最新全球心梗统一定义 英文翻译版
全科医生小词典——修订版心肌梗死全球统一定义
７ 朱理敏 ，王宪衍 ．脉压 与心脑血管 疾病危险 因子 ［ Ｊ ］ ． 中华 心血
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种 补 充 和探 索 ，管 理 内容 和模 式 尚需 进 一 步 充 实 和 完善 ，管
８ 胡小平 ，王 占成 ，刘 经磐 ，等 脉压 与脑 卒 中发 生 的临 床研 究 ［ Ｊ ］ ．高血压杂志 ，２ ０ ０ ２ ，１ ０（ ４ ） ：３ ２ ６—３ ２ ８ ．
要求 。社区高血压细节 管理 ，作为 目前管 理模式 的一 种补充 ，
即在 现 行 的 管 理模 式 基 础 上 ，对 各个 管 理 细 节 进 行 完 善 ，通 过
４ 钱伟峰 ．社 区健康教 育对高血压 患者易感 因素的影响研 究 ［ Ｊ ］．
中 国 全科 医学 ，２ ０ １ ２，１ ５（ ４） ：１ ３ ０ ０ ．
一
５ 中国高血压 防治指南修订委员会 ．中国高血压防治指南 ２ ０ １ ０［ Ｊ ］ ．
中 国 医 学前 沿 杂 志 （ 电子版） ，２ ０ １ ｌ ，３ （ ５） ：４ ２—９ ３ ．
６ 许予明 ，谭颂 ，刘铭 ，等 ．脑 血管疾病诊断与治疗 临床指南 ［ Ｊ ］ ．
内 科 急 危 重症 杂 志 ，２ ０ ０ ５，１ １（ ５ ） ：２ ４ ３— ２ ４ ５ ．
的第 ３版 《 心肌梗死全球统一定义》 。新定义要点如下 ：
１ 逐 渐 增 加 、小 批 量 心 肌 坏 死 可 通 过 敏 感 性 和 心 肌组 织 特 异 性 标 志 物 增 加来 监测 。 ２ 心 肌 坏 死 可 能 源 于非 缺 血 性 机 制 如 心 力 衰竭 ，可称 为心 肌 损 伤 而 不 称 心 肌 梗死 。
急性心肌梗死全球统一定义
医学ppt
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2007版 cTn升高的非缺血性心脏病原因
• 肾功能衰竭 • 急性神经系统疾病,包括卒中或蛛网膜下腔出血 • 浸润性疾病,如淀粉样变性、血色病、肉状瘤病、硬皮
病
• 炎症性疾病,如心肌炎、心肌扩张性疾病、心内膜炎、心 包炎
• 药物毒性或毒素 • 危重患者,尤其是呼吸衰竭或脓毒症患者 烧伤患者,尤其
医学ppt
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2007版 陈旧性心肌梗死的ECG表现
• V2-V3导联Q波≥0.02 s 或呈QS型 • 两个相邻导联(I、aVL、V6;V4-V6;Ⅱ、Ⅲ、aVF)中Q波
≥0.03 s,深度≥0.1 mV或呈QS型 • V1-V2导联R波≥0.04 s以及R/S≥1合并直立T波(无传导
缺陷)
医学ppt
是烧伤>30%体表面积者 • 过度劳累者
医学ppt
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2007版 急性心肌缺血的ECG表现
• 急性心肌缺血的ECG表现(无左心室肥厚和LBBB) • ST段抬高 相邻2个导联新发ST段J点抬高:V2-V3导联
男性≥0.2 mV、女性≥0.15 mV,和(或)其他导联≥0.1 mV • ST段压低和T波改变 相邻2个导联新发ST段水平或下斜 性压低≥0.05 mV,和(或)相邻2个导联T波倒置≥0.1 mV 合并高大R波或R/S>1
死:
• 新出现的病理性Q波(伴或不伴症状)。
• 影像学证据显示局部存活心肌丢失(变薄、无收缩),缺乏非 缺血性原因。
• 病理发现已经愈合或正在愈合的心肌梗死。
医学ppt
72007版 cTn升高的非缺性心脏病原因• 心脏挫伤,或由手术、消融、起搏器等引起的心脏创 伤 急性或慢性充血性心力衰竭
• 主动脉夹层 • 主动脉瓣膜疾病 • 肥厚型心肌病 • 快速或缓慢性心律失常,或心脏传导阻滞 • 心尖球形综合征：急性扩张性心肌病 • 横纹肌溶解伴心肌损伤 • 肺栓塞、严重肺动脉高压
2024年ESCST抬高型心肌梗死诊疗指南中文翻译版
2024年ESCST抬高型心肌梗死诊疗指南的中文翻译版如下：
抬高型心肌梗死（ST段抬高型心肌梗死，ST-elevation myocardial infarction，STEMI）是心肌梗死的严重类型，通常由冠状动脉阻塞引起。
