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一、前景理论前景理论(Prospect Theory)金融学的四大研究成果,即前景理论(或视野理论)(Prospect Theory)、后悔理论(Regret Theory)、过度反应理论(Overreaction Theory)及过度自信理论(Over confidence Theory)。
前景理论概述很多学者研究风险以及不确定性条件下的决策，提出的模型非常多，其中最常用的被接受的理性选择模型是Von Neumann和Morgenstern(1953)发展的财富预期效用理论。
该理论提供了数学化的公理，是一个标准化的模型(解决了当人们面对风险选择时他们应该怎样行动的问题)，应用起来比较方便。
但是在最近的几十年，该理论遇到了很多问题，它不能解释众多的异象，它的几个基础性的公理被实验数据所违背，这些问题也刺激了其它的一些试图解释风险或者不确定性条件下个人行为的理论的发展。
前景理论(Prospect Theory)就是其中比较优秀的一个。
前景理论认为人们通常不是从财富的角度考虑问题，而是从输赢的角度考虑，关心收益和损失的多少。
前景理论的产生前景理论（PT）首先由国外学者Kahneman和阿莫斯·特沃斯基（Amos Tversky）(1979)(用KT代表两个作者)明确的提出，他们认为个人在风险情形下的选择所展示出的特性和VonNeumann—Morgenstem的效用理论的基本原理是不相符的。
一是他们发现和确定性的结果相比个人会低估概率性结果，他们称之为确定性效应(Certainty Effect)。
KT还指出确定性效应导致了当选择中包含确定性收益时的风险厌恶以及当选择中包含确定性损失的风险寻求。
二是他们还发现了孤立效应(Isolation Effect)，即当个人面对在不同前景的选项中进行选择的问题时，他们会忽视所有前景所共有的部分。
孤立效应会导致当一个前景的描述方法会改变个人决策者决策的变化。
基于PROSPECT模型的植物叶片干物质估测建模研究王洋;肖文;邹焕成;陆婧楠;曹英丽;于丰华【摘要】为了快速、准确估测植物叶片干物质含量,为作物长势及健康状况监控提供数据支撑,利用光谱分析技术探讨了干物质含量敏感光谱波段提取方法及其估测建模方法.试验数据由叶片辐射传输模型PROSPECT在干物质含量(0.001~0.02)g?cm-2范围内进行模拟,随机产生1000条400~2500nm的光谱曲线,其中600条光谱曲线用于建模研究、400条光谱曲线作为模型验证数据,同时应用叶片光学特性数据库LOPEX93中325条叶片光谱-干物质含量数据进行进一步验证.首先应用试验数据进行局部敏感性分析,初步得到叶片干物质敏感波段范围,再运用改进Sobol算法进行全局敏感性分析,提取了干物质含量敏感的光谱波段范围,在此敏感波段范围运用波段组合算法计算归一化植被指数NDVI与叶片干物质含量相关系数,优选了4组相关性大的波段组合建立归一化干物质指数NDMI(1644,1719)、NDMI(1871,2294)、NDMI(2150,2271)、NDMI(1496,2282)用于干物质含量估测建模.结果表明:NDMI(1644,1719)和NDMI(1871,2294)模型中三次多项式形式(cubic)效果最佳、NDMI(1496,2282)模型中幂指数形式(power)效果最佳,三者中NDMI(1871,2294)的三次多项式模型最优,决定系数R2为0.837,对叶片干物质含量具有较好的估测能力.%In order to estimate the dry matter of plant leaves quickly and accurately and provide data support for crop growth and health status monitoring, we used spectral analysis technique to explore the extraction method of dry matter sensitive spectral bands and its estimation modeling method. The experimental data were simulated by leaf optical properties spectra (PROSPECT) in direct mode, when dry matter in the range of 0.001-0.02g?cm-2. From the randomly generated 1000 spectral curves between 400 nm and 2500 nm, 600 spectral curves were used for modeling studies, and 400 spectral curves were used as model validation data. The models were further validated by the 325 leaves spectral-dry matter data from the Leaf Optical Properties Experiment 93(LOPEX93). Firstly, local sensitivities of leaf dry matter were preliminarily obtained by using the experimental data, and then global sensitivity was analyzed by using the improved Sobol algorithm. The range of spectral bands sensitive to dry matter was extracted, and the spectral combination algorithm was used to calculate the correlation coefficient between the normalized vegetation index NDVI and the dry matter of plant leaves. Four groups of correlation bands NDMI (1644,1719), NDMI (1871,2224), NDMI(2150,2271) and NDMI (1496, 2282) were used as characteristic bands for dry matter estimation modeling. The results showed that the cubic polynomials in NDMI(1644,1719)andNDMI(1871, 2294)models were the best, and that the power exponent in NDMI(1496,2282)model was the best. Among the three models, the third-order polynomial model of NDMI(1871, 2294)was the best, and the coefficient of determination R2was 0.837, which had good estimation ability.【期刊名称】《沈阳农业大学学报》【年(卷),期】2018(049)001【总页数】7页(P121-127)【关键词】叶片干物质含量;敏感性分析;PROSPECT模型;LOPEX93数据集;光谱指数【作者】王洋;肖文;邹焕成;陆婧楠;曹英丽;于丰华【作者单位】沈阳农业大学辽宁省农业信息化工程技术中心/信息与电气工程学院,沈阳110161;沈阳农业大学辽宁省农业信息化工程技术中心/信息与电气工程学院,沈阳110161;沈阳农业大学辽宁省农业信息化工程技术中心/信息与电气工程学院,沈阳110161;沈阳农业大学辽宁省农业信息化工程技术中心/信息与电气工程学院,沈阳110161;沈阳农业大学辽宁省农业信息化工程技术中心/信息与电气工程学院,沈阳110161;沈阳农业大学辽宁省农业信息化工程技术中心/信息与电气工程学院,沈阳110161【正文语种】中文【中图分类】Q948;TP79植物叶片干物质含量是重要的生化参数之一，叶片干物质的有效积累可促进植物生长、提高植物光合作用效率，且与叶片寿命、抗逆性具有很大相关性[1-3]，是作物长势和健康状态的重要指标。
关于PROSPECT 建议的说明
PROSPECT 根据已发表的证据和专家意见，为临床医生提供赞成和反对使用各种术后疼痛干预措施的支持性论据。
临床医生必须根据临床情况和当地法规做出判断。
任何时候都必须参考所提及药物的当地处方信息。
建议等级（GoR ）根据建议所依据的总体证据级别（LoE ）进行指定，这取决于证据的质量和来源。
证据级别和建议等级。
汇总表
Study type
研究类型
可以在以下链接中找到如何执行研究质量评估以确定LoE和GoR的说明：剖宫产：证据级别和建议等级。
研究和评估指南（AGREE） II的工具（Brouwers，2010年）在国际上被用于评估实践指南的方法严谨性和透明度。
PROSPECT剖宫产审核的方法尽可能符合AGREE II工具“领域3：制定的严谨性”的要求：
∙用系统方法来搜索证据。
∙清楚地描述了选择证据的标准。
∙明确描述了证据的优点和局限性。
∙清楚地描述了制定建议的方法。
∙在制定建议时考虑了健康益处、副作用和风险。
∙建议与支持性证据之间存在明确的联系。
∙专家在该指南出版前已对该指南进行了外部审核。
[证据和建议将在PROSPECT网站上公布后提交给同行评审]
∙提供了更新指南的程序。
[提供方法，以便根据需要对系统性评价进行更新]
摘要建议
总体建议：择期剖宫产手术的疼痛管理
不建议用于剖宫产。
・２３４・医堂绫述！Ｑ塑生！旦筮！！鲞箍！翅丛！！ｉ趔曼璺：！唑！！坐：』塑！Ｑ塑：Ｙ生：！§：丛！：呈超声心动图在心脏再同步化治疗中的应用现状和进展曹睿△（综述），吴棘（审校）（广西医科大学第一附属医院超声诊断科，南宁５３００２１）中图分类号：１１５４１．６；Ｒ４４５．１文献标识码：Ａ文章编号：１００６－２０８４（２００９）０２４３２３４－０４摘要：心脏再同步化治疗（ＣＲＴ）已经成为对于严重心力衰竭及内科难治性心力衰竭患者的一种可选择性治疗方法，几项较大的研究已经证明了ＣＲＴ的有效性。
