49] Fujii K, Carlier SG, Mintz GS, et al. Intravascular ultrasound study of patterns of calcium in ruptured coronary plaques[J]. Am J Cardiol 2005;96:352-357.
[50] Mintz GS, Pichard AD, Kent KM, et al. Axial plaque redistribution as a mechanism of percutaneous transluminal coronary angioplasty[J]. Am J Cardiol, 1996, 77: 427-430.
[51] Honda Y, Yock CA, Hermiller JB, et al. Longitudinal redistribution of plaque is an important mechanism for lumen expansion in stenting. J Am Coll Cardiol, 1997, 29 (suppl A) : 281A.
[52] Maehara A, Takagi A, Okura H, et al. Longitudinal plaque redistribution during stent expansion[J]. Am J Cardiol, 2000, 86: 1069-1072.
[53] Algowhary M, Matsumura A, Hashimoto Y, et al. Poststenting axial redistribution of atherosclerotic plaque into the reference segments and lumen reduction at the stent edge[J].Int Heart J, 2006, 47: 159-171.
[54] Ahmed JM, Mintz GS, Weissman NJ, et al. Mechanism of lumen enlargement during intracoronary stent implantation: an intravascular ultrasound study[J]. Circulation, 2000, 102:7-10.
[55] Dudek D, Legutko J, Kaluza GL, et al. Intravascular ultrasonic evaluation of the magnitude of stent expansion and the mechanisms of lumen enlargement after direct stenting and after conventional stenting with balloon predilatation[J]. Am J Cardiol, 2002, 90: 639-641.
[56] Finet G, Weissman NJ, Mintz GS, et al. Comparison of luminal enlargement by direct coronary stenting versus predilation coronary stenting by three-dimensional volumetric intravascular ultrasound analysis[J]. Am J Cardiol, 2001, 88: 1179-1182.
[57] Albertal M, Abizaid A, Munoz JS, et al. A novel mechanism explaining early lumen loss following balloon angioplasty for the treatment of in-stent restenosis[J]. Am J Cardiol, 2005,95: 751-754.
[2] Nissen SE, Tuzcu EM, Schoenhagen P, et al. Effect of intensive compared with moderate lipid-lowing therapy on progression of coronary atherosclerosis: a randomized controlled trial (REVERSAL) [J]. JAMA, 2004, 291: 1071-1080.
[3] Yamada T, Azuma A, Sasaki S, et al. Randomized evaluation of atorvastatin in patients with coronary heart disease: a serial intravascular ultrasound study[J]. Circ J, 2007, 71:1845-1850.
[4] Okkels Jensen L, Thayssen P, Pederson KE, et al. Regression of coronary atherosclerosis by simvastatin: a serial intravascular ultrasound study[J]. Circulation, 2004, 110: 265-270.
[5] Konig A, Kilian E, Rieber J, et al. Assessment of early atherosclerosis in de novo heart transplant recipients: analysis with intravascular ultrasound-derived radiofrequency analysis[J]. J Heart Lung Transplant, 2008, 27: 26-30.
[6] Kavamoto T, Okura H, Koyama Y, et al. The relationship between coronary plaque characteristics and small embolic particles during coronary stent implantation[J]. J Am Coll Cardiol, 2007, 50: 1635-1640.
[7] Von Birgelen C, Hartmann M, Mintz GS, et al. Relationship between cardiovascular risk as predicted by established risk scores versus plaque progression as measured by serial intravascular ultrasound in left main coronary arteries[J]. Circulation, 2004, 110: 1579-1585.
[8] Von Birgelen C, Hartmann M, Mintz GS, et al. Spectrum of remodeling behavior observed with serial long-term (>/=12 months) follow-up intravascular ultrasound studies in left main coronary arteries[J]. Am J Cardiol, 2004, 93: 1107-1113.
[9] Shiran A, Mintz GS, Leiboff B, et al. Serial volumetric intravascular ultrasound assessment of arterial remodeling in left main coronary artery disease[J]. Am J Cardiol, 1999, 83:1427-1432.
[10] Schartl M, Bocksch W, Fateh-Moghadam S, on behalf of the GAIN-Study group. Effects of lipid-lowing on coronary artery remodeling[J]. Coron Artery Dis, 2004, 15: 45-51.
[11] Sipahi I, Tuzcu EM, Moon KW, et al. Do the extent and direction of arterial remodelling predict subsequent progression of coronary atherosclerosis? A serial intravascular ultrasound study[J]. Heart, 2008, 94: 623-627.
[12] Kume T, Okura H, Kawamoto T, et al. Relationship between coronary remodeling and plaque characterization in patients without clinical evidence of coronary artery disease[J].Atherosclerosis, 2008, 197: 799-805.
[13] GyOngyOsi M, Yang P, Hassan A, et al. Arterial remodeling of native human coronary arteries in patients with unstable angina pectoris: a prospective intravascular ultrasound study[J]. Heart, 1999, 82: 68-74.
[14] 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: 804-808.
[15] Mintz GS, Pichard AD, Kent KM, et al. Axial plaque redistribution as a mechanism of percutaneous transluminal coronary angioplasty[J]. Am J Cardiol, 1996, 77: 427-430.
[16] Honda Y, Yock CA, Hermiller JB, et al. Longitudinal redistribution of plaque is an important mechanism for lumen expansion in stenting[J]. J Am Coll Cardiol, 1997, 29 (suppl A) :281A.
[17] Maehara A, Takagi A, Okura H, et al. Longitudinal plaque redistribution during stent expansion[J]. Am J Cardiol, 2000, 86: 1069-1072.