早期诊断和治疗可以显著改善患者的预后。
以下是ESCST（欧洲心脏病协会和欧洲心脏协会）发布的2024年抬
高型心肌梗死诊疗指南的要点：
1.快速进行心电图（ECG）检查，以确认ST段抬高型心肌梗死诊断。
2.立即进行溶栓治疗或急诊冠脉介入手术（PCI），以恢复冠状动脉
的血流。
3.根据患者的具体情况，确定是否需要进行其他治疗，如抗血小板药物、抗凝药物等。
4.在患者稳定后，对其进行心理支持和康复服务，以促进身心康复和
预防再发。
这些指南旨在帮助医疗机构和医生提供高质量的抬高型心肌梗死诊疗
服务，以降低患者的死亡率和并发症发生率。
第三次心肌梗死全球通用定义(中译全文)
2012年第三次心肌梗死全球通用定义（中译全文）2013-07-08 05:58:24| 分类：冠心病 | 标签： |举报 |字号大中小订阅ESC/ACC/HAH/WHF心肌梗死全球通用定义工作组柳州市人民医院心内科胡世红教授译自：European Heart Journal (2012) 33, 2551–2567内容表缩略语和词头语心肌梗死的定义急性心肌梗死的定义既往心肌梗死的定义引言心肌缺血和梗死的病理特征心肌损伤伴坏死的生物标志物的检出心肌缺血和心肌梗死的临床特征心肌梗死的临床分型自发性心肌梗死（1型心肌梗死）继发于氧供需不平衡的心肌梗死（2型心肌梗死）由于心肌梗死所致的心脏死亡（3型心肌梗死）与血运重建术相关的心肌梗死心肌梗死的心电图检出既往心肌梗死无症状性心肌梗死与心肌梗死心电图诊断相混淆的情况成像技术超声心动图放射性核素成像磁共振成像计算机体层摄影术应用于急性心肌梗死的成像应用于心肌梗死晚期表现的成像伴随PCI的心肌梗死诊断的诊断标准（4型心肌梗死）伴随CABG的心肌梗死的诊断标准（5型心肌梗死）对拟行其它心脏手术患者心肌梗死的评估与非心脏手术相关的心肌梗死在重症监护病房的心脏梗死再发心肌梗死与心力衰竭相关的心肌损伤或心肌梗死在临床试验中心肌梗死的应用和质量保证方案调整心肌梗死定义的公共政策意义心肌梗死定义的全球看法利益冲突致谢参考文献缩略语和词头语ACCF 美国心脏病学院基金会ACS 急性冠脉综合征AHA 美国心脏病协会CAD 冠心病CABG 冠状动脉旁路移植术CKMB 肌酸激酶MB同工酶cTn 心肌肌钙蛋白CT 计算机体层摄影CV 变异系数ECG 心电图FDG 氟脱氧葡萄糖HF 心力衰竭LBBB 左束支传导阻滞LV 左心室LVH 左心室肥厚MI 心肌梗死mIBG 间碘苯甲胍MONICA 心血管病趋势和决定因素的多国监测MPS 心肌灌注闪烁扫描术MRI 磁共振成像mV 毫伏Non-Q MI 无Q波型心肌梗死NSTEMI 非ST-段抬高型心肌梗死PCI 经皮冠状动脉介入治疗PET 正电子发射断层摄影Q wave MI Q波型心肌梗死RBBB 右束支传导阻滞SPECT 单光子发射计算机断层摄影的闭塞；或（3）有活力的心肌新的丢失或新的局部室壁运动异常的影像证据。
全球心梗统一定义
根据临床、病理以及其他特征可分四期
1、急性进展期（<6小时） 2、急性期（6小时--7天） 3、愈合期（7天--28天） 4、陈旧期(痊愈期)（≥29天）
需要强调的是，临床和ECG所记录的心梗分期与实际病理学分 期并不一定完全相符。例如，ECG显示ST-T变化、心脏标志物升 高时往往提示新近发生的心梗，但病理学分期可能已处于愈合期。
全球心肌梗死新定义
全球心肌梗死定义
—ESC/ACC/AHA/EHS/WHF 标准
心肌梗死的病理学定义
★心肌缺血时间过长所导致的心肌细胞坏死
★细胞坏死定义为细胞凝固和（或）收缩带的坏死
全球心肌梗死定义
—ESC/ACC/AHA/EHS/WHF 标准
心肌梗死分类
★根据梗死面积分类
★病理学分类
★临床分类
急性心肌梗死诊断—ESC/ACC/AHA/EHS/WHF 标准
PCI相关性心梗 1. 基 线 cTn 水 平 正 常 者 接 受 经 皮 冠 脉 介 入 治 疗 （PCI）后，如心脏标志物水平升高超过URL99百分位 值，则提示围手术期心肌坏死 2.心脏标志物水平超过URL99百分位值的3倍被定 义位与PCI相关的心肌梗死 3.一个亚型是支架内血栓相关性心肌梗死 PCI术 后心肌梗死,且造影或影象学证实支架内血栓
①急性和慢性充血性心力衰竭
②肾功能衰竭 ③快速性或缓慢性心律失常，或心脏传导阻滞 ④急性神经系统疾病包括卒中或蛛网膜下腔出血
心肌梗死相关表现的定义
心肌坏死生化标志物改变的定义
⑤肺栓塞和肺动脉高压