ＣＲＴ的治疗机制是改善房室同步性、室问同步性和室内同步性。
超声心动图（ＥＣＧ）尤其是各种新技术在准确评估心脏机械不同步运动的部位、范围及程度方面均具有重大作用。
现详细介绍二维、Ｍ型及脉冲多普勒３种传统ＥＣＧ技术和组织多普勒成像、￡维斑点追踪成像和三维全客积等新技术如何评价心脏机械同步性。
ＥＣＧ在为ＣＲＴ筛选合适患者，优化起搏程序，评价并随访疗效等方面具有重要临床意义。
关键词：超声心动图；机械同步性；心脏再同步化治疗；心力衰竭ＡｄｖａｎｃｅｓｉｎＥｃｈｏｃａｒｄｉｏｇｒａｐｈｙｏｎＣａｒｄｉａｃＲｅｓｙｎｃｈｒｏｎｉｚａｔｉｏｎＴｈｅｒａｐｙＣＡＯＲｕｉ，ＷＵ且．（Ｄｅｐａｒｔｍｅｎｔ矿Ｕｌｔｒａｓｏｎｏｇｒａｐｈｙ，ｔｈｅＦｉｒｓｔＡｆｆｉｌｉａｔｅｄＨｏｓｐｉｔａｌｏｆＧｕａｎｇｘｉＭｅｄｉｃａｌＵｎｈｅｒｓ蚵，Ｎａｎｎｉｎｇ５３００２１，Ｃｈｉｎａ）Ａｂｓｔｒａｃｔ：Ｃａｒｄｉａｃｒｅｓｙｎｃｈｒｏｎｉｚａｔｉｏｎｔｈｅｒａｐｙ（ＣＲＴ）ｈａｓｂｅｃａｍｅａｎａｌｔｅｒｎａｔｉｖｅｔｒｅａｔｍｅｎｔｉｎｐａｔｉｅｎｔｓｗｉｔｈｓｅｖｅｒｅｍｅｄｉｃａｌｌｙｒｅｆｒａｃｔｏｒｙｈｅａｒｔｆａｉｌｕｒｅｉｎｒｅｃｅｎｔｙｅａｒｓ．Ｓｅｖｅｒａｌｌａｒｇｅｓｔｕｄｉｅｓｈａｖｅｄｅｍｏｎｓｔｒａｔｅｄｔｈｅｅｆ－ｆｅｃｔｉｖｅｎｅｓｓｏｆＣＲＴ，ｗｈｉｃｈｃａｎｉｍｐｒｏｖｅｔｈｅａｔｒｉｏｖｅｎｔｒｉｅｕｌａｒ，ｉｎｔｅｒｖｅｎｔｒｉｃｕｌａｒ，ａｎｄｉｎｔｒａｖｅｎｔｒｉｃｕｌａｒｄｙｓｓｙｎｃｈｒｏ—ｎｙ．Ｅｃｈｏｃａｒｄｉｏｇｒａｐｈｙｐｌａｙｓａｎｉｍｐｏｒｔａｎｔｒｏｌｅｉｎｐｒｅｃｉｓｅａｓｓｅｓｓｍｅｎｔｌｏｃａｔｉｏｎ．ｒａｎｇｅａｎｄｄｅｇｒｅｅｏｆｃａｒｄｉａｃｍｅ．ｃｈａｎｉｅａｌｄｙｓｓｙｎｃｈｍｎｙ．Ｔｈｉｓａｒｔｉｃｌｅｉｎｔｒｏｄｕｃｅａｓｅｒｉｅｓｏｆｔｒａｄｉｔｉｏｎａｌａｎｄｎｏｖｅｌｔｅｃｈｎｉｑｕｅｏｆｅｅｈｏｃａｒｄｉｏｇｒａｐｈｙ．ｉｎｃｌｕｄｉｎｇＭｍｏｄｅｌ，ｐｕｌｓｅｗａｖｅＤｏｐｐｌｅｒ，ｔｉｓｓｕｅＤｏｐｐｌｅｒｉｍａｓｉｎｇ，ｓｐｅｃｋｌｅｔｒａｃｋｉｎｇｉｍａｇｉｎｇａｎｄｔｈｒｅｅ—ｄｉｍｅｎ—ｓｉｏｎａｌｆｕｌｌｖｏｌｕｍｅ．ＥｅｈｏｃａｒｄｉｏｇｒａｐｈｙｓｈｏｗｓｉｍｐｏｒｔａｎｔｃｌｉｎｉｃａｌｍｅａｎｉｎｇｉｎｓｅａｒｃｈｉｎｇｓｕｉｔａｂｌｅｐａｔｉｅｎｔｓｆｏｒＣＲＴ，ｏｐｔｉｍｉｚｉｎｇＡＶａｎｄＶＶｄｅｌａｙ，ｅｖａｌｕａｔｉｎｇａｎｄｆｏｌｌｏｗｉｎｇｕｐｅｆｆｅｃｔｏｆＣＲＴ，Ｋｅｙｗｏｒｄｓ：Ｅｃｈｏｃａｒｄｉｎｇｒａｐｈｙ；Ｍｅｃｈａｎｉｃａｌｓｙｎｃｈｒｏｎｉｃｉｔｙ；Ｃａｒｄｉａｃｒｅｓｙｎｃｈｒｏｎｉｚａｔｉｏｎｔｈｅｒａｐｙ；Ｈｅａｒｔｆａｉｌｕｒｅ心力衰竭是目前心血管领域非常重要的一项公共健康问题，世界总人口的１％一５％都曾罹患心力衰竭。
急性冠脉综合征（ACS ）是一组由于易损斑块破裂或侵蚀引起的冠脉内急性血栓形成的严重临床综合征，其发病率和死亡率位居各类疾病前列［1］。
许多国家心肌梗死发病率大幅下降源于积极有效地进行传统ACS危险因素干预［2-3］，早期发现、预防高危斑块形成，尤其是临床症状不典型的患者，对减少心血管相关事件至关重要。
近年来，越来越多的研究证实了许多ACS 事件发生在血管造影提示管腔轻-中度狭窄的情况下。
目前ACS 的诊断依赖心电图、心肌酶水平、冠脉造影等检查手段。
但心肌酶的敏感度和特异性不够理想，而冠脉造影检查需要待官腔狭窄到一定程度方能明确诊断，血管内成像设备又因其无法实现对动脉管壁细胞结构的准确判断，无法评估动脉粥样硬化斑块的特征等因素限制了广泛使用。
因此，研究高敏感度、高特异性、高便捷性的诊断新方法，具有良好的临床应用价值和社会经济效益。
虽然冠状动脉造影是明确ACS 的金标准，但由于缺乏高效的生物标记物评估系统和精确地在体腔内影像学探测手段识别高危易损斑块，无法将临床实验室检查结果与动脉粥样硬化斑块负荷、面积等进行整合分析得出可靠的相关性数据。
如何避免慢性冠状动脉综合征患者发生急性冠状动脉事件成为研究热点。
各种血管内成像技术致力于对斑块稳定性的评估——包括血管内超声、心肌磁共振成像、PET 成像、光学相干断层扫描、近红外光谱和光学相干弹性成像等单模态或多模态影像技术应运而生。
近年来，心脏病专家与医学工程师通力合作，突破了台式成像设备转为床旁时遇到的瓶颈，兴起了多模态血管内成像技术的临床研究。
受益于多学科协同合作发展、科研院所、企业和政府资助，多模态血管内成像的临床转化可以深入了解冠状动脉疾病病理生理过程，终极目标是通过多模态成像帮助临床医生优化个体化治疗方案和改善预后。
Advances in Multimodality Intravascular Imaging for Identification of High-risk Vulnerable Plaques in Coronary ArteriesYANG Fan 1,WU Jianjun 1,21Key Laboratory of Myocardial Ischemia,Ministry of Education,2Department of Cardiology,The Second Affiliated Hospital of Harbin Medical University,Harbin 150001,China摘要：冠状动脉粥样硬化斑块破裂或侵蚀引起的血栓形成造成心肌梗死事件的发生。
冠脉腔内影像学进展重点内容目前经皮冠脉介入治疗（PCI）正逐渐步入“精准PCI”时代，即应用腔内影像（OCT、IVUS等）及生理学检查（FFR、iFR等）手段更加精准地为每位患者制定个体化治疗方案，最终获得更好的疗效。
冠脉腔内影像学技术不仅可以提供更多的冠脉解剖信息，而且可以指导优化手术策略，提高手术安全性以及改善患者预后。
因此被国内外众多PCI指南或专家共识推荐。
现将近2年冠脉腔内影像学的最新进展进行简要的介绍。
一、腔内影像指导PCI的真实世界研究：ULTIMATE研究是南京市第一医院陈绍良教授牵头的前瞻性、多中心、随机对照研究，共纳入1448例拟接受DES置入的患者，按1:1随机分为造影组和IVUS指导组，研究定义了IVUS评估支架置入满意的标准需同时满足1）支架段内最小管腔面积（MLA）大于5.0mm2或远端参考段内最小管腔面积的90%；2）支架边缘近端或远端5mm斑块负荷小于50%；3）边缘夹层累及中膜不超过3mm，如不能同时满足则定义为次优标准。
术后1年的随访结果显示IVUS组的靶血管失败（TVF）显著降低。
2020年公布的三年随访结果显示IVUS组TVF、支架内血栓发生率更低。
同时IVUS最优组3年内TVF发生率低于次优组。
研究提示：IVUS指导下的DES植入术可以使患者的获得更好的临床结局，尤其在IVUS指导下获得最佳优化的患者中获益更明显。
二、腔内影像对高危斑块识别的最新研究：CLIMA研究前瞻性纳入了1003例对非罪犯病变的前降支行OCT检查的STEMI患者，将同时符合最小管腔面积＜3.5mm2，纤维帽厚度＜75μm，脂质角度＞180°以及巨噬细胞浸润定义为OCT-高危斑块。
术后1年的随访结果显示OCT-高危斑块是主要冠脉事件（心源性死亡和靶血管节段心肌梗死）的独立预测因子。
该研究提示应用OCT对高危斑块的判定有利于识别高危人群。
2020年7月哈医大二院于波教授团队在《JACC Cardiovascular Imaging》杂志上发表了一项旨在揭示STEMI患者全冠脉斑块特征的OCT 研究结果。
冠脉CT血管造影诊断高危斑块病变影像学特征分析心血管疾病已经成为全球第一死因。
大多数心血管病患者都是死于冠心病和卒中，死亡人数将从2008年的1730万激增到2030年的2330万。
急性心肌梗死和心脏性猝死是导致患者死亡率急剧上升的罪魁祸首，大多数患者在冠脉事件（急性冠脉综合征【ACS】或突发心脏性猝死）急性发作之前都没有任何征状或者警示征兆。
目前看来，想有效地减轻心血管疾病所带来的负担以及降低死亡率和发病率，只有做好急性冠脉事件的预防工作。
但是，如何使用心血管影像学来确定患者是否处于急性冠脉事件的边缘，也是一个急需解决的难题。
当下的诊断策略显然侧重于检测有无心肌缺血和血流动力学管腔狭窄，而不是针对冠状动脉粥样硬化斑块本身。
这种策略适合已经出现症状的患者，却忽略了以急性冠脉事件为始发症状的CAD患者。
尸检报告显示，大多数急性冠脉事件的发生，是由于斑块破裂，导致突发管腔内血栓形成所诱发的。
易于破裂的冠脉病变斑块在形态上与稳定型斑块截然不同（见图1），利用这点，可以在早期采用非有创的影像学检查来鉴别易损斑块。
而且，相对于传统的检测管腔狭窄，检测冠脉斑块的组成和尺寸更有利于早期诊断急性冠脉事件。
图 1 稳定型斑块和易损斑块的形态学与功能特征冠状动脉CT血管造影（CCTA）可以对冠状动脉粥样硬化斑块进行无创性评估，而不仅限于检测冠脉管腔。
CCTA可以明确冠脉的分支走向和动脉粥样硬化斑块的整体情况，但一般的检测方法只能辨别管腔狭窄与否或者根据钙离子水平判断斑块类型。
有了新的应用设备，影像指导下的预防、药物治疗和冠脉介入治疗效果都能得到相应的改善。
根据斑块特性进行分层，可制定相应的个性治疗方案。
因此，我们需要掌握解析CCTA的能力，而不仅仅是判断管腔狭窄情况。
本文既描述了CCTA如何检测并描述易损斑块的形态和功能特性，也展示了最新的图像后处理技术和计算机流体力学模拟技术如何评估冠脉斑块与狭窄。
最后，文章还探讨未来的成像技术如何在检测动脉粥样硬化斑块和早期诊断ACS患者方面有着重大的临床意义。