[18] Algowhary M, Matsumura A, Hashimoto Y, et al. Poststenting axial redistribution of atherosclerotic plaque into the reference segments and lumen reduction at the stent edge[J].Int Heart J, 2006, 47: 159-171.
[19] The Long-Term Intervention with Pravastatin in Ischaemic Disease(L[PlD) Study Group.Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels[J]. N Engl J Med, 1998, 339:1349-1357.
[20] Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: A randomised placebo-controlled trial[J]. Lancet, 2002, 360: 7-22.
[21] Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia: West of Scotland Coronary Prevention Study Group[J]. N Engl J Med, 1995, 333: 1301- 1307.
[22] Sacks FM, Tonkin AM, Shepherd J, et al for the Prospective Pravastatin Pooling Project Investigators Group. Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: The Prospective Pravastatin Pooling Project[J]. Circulation, 2000,102: 1893-1900.
[23] Cannon CP, Braunwald E, McCabe CH, et al for the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes[J]. N Engl J Med,2004,350: 1495-1504.
[24] Takashi Y, Akihiro A, Susumu S, et al. Randomized Evaluation of Atorvastatin in Patients With Coronary Heart Disease A Serial Intravascular Ultrasound Study[J]. Circ J, 2007, 71:1845-1850.
[25] Nissen SE, Tuzcu EM, Schoenhagen P, et al; REVERSAL Investigators. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis:A randomized controlled trial[J]. JAMA, 2004, 291:1071-1080.
[26] Nissen SE, Nicholls SJ, Sipahi I, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: The ASTEROID trial[J]. JAMA, 2006, 295:1556-1565.
[27] Campbell CY, Rivera JJ, Blumenthal RS. Residual risk in statin-treated patients: future therapeutic options[J]. Curr Cardiol Rep, 2007;9(6):499-505.
[28] Roze S, Ferrieres J, Bruckert E, et al. Cost-effectiveness of raising HDL cholesterol by adding prolonged-release nicotinic acid to statin therapy in the secondary prevention setting:a French perspective[J]. Int J Clin Pract, 2007;61(11):1805-11.
[29] Steven E, Stephen J, Ilke S, et al. Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis The ASTEROID Trial[J], JAMA, 2006, 295: 1556-1565.
[30] Jukema JW, Liem AH, Dunselman PH, et al. LDL-C/HDL-C ratio in subjects with cardiovascular disease and a low HDL-C: results of the RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) study. Curr Med Res Opin[J],2005;21(11):1865-74.
[31] Jones PH, Davidson MH, Stein EA, et al. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial) [J]. Am J Cardiol, 2003;92(2):152-60.
[32] Jensen LO, Thayssen P, Mintz GS, et al. Intravascular ultrasound assessment of remodelling and reference segment plaque burden in type-2 diabetic patients[J]. Eur Heart J, 2007,28:1759-1764.
[33] Schukro C, Syeda B, Yahya N, et al. Volumetric intravascular ultrasound imaging to illustrate the extent of coronary plaque burden in type 2 diabetic patients[J]. J Diabetes Complication,2007,21:381-386.
[34] Tauth J, Pinnow E, Sullebarger JT, et al. Predictors of coronary arterial remodeling patterns in patients with myocardial ischemia[J]. Am J Cardiol, 1997, 80:1352-1355.
[35] Nishioka T, Nagai T, Luo H, et al. Coronary remodeling of proximal and distal stenotic aterosclerotic plaque within the same artery by intravascular ultrasound study[J]. Am J Cardiol, 2001, 87:387-391.
[36] Burke AP, Weber DK, Kolodgie FD,et al. Pathophysiology of calcium deposition in coronary arteries[J]. Herz 2001;26:239-244.
[37] Ramakrishna G, Miller TD, Breen JF, et al. Relationship and prognostic value of coronary artery calcification by electron beam computed tomography to stress-induced ischemia by single photon emission computed tomography[J]. Am Heart J 2007; 153:807-814.
[38] Shisen J, Leung DY, Juergens CP. Gender and age differences in the prevalence of coronary artery calcification in 953 Chinese subjects[J]. Heart Lung Circ 2005; 14:69-73.
[39] Keelan PC, Bielak LF, Ashai K, Jamjoum LS, Denktas AE, Rumberger JA, Sheedy II PF,Peyser PA, Schwartz RS. Long-term prognostic value of coronary calcification detected by electron-beam computed tomography in patients undergoing coronary angiography[J].Circulation 2001;104:412-417.
[40] Arad Y, Spadaro LA, Goodman K, et al. Prediction of coronary events with electron beam computed tomography[J]. J am Coll Cardiol 2000;36:1253-1260.
[41] Raggi P, Callister TQ, Cooil B, et al. Identification of patients at increased risk of first unheralded acute myocardial infarction by electron-beam computed tomography[J].Circulation 2000;101:850-855.
[42] Konieczynska M, Tracz W, Pasowicz M, Przewlocki T. Use of coronary calcium score in the assessment of atherosclerotic lesions in coronary arteries[J]. Kardiol Pol 2006;64:1073-1079.
[43] de Feyter PJ, Ozaki Y, Baptista J, et al. Ischemia-related lesion characteristics in patients with stable or unstable angina. A study with intracoronary angioscopy and ultrasound[J].Circulation 1995;92:1408-1413.
[44] Beckman JA, Ganz J, Creager MA, et al. Relationship of clinical presentation and calcification of culprit coronary artery stenoses[J]. Arterioscler Thromb Vasc Biol 2001;21:1618-1622.
[45] Mintz GS, Pichard AD, Popma JJ, et al. Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study[J]. J Am Coll Cardiol 1997;29:268-274.
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