⑥心脏挫伤、消融、起搏和心脏复律 ⑦浸润性心脏疾病，如淀粉样变形和硬皮病
—ESC/ACC/AHA/EHS/WHF 标准
心肌梗死的全球统一定义 共37页
④
基线肌钙蛋白值正常行经冠脉旁路移植术（CABG） 的患者，心脏生物标志物升高超过URL的第99百分 位值提示围手术期心肌坏死（indicative of periprocedural myocardial necrosis）。按习用裁定（by convention，按惯例），生物标志物升高超过URL 的5倍加上新的病理性Q波或新的左束支阻滞，或 冠脉造影证实新的移植的或自身的冠脉闭塞，或有 活力心肌丧失的影像学证据，定为与CABG相关的 心肌梗死（CABG-related myocardial infarction）。其 中一个亚型与支架血栓形成有关
缺血症状并不特异，有时不典型，甚至 没有任何症状
如果症状不典型或没有症状，AMI的诊断将更多的 依赖心电图、心脏生物标记物及心脏成像技术 （cardiac imaging）的检查结果
②
突发、意外的心脏性死亡，涉及（involving）心 脏骤停（cardiac arrest），常伴有提示心肌缺血 的症状、及推测（presumably）为新的ST段抬高 或新的左束支阻滞、和/或冠脉造影和/或尸检有新 鲜血栓的证据。死亡发生在可取得血标本之前或 生物标志物在血中状：静息或用力时胸部、上 肢、下颌或上腹部的不适（discomfort）， 部位可有不同组合
AMI相关胸部不适常表现为：时间至少 超过20 min，部位呈弥散性（diffuse） 而非局限性（not localized），非体位性 （not positional）且不受局部运动影响 （not affected by movement of the region），可 伴有呼吸困难、出汗、恶心或晕厥
ST段抬高31 min后出现室颤，猝死
心脏性猝死的患者尽管来不及采血测定 肌钙蛋白，或即使采血检测肌钙蛋白不 高，即缺乏心脏生物标志物证据，如猝 死前有心肌缺血的临床证据，此时仍应 诊为（致命的）心肌梗死。如有冠脉造 影（假使有可能）和/或尸检证实有新鲜 血栓，AMI的诊断将更为明确
医学--第三版心肌梗死统一定义
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心肌损伤标志物
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心肌损伤标志物
特异性和敏感性：cTn>CK-MB参考值：>99th URL，CV<10%〔CV>20%时禁用〕采样要求：首诊、3-6h、必要时升高而无缺血证据时应查找其他病因：心肌炎、主动脉夹层、肺栓塞、心力衰竭 、肾衰竭等
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肌钙蛋白升高
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原发心肌缺血性损伤
继发心肌缺血性损伤
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SPECT
27
PET
28
MRI
29
15
性别和年龄特异性
急性非ST段抬高心梗ECG标准
两连续导联ST段水平或下斜型压低≥0.05mv，或R波为主或R/S>1的导联T波倒置≥0.1mv
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陈旧性心肌梗死ECG标准
V₂-V₃导联Q波≥0.02s或呈QS波；任意组(Ⅰ，aVL，V₆；V₄-V₆；Ⅱ，Ⅲ，aVF)两导联Q波≥0.02s且≥0.1mv或呈QS波；无传导阻滞时V₁-V₂导联R≥0.04s波和T波直立R/S≥0.1
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急性心肌梗死标准
检出生物学标志(尤其是肌钙蛋白)升高和/或降低且至少一次>99th URL，并有以下之一：①心肌缺血病症；②新的缺血性ST/LBBB改变；③出现病理性Q波；④影像示新出现的活力心肌丧失或局部室壁运动异常；⑤造影或活检证实的冠状动脉内血栓猝死PCI相关CABG相关
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心肌梗死1型