Relation Between Angiographic Lesion Severity,Vulnerable Plaque Morphology and Future Adverse Cardiac Events(from the Providing Regional Observations to Study Predictors of Events inthe Coronary Tree Study)Kyeong Ho Yun,MD a,b,c,Gary S.Mintz,MD b,Naim Farhat,MD d,Steven P.Marso,MD e, Nevio Taglieri,MD f,Stefan Verheye,MD g,Michael C.Foster,MD h, M.Pauliina Margolis,MD,PhD i,Barry Templin,MBA j,Ke Xu,PhD b,Ovidiu Dressler,MD b, Roxana Mehran,MD b,k,Gregg W.Stone,MD a,b,and Akiko Maehara,MD a,b,*Previous angiographic studies have suggested that the future risk for major adversecardiovascular events(MACEs)is related to coronary stenosis severity.The aim of thisstudy was to use the grayscale and virtual histology(VH)–intravascular ultrasound(IVUS)data from the Providing Regional Observations to Study Predictors of Events in theCoronary Tree(PROSPECT)study to identify underlying lesion morphologic character-istics that might explain thesefindings.In PROSPECT,patients presenting with acutecoronary syndromes in whom percutaneous coronary intervention was successful under-went3-vessel grayscale and VH-IVUS and were followed for a median of3.4years for theincidence of MACEs.Overall,3,115nonculprit lesions detected by IVUS were divided intoquartiles according to baseline angiographic diameter stenosis.From thefirst to fourthquartiles,there were increases in the prevalence of lesions with IVUS minimum luminalareas<4mm2,IVUS plaque burden>70%,and VH-IVUS thin-capfibroatheroma(13.4%,22.0%,24.2%,and30.3%,respectively,p<0.001),along with an increased frequency ofplaque ruptures and greater necrotic core volumes.The incidence of lesions with plaqueburden>70%,minimum luminal area<4mm2,and VH thin-capfibroatheroma washighest in the fourth quartile(0%,0.4%,0.4%,and2.8%in thefirst through fourthquartiles,respectively,p<0.001).Three-year MACE rates were also highest in the fourthquartile(0.3%,0.7%,1.3%,and5.1%,respectively,p<0.001).In conclusion,increasingangiographic diameter stenosis was associated with an increased frequency of grayscaleand VH-IVUS lesion morphologic features that have been associated with adverse eventsand that may,in part,explain why future MACEs were related to baseline lesionseverity.©2012Elsevier Inc.All rights reserved.(Am J Cardiol2012;110:471–477)Virtual histology(VH)–intravascular ultrasound(IVUS) correlates well with histopathology and potentially classi-fied plaques into phenotypical subtypes.1Patients enrolled in the Providing Regional Observations to Study Predictors of Events in the Coronary Tree(PROSPECT)study under-went3-vessel coronary angiography and grayscale and VH-IVUS after culprit lesions were successfully treated.2Al-though nonculprit lesions that subsequently resulted in future adverse cardiac events showed angiographically mild stenosis,by multivariate analysis,the independent predic-a Columbia University Medical Center;b The Cardiovascular Research Foundation,New York,New York;c Regional Cardiocerebrovascular Center, Wonkwang University Hospital,Iksan,South Korea;d North Ohio Heart Cen-ter/Elyria Memorial Hospital Regional Medical Center,Elyria,Ohio;e St. Luke’s Hospital,Kansas City,Missouri;f Azienda Ospedaliero-Universitaria Policlinico St.Orsola/Malpighi,Bologna,Italy;g Cardiovascular Center,ZNA Middelheim,Antwerp,Belgium;h Sisters of Charity Providence Hospitals, Columbia,South Carolina;i Volcano Corporation,Rancho Cordova,Califor-nia;j Abbott Vascular,Santa Clara,California;andk Mount Sinai Medical Center,New York,New York.Manuscript received April5,2012;revised manuscript received and accepted April17,2012.The Providing Regional Observations to Study Predictors of Events in the Coronary Tree(PROSPECT)study was funded by Abbott Vascular, Santa Clara,California,and funding was provided by Abbott Vascular and Volcano Corporation(Rancho Cordova,California).Dr.Yun has received grants from the Sung San Fellowship at Wonkwang University,Iksan,South Korea.Dr.Mintz has received research and grant support from Volcano Corporation and Boston Scientific Corporation,Natick,Massa-chusetts,and speaking honoraria from Boston Scientific Corporation.Dr. Mintz is a consultant for Volcano Corporation.Dr.Marso has received research grant support from Abbott Vascular;Boston Scientific Corpora-tion;Volcano Corporation;and Terumo Medical,Somerset,New Jersey. Dr.Foster has received speaking honoraria from Volcano Corporation and Boston Scientific Corporation.Dr.Margolis is an employee of Volcano Corporation.Mr.Templin was an employee of Abbott Vascular.Dr.Stone is a consultant to Abbott Vascular;Boston Scientific Corporation; Medtronic,Inc.,Minneapolis,Minnesota;Volcano Corporation;and InfraReDx,Burlington,Massachusetts.Dr.Maehara has received research grant support from Boston Scientific Corporation and speaking honoraria from Volcano Corporation.*Corresponding author:Tel:646-434-4569;fax:646-434-4464.E-mail address:amaehara@(A.Maehara).0002-9149/12/$–see front matter©2012Elsevier Inc.All rights /10.1016/j.amjcard.2012.04.018tors of nonculprit lesion–related events at3years of fol-low-up were the IVUS parameters of plaque burdenϾ70%, minimum luminal area(MLA)Ͻ4mm2,and VH-IVUS thin-capfibroatheroma(VH-TCFA).In the present study, we compared residual nonculprit angiographic stenosis se-verity to grayscale and VH-IVUS lesion morphology.Our hypothesis was that residual nonculprit lesions with increas-ing angiographic diameter stenoses would have larger plaque burdens,smaller MLAs,and more VH-TCFAs and would be associated with a higher rate of future major adverse cardiac events(MACEs).MethodsThe PROSPECT study design,major inclusion and ex-clusion criteria,end points,and definitions have been pre-viously described in detail.2In brief,697patients with acute coronary syndromes(ST-segment elevation myocardial in-farctionϾ24hours,non–ST-segment elevation myocardial infarction,or unstable angina)underwent angiography and multimodality intracoronary imaging of the proximal6to8 cm of all3coronary arteries after the performance of suc-cessful percutaneous coronary intervention of all coronary lesions responsible for the index event(culprit lesions)and other severe angiographic stenoses.Of the697patients enrolled in PROSPECT,angiographic and IVUS data wereavailable in659patients,thus constituting the study popu-lation.Intracoronary imaging,grayscale and VH-IVUS,was obtained using a synthetic-aperture-array,20-MHz,3.2Fr catheter(Eagle Eye,In-Vision Gold;Volcano Corporation, Rancho Cordova,California)with motorized catheter pull-back(0.5mm/s).Patients were then followed for a median of3.4years to relate subsequent events to the morphologies of the lesions detected at baseline.The study was approved by the institutional review board or medical ethics commit-tee at each participating center,and all patients gave written informed consent.Baseline and follow-up angiograms and baseline gray-scale and VH-IVUS studies were analyzed at separate core laboratories that were blinded to clinical outcomes(Cardio-vascular Research Foundation,New York,New York). Quantitative coronary angiography was performed using Medis CMS software version7.0(Medis Medical Imaging, Leiden,The Netherlands).All culprit and nonculprit lesions (defined asՆ30%angiographic visual angiographic diam-eter stenosis)were identified and located in relation to the corresponding coronary artery ostium and nearby side branches.All3epicardial vessels as well as all side branchesՆ1.5mm in diameter were divided into29Cor-onary Artery Surgery Study(CASS)segments.Each CASS segment was then subdivided into subsegments1.5mm in length and analyzed.Measurements of each1.5-mm sub-segment included minimum luminal diameter,reference vessel diameter,and diameter stenosis.Grayscale and VH-IVUS analyses were performed using QCU-CMS software(Medis Medical Imaging),pcVH ver-sion2.1software(Volcano Corporation),and proprietary qVH software(Cardiovascular Research Foundation).The external elastic membrane and luminal borders were con-toured for each frame.Quantitative grayscale IVUS mea-surements included the cross-sectional areas of the external elastic membrane,lumen,and plaque and media(externalelastic membrane minus lumen)and plaque burden(plaqueand media divided by external elastic membrane).The re-modeling index was calculated as the external elastic mem-brane cross-sectional area at the MLA slice divided by theaverage of the proximal and distal reference external elasticmembrane cross-sectional area.Qualitative grayscale IVUSmorphology included plaque rupture(intraplaque cavity thatcommunicated with the lumen with an overlying residualfibrous cap fragment)and echolucent plaque(a plaque con-taining a non-echo-reflective dark zone).3,4An IVUS non-culprit lesion was defined by a plaque burden ofϾ40%in Ն3consecutive frames.Lesions were considered separate if there was aՆ5-mm-long segment withϽ40%plaque bur-den between them.On the basis of VH-IVUS,plaque com-ponents were categorized as dense calcium,fibrous tissue,fibrofatty plaque,or necrotic core(NC)and reported per-centages of total plaque areas and volumes.Lesions werethen classified by VH-IVUS as1of the following:VH-TCFA,thick-capfibroatheroma(ThCFA),pathologic inti-mal thickening,fibrotic plaque,orfibrocalcific plaque,aspreviously reported.1,5–7Fibrotic plaque had mainlyfibroustissue withϽ10%confluent NC,Ͻ10%confluent densecalcium,andϽ15%fibrofattty plaque.Fibrocalcific plaquehad mainlyfibrous tissue withϾ10%confluent dense cal-cium butϽ10%confluent NC.Pathologic intimal thicken-ing was a mixture of all plaque components,but dominantlyfibrofatty plaque withϽ10%confluent NC andϽ10%con-fluent dense calcium.Fibroatheroma(VH-TCFA andThCFA)was defined asϾ10%confluent NC(spotty redcolor was not considered as confluent NC).Because theresolution of VH-IVUS is150to250m,it was not pos-sible to detectfibrous cap thicknessϽ65m(the typical pathologic definition of a a thinfibrous cap).Therefore,if there wasϾ30°of NC abutting to the lumen in3consec-Table1Baseline characteristics of the patients(nϭ659)Characteristic ValueAge(years)58.1(50.7–66.7) Men507/659(76.9%) Diabetes mellitus113/656(17.2%) Hypertension305/653(46.7%) Current smokers310/650(47.7%) Previous myocardial infarction70/655(10.7%) Clinical presentationST-segment elevation myocardial infarction198/659(30.0%)Non–ST-segment elevation myocardialinfarction436/659(66.2%) Unstable angina pectoris25/659(3.8%)Total cholesterol(mg/dl)172.0(149.5–200.0) Low-density lipoprotein cholesterol(mg/dl)100.8(79.2–127.4) High-density lipoprotein cholesterol(mg/dl)38.6(34.0–46.0) Triglycerides(mg/dl)125.0(88.6–177.1) Estimated creatinine clearanceՅ60ml/min61/622(9.8%)High-sensitivity C-reactive protein(mg/l),day07.3(2.4–19.0) Worst nonculprit lesion on quantitativecoronary angiography(%)46.2(37.6–57.9) IVUS nonculprit lesion per patient 5.0(4.0–6.0) Continuous variables are presented as median(interquartile range).472The American Journal of Cardiology()utive slices,the fibroatheroma was classified as VH-TCFA;otherwise,it was classified as ThCFA.Fibroatheromas were considered multiple and distinct if they were separated by Ն3consecutive slices containing a different fibroatheroma subtype (VH-TCFA or ThCFA)or nonfibroatheroma phe-notype,and the length of each fibroatheroma was analyzed and summed per lesion.The total NC abutting the lumen was measured in degrees and analyzed at the maximum arc of NC abutting to the lumen within each VH-TCFA.7Fi-broatheromas were subclassified as having single or multi-ple confluent NCs.Each IVUS lesion was coregistered to the angiographic road map using fiduciary branches for alignment as previously described.2The primary end point was the incidence of MACEs (the composite of death from cardiac causes,cardiac arrest,myocardial infarction,or rehospitalization for unstable or progressive angina according to the Braunwald unstable angina classification and the Canadian Cardiovascular So-ciety angina classification).The primary end point was adjudicated by an independent clinical events committee.On the basis of follow-up angiography,MACEs were at-tributed to a nonculprit lesion site if the site associated with an event was previously untreated.If follow-up angiogra-phy was not performed,the lesion site was classified as indeterminate and excluded from this analysis.All statistical analyses were performed using SAS ver-sion 9.2(SAS Institute Inc.,Cary,North Carolina).Cate-gorical variables were summarized using percentages and counts and were compared using chi-square tests or Fisch-er’s exact tests as appropriate.Lesions were divided into quartiles on the basis of the angiographic diameter stenosis.For fibroatheroma-and lesion-level data,a model with a generalized estimating equation approach was used to com-pensate for potential cluster effects of multiple lesions in the same patient and presented as least square means with 95%confidential intervals.Continuous variables were compared using analysis of variance and unpaired Student’s t tests.Time-to-event data are presented as Kaplan-Meier estimates and were compared using generalized estimating equation adjusted log-rank tests.A p value Ͻ0.05was considered statistically significant.ResultsPatient characteristics are described in Table 1.The me-dian patient age was 58.1years,17.2%of the patients had diabetes mellitus,and 66.2%of the patients presented with non-ST-segment elevation myocardial infarctions and 30.0%with ST-segment elevation myocardial infarctions.By quantitative angiographic analysis,the median diam-eter stenosis of the worst untreated nonculprit lesion in eachTable 2Quantitative findings of coronary angiography according to quartile of angiographic diameter stenosis VariableQuartile 1(n ϭ778)Quartile 2(n ϭ779)Quartile 3(n ϭ779)Quartile 4(n ϭ779)p Value Diameter stenosis (%)2.8(2.6–3.1)10.0(9.8–10.1)17.7(17.5–17.9)33.5(32.9–34.1)Ͻ0.001*Reference vessel diameter (mm) 3.25(3.20–3.30) 3.07(3.02–3.13) 3.01(2.96–3.06) 3.00(2.95–3.06)Ͻ0.001*Minimal luminal diameter (mm)3.15(3.10–3.21)2.76(2.72–2.81)2.47(2.43–2.51)2.01(1.97–2.05)Ͻ0.001*Data presented as least square means (95%confidential intervals).*Analysis of variance.Table 3Quantitative and qualitative findings of intravascular ultrasound according to quartile of angiographic diameter stenosis VariableQuartile 1(n ϭ778)Quartile 2(n ϭ779)Quartile 3(n ϭ779)Quartile 4(n ϭ779)p ValueVolumetric analysisAverage EEM area (mm 3/mm)17.5(17.0–18.0)16.5(16.0–16.9)15.8(15.4–16.2)15.5(15.1–15.9)Ͻ0.001*Average luminal area (mm 3/mm)9.4(9.1–9.7)8.7(8.4–8.9)8.0(7.8–8.3)7.5(7.3–7.7)Ͻ0.001*Average P&M area (mm 3/mm)8.1(7.9–8.3)7.8(7.6–8.0)7.8(7.5–8.0)7.9(7.7–8.2)0.11*Plaque burden (%)46.2(45.8–46.6)47.4(47.0–47.8)49.0(48.6–49.4)51.1(50.6–51.5)Ͻ0.001*Lesion length (mm)7.6(7.2–8.1)13.8(13.0–14.6)18.7(17.6–19.7)23.6(22.4–24.8)Ͻ0.001*MLA site analysis EEM area (mm 2)16.5(16.1–17.0)15.2(14.8–15.6)14.4(14.0–14.8)13.9(13.5–14.3)Ͻ0.001*MLA (mm 2)7.9(7.7–8.1) 6.9(6.7–7.1) 6.1(5.9–6.2) 5.2(5.0–5.4)Ͻ0.001*MLA Յ4mm 278(10.0%)93(11.9%)157(20.2%)271(34.8%)Ͻ0.001†Plaque burden (%)52.1(51.5–52.6)54.5(53.9–55.1)57.3(56.7–58.0)61.6(60.1–62.3)Ͻ0.001*Plaque burden Ն70%13(1.7%)28(3.6%)77(9.9%)160(20.5%)Ͻ0.001†Remodeling index 0.95(0.94–0.96)0.92(0.91–0.93)0.91(0.90–0.92)0.89(0.88–0.90)Ͻ0.001*Morphologic analysis Echolucent plaque 3(0.4%)16(2.1%)30(3.9%)78(10.0%)Ͻ0.001†Plaque rupture6(0.8%)11(1.4%)26(3.3%)58(7.4%)Ͻ0.001†Continuous variables presented as least square means (95%confidential intervals).*Analysis of variance.†Chi-square statistics.EEM ϭexternal elastic membrane;P&M ϭplaque and media.473Coronary Artery Disease/Lesion Severity,Morphology,and Prognosispatient was 46.2%(interquartile range 37.6%to 57.9%,range 1.1%to 96.0%),and 41.6%of patients had Ն1lesion with a Ͼ50%diameter stenosis.When lesions were divided into quartiles on the basis of the lesion with the worst diameter stenosis,the least square means angiographic di-ameter stenoses among the 4quartiles were 2.8%,10.0%,17.7%,and 33.5%in the first through fourth quartiles,respectively (p Ͻ0.001;Table 2).The incidence of impaired renal function (estimated creatinine clearance Յ60ml/min)was significantly higher in the fourth quartile than intheFigure 1.Incidence of plaque phenotype according to quartile of angiographic diameter stenosis.PIT ϭpathologic intimal thickening.Table 4Virtual histology intravascular ultrasound findings according to quartile of angiographic diameter stenosis VariableQuartile 1(n ϭ702)Quartile 2(n ϭ692)Quartile 3(n ϭ696)Quartile 4(n ϭ690)p ValueVolumetric analysis NC volume (%)12.3(11.6–13.0)12.5(11.8–13.2)13.0(12.3–13.7)14.0(13.3–14.7)Ͻ0.001*Dense calcium volume (%) 6.0(5.4–6.6) 6.1(5.7–6.6) 6.5(6.0–7.0)7.2(6.6–7.7)Ͻ0.001*Fibrous tissue volume (%)59.4(58.6–60.2)59.8(59.0–60.6)59.8(59.1–60.6)59.1(58.4–59.8)0.33*Fibrofatty volume (%)22.3(21.3–23.4)21.6(20.6–22.6)20.6(19.7–21.5)19.7(18.8–20.6)Ͻ0.001*MLA site analysis NC volume (%)12.8(12.0–13.6)13.3(12.5–14.1)13.7(12.9–14.6)15.2(14.3–16.1)Ͻ0.001*Dense calcium volume (%) 5.8(5.2–6.4) 6.4(5.8–7.0) 6.6(5.9–7.3) 6.8(6.2–7.5)0.06*Fibrous tissue volume (%)59.2(58.3–60.2)59.4(58.4–60.4)60.1(59.2–61.0)59.6(58.6–60.5)0.55*Fibrofatty volume (%)22.1(20.9–23.3)20.9(19.8–22.1)19.4(18.4–20.5)18.4(17.3–19.5)Ͻ0.001*Morphologic analysisVH-TCFA with multiple confluent NC 53(7.5%)115(16.6%)114(16.4%)164(23.8%)Ͻ0.001†VH-TCFA with single confluent NC 41(5.8%)37(5.3%)56(8.0%)45(6.5%)0.19†Total VH-TCFA length per lesion (mm)2.0(1.6–2.4)3.2(2.7–3.7) 3.4(2.9–4.0) 4.2(3.6–4.7)Ͻ0.001*Maximal arc of NC abutting to the lumen (°)71.2(65.7–76.7)74.8(70.5–79.0)78.6(72.9–84.3)80.2(76.1–84.2)0.04*ThCFA with multiple confluent NC 144(20.5%)151(21.8%)185(26.6%)209(30.3%)0.002†ThCFA with single confluent NC 103(14.7%)86(12.4%)85(12.2%)81(11.7%)0.45†Total ThCFA length per lesion (mm)3.1(2.7–3.4)5.0(4.4–5.7)6.2(5.5–6.8)7.7(7.0–8.5)Ͻ0.001*Continuous variables presented as least square means (95%confidential intervals).*Analysis of variance for continuous variables.†Chi-square statistics.474The American Journal of Cardiology ()other 3quartiles (6.5%,6.3%,9.8%,and 16.7%in the first through fourth quartiles,respectively,p ϭ0.006).However,other characteristics such as age,incidence of diabetes,and level of low-density lipoprotein cholesterol were similar among the 4patient groups (data not shown).Overall,there were 3,115nonculprit lesions detected by IVUS.The IVUS MLA decreased across the first to the fourth quartiles of the quantitative angiographic diameter stenosis;thus,the frequency of lesions with MLAs Յ4mm 2was highest in the fourth angiographic quartile (10.0%,11.9%,20.2%,and 34.8%in the first through fourth quar-tiles,respectively,p Ͻ0.001;Table 3).The magnitude of plaque burden at the MLA site (61.6%in the fourth quartile)and the prevalence of lesions with plaque burden Ն70%at the MLA site were also highest in the fourth angiographic quartile (1.7%,3.6%,9.9%,and 20.5%in the first through fourth quartiles,respectively,p Ͻ0.001).The frequency of echolucent plaques and plaque ruptures also increased from the first through the fourth angiographic quartiles (Table 3).Overall,VH-IVUS data were available for 2,780of the 3,115IVUS lesions.VH-IVUS volumetric analysis showed that percentage NC volume and percentage dense calcium volume increased significantly from the first to the fourth angiographic quartile,while percentage fibrofatty volume decreased from the first to the fourth quartile (all p values Ͻ0.001).MLA site analysis also showed similar results (Table 4).There was a monotonic increase in the frequency of VH-TCFAs from the first to the fourth angiographic quartile (13.4%,22.0%,24.4%,and 30.3%,respectively,p Ͻ0.001;Figure 1).The frequency of ThCFA also in-creased among the 4groups (p for trend ϭ0.03).Thus,combining VH-TCFAs and ThCFAs,the fibroatheroma fre-quency increased from 48.6%in the first quartile,to 56.2%in the second quartile,to 63.2%in the third quartile,and to 72.3%in the fourth quartile (p Ͻ0.001;Figure 1).In con-trast,the incidence of pathologic intimal thickening de-creased from the first to the fourth angiographic quartile (p Ͻ0.001).The frequencies of VH-TFCAs and ThCFAs with multiple confluent NCs increased from the first to the fourth angiographic quartile.The maximal arc of NC abut-ting to the lumen in lesions classified as VH-TCFAs signif-icantly increased from the first to the fourth angiographic quartile.Similarly,total VH-TCFA length increased from 2.0mm (range 1.6to 2.4)in the first quartile to 4.2mm (range 3.6to 4.7)in the fourth quartile (p Ͻ0.001).The incidence of lesions that had all 3previously re-ported predictors of future nonculprit events at 3years (plaque burden Ն70%,MLA Յ4mm 2,and aVH-TCFA)Figure 2.Incidence of lesions with predictors of nonculprit events at 3years (plaque burden Ն70%,MLA Յ4mm 2,and VH-TCFA)according to quartile of angiographic diameter stenosis.Table 5Nonculprit lesion level event rates according to quartile of angiographic diameter stenosis VariableQuartile 1(n ϭ778)Quartile 2(n ϭ779)Quartile 3(n ϭ779)Quartile 4(n ϭ779)p Value Cardiac death 0000—Cardiac arrest0000—Myocardial infarction 001(0.1%)2(0.3%)Ͻ0.001*Rehospitalization2(0.3%)5(0.7%)8(1.2%)35(4.9%)Ͻ0.001*Rehospitalization for unstable angina 02(0.3%)4(0.6%)10(1.4%)Ͻ0.001*Rehospitalization for increasing angina 2(0.3%)3(0.4%)4(0.6%)25(3.5%)Ͻ0.001*Composite cardiac events 2(0.3%)5(0.7%)9(1.3%)37(5.1%)Ͻ0.001**Chi-square statistics.475Coronary Artery Disease/Lesion Severity,Morphology,and Prognosiswas highest in the fourth quartile (0%,0.4%,0.4%,and 3.2%in the first through fourth quartiles,respectively,p Ͻ0.001;Figure 2).MACEs occurred in 53nonculprit lesions (1.9%)during 3-year follow-up (Table 5).Most events were rehospitaliza-tions for unstable or progressive angina (0.3%,0.7%,1.2%,4.9%in the first through fourth angiographic quartiles,re-spectively,p Ͻ0.001).However,the incidence of myocar-dial infarction also increased from the first to the fourth quartile (0%,0%,0.1%,and 0.3%,respectively,p Ͻ0.001).Kaplan-Meier curves showed the highest cumulative inci-dence of MACEs in the fourth angiographic quartile (0.3%,0.7%,1.3%,and 5.1%in the first through fourth quartiles,respectively,p Ͻ0.001;Figure 3).DiscussionThe present analysis of the PROSPECT study data con-firms the clinical observation the CASS investigators made Ͼ2decades ago that on a per lesion basis,the propensity of a lesion to result in future myocardial infarction and MACEs was related to the baseline angiographic diameter stenosis.However,the present analysis also explains this phenomenon.The issue is not just luminal compromise but underlying lesion morphology.In the present study,the prevalence of plaque burden Ն70%,MLA Յ4mm 2,and a VH-TCFA (the triad of predictors of nonculprit lesion–related future MACEs in PROSPECT)all increased in fre-quency with increasing angiographic diameter stenosis,although most of these lesions were still considered angio-graphically mild or intermediate in severity.In particular,there was a striking gradient in the prevalence of a fibro-atheroma from the first to the fourth angiographic diameter stenosis quartile,such that 72.3%of lesions with angio-graphic median diameter stenoses of 33.5%(range 32.9%to 34.1%)had VH-IVUS characteristics of a fibroatheroma,and 30.3%had rupture-prone VH-TCFA (vulnerable plaque)morphologic features.Atherosclerosis begins early in life,but it usually takes decades to form a stenosis responsible for ischemia.This process can be slow and progressive,episodic with subclin-ical plaque rupture and healing,or present as plaque rupture with occlusive thrombosis and an acute coronary event,as has been shown in several autopsy studies.Mann and Da-vies 8reported that repeated silent ruptures that heal are the cause of progressive and worsening luminal compromise.Similarly,in another autopsy study,Burke et al 9reported that plaque burden and percentage luminal narrowing in-creased with the number of previous ruptures at that partic-ular site and that percentage luminal narrowing was greater for acute compared to healed ruptures.The precursor lesion of plaque rupture is the TCFA.Plaque rupture develops in a lesion with a large NC and overlying thin fibrous cap containing numerous inflammatory cells.10,11Finn et al 11reported that 65%of lesions with plaque burden Ͼ50%had pathologic plaque rupture and 42%contained TCFAs,while 35%of lesions with plaque burden Ͻ50%had plaque rup-ture and 57%had TCFAs.Therefore,pathologic autopsy studies demonstrated that acute and healed ruptures were more common in lesions with greater plaque burden,whereas TCFAs were more common in lesions with less plaque burden.The present clinical study extends these findings by demonstrating that lesions with the worst an-giographic diameter stenosis have the highest frequencies of incidental plaque ruptures as well as VH-TCFAs whose rupture could contribute to progression.However,not all TCFAs progress to rupture.As has been shown in autopsy studies,a TCFA with a large NC,which increases in size as plaque burden increases,is more likely to rupture than a TCFA with a small NC.11,12One clinical VH-IVUS study also reported a significant correlation be-tween plaque area and percentage of NC in patients with acute coronary syndromes.13In the present clinical study in lesions with worsening luminal stenosis,the NC not only increased as a percentage of plaque area,but the NC also increases in length,in the arc abutting to the lumen,and in the number of individual NCs contained within the VH-TCFA,all evidence of increasing VH-TCFA instability of the TCFA with worsening diameter stenosis.In particular,multiple NCs were evidence of the cycle of NC,rupture,and healing leading to lesion progression.9Not all plaque ruptures cause events.In 1clinical IVUS study,Fujii et al 14showed that ruptured plaques that caused events had larger plaque burden,more luminal compromise,and more frequent thrombus formation than plaques that ruptured silently;that is,plaque ruptures do not cause acute events unless there is thrombus formation and/or significant luminal compromise.In CASS,the risk for myocardial infarction and coronary occlusion increased with increasing baseline angiographic lesion severity.15,16The present le-sion-level analysis from PROSPECT similarly demonstrates that the incidence of events increased with increasing an-giographic diameter stenosis.Moreover,the frequency of a VH-TCFA increased and the size and distribution of its NC worsened with increasing angiographic diameter stenosis of the lesion.Thus,angiographically more severe lesions are more unstable not only because the plaque burden is greater and the lumen smaller but also because they more oftenN o n -C u l p r i t M A C E (%)0123456Time in Months61218243036778726717693680655416779721711692679659411779707693675652630379779722706684668654430Number at risk First quartile Second quartile Third quartile Fourth quartileGEE Adjusted Log-Rank P < 0.0010.3%0.7%1.3%5.1%Q1Q2Q3Q4Figure 3.Kaplan-Meier curves for MACEs in nonculprit lesions according to quartile of angiographic diameter stenosis.The 3-year cumulative rates of MACEs at site of nonculprit lesion were 0.3%,0.7%,1.3%,and 5.1%in the first through fourth quartiles,respectively.MACEs were defined as death from cardiac causes,cardiac arrest,myocardial infarction,and re-hospitalization for unstable or progressive angina.GEE ϭgeneralized estimating equation.476The American Journal of Cardiology ()。