自发性心肌梗死粥样硬化斑块破裂、溃疡、侵蚀、裂隙、夹层等致一支或多支冠脉腔内血栓，进而心肌血流减少或远端血小板栓塞、心肌坏死，通常有严重的CAD，偶然(5~20%)非阻塞性或无CAD
ቤተ መጻሕፍቲ ባይዱ2023/6/19
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血管内超声
Intravascular ultrasonography, IVUS有创操作(在冠脉造影中联合操作)可以显示冠脉管壁细节不能同步显示冠脉管腔还需更好的不稳定斑块参数
心肌梗死的重新定义
心肌梗死的重新定义欧洲心脏学会/美国心脏病学会心肌梗死重新定义联合委员会文件一、心肌梗死的概念与定义心肌梗死(myocardial infarction)的定义可以根据临床、心电图、生物化学和病理学特征做出。
心肌梗死术语还具有社会与心理学方面的意义，表现在作为严重健康疾病的一个晴雨表和作为人口统计学中疾病发生率和临床试验结果的参数(图1)。
过去，有关心肌梗死相关概念在临床上已达成共识。
在世界卫生组织(World Health Organization，WHO)有关疾病发生率的研究中，具备下述3个特征中的2个即可诊断心肌梗死：典型症状(即胸痛)、心肌酶升高和出现Q波的典型心电图表现。
但是，目前的临床实践、医疗卫生系统以及流行病研究和临床试验，都需要对心肌梗死做出更精确的定义。
而且，更敏感、更精确的血清生化标记物与更精确影像技术的出现，需要对原来心肌梗死的定义进行重新评价。
影像技术的进步，使得影像检查的敏感性提高，发现过去不能诊断的非常小的心肌梗死灶。
现有的技术已经能鉴别重量<1克的心肌坏死灶。
我们越来越接受这样一个概念，即心肌缺血引起的所有大小的坏死均应定义为心肌梗死(正如本次会议提出的)。
重新审视过去所诊断的严重、稳定型或不稳定型心绞痛的病人，在今天就应该被诊断为小灶性心肌梗死。
心肌梗死诊断标准敏感性的增高，意味着会发现更多的病例。
另一方面，诊断标准特异性增高，会减少诊断心肌梗死假定阳性病例数。
心肌梗死定义的这种变化，将会对疾病发生率的传统监测方法及结果评估产生明显的影响。
随着对心肌梗死诊断水平的不断提高，ESC和ACC于1999年7月曾召集会议，重新修订心肌梗死的定义。
对心肌梗死新定义的科学与社会意义的评价，将在病理学、生物化学、心电图检查、影像检查、临床试验、流行病学和公共政策等方面进行。
显然，无论是在临床实践还是在人口研究中，对心肌梗死定义若不进一步明确，则阻碍了其广泛使用。
这种进一步定义涉及到心肌细胞损伤(梗死范围)、导致梗死的诱因(自发性还是在冠状动脉诊断性或治疗性操作中发现)、以及观察心肌坏死动态衍变的过程(进展性、正在愈合或已经愈合的心肌梗死)。
心肌梗死新定义
全球心肌梗死工作组（ESC/ACC/AHA/EHS/WHO）发布心肌梗死新定义转载请注明来自丁香园长期以来，急性心肌梗死的诊断都是根据临床症状、心电图改变和以肌酸激酶（CK）和肌酸激酶同工酶（CK-MB）为主的血清心肌酶学改变而作出的。
随着敏感性和特异性更高的心肌坏死生化标志物——心脏肌钙蛋白（cTn）的推广和应用，以及新的影像学技术的进展，人们对心肌梗死有了新的认识。
研究显示，应用心脏肌钙蛋白T（cTnT）升高作为心肌梗死的诊断标准，与CK相比，诊断率增加74%，与CK-MB相比，诊断率增加41%。
基于上述现状，全球心肌梗死工作组[ 欧洲心脏病学会（ESC）、美国心脏病学会（ACC）、美国心脏学会（AHA）、欧洲高血压学会（EHS）和世界卫生组织（WHO）对心肌梗死进行了新的定义。
新定义在2006年第16届世界心脏病大会暨ESC年会（WCC/ESC）上进行了公布。
ESC/ACC对急性进展性和陈旧性心肌梗死的定义急性进展性心肌梗死定义以下任何一项标准均可诊断急性、进展性心肌梗死：1. 心肌坏死生化标志物典型的升高和降低，至少伴有下述情况之一：（1）心肌缺血症状；（2）心电图病理性Q波形成；（3）心电图ST段改变提示心肌缺血；（4）冠状动脉介入治疗，如血管成形术。
2. 病理发现急性心肌梗死。
陈旧性心肌梗死定义1. 系列心电图检查提示新出现的病理性Q波，患者可有或可不记得有任何症状，心肌坏死生化标志物可已降至正常。
2. 病理发现已经或正在愈合的心肌梗死。
ESC/ACC/AHA/EHS/WHO对心肌梗死相关表现的定义急性心肌梗死的病理学定义急性心肌梗死定义为长时间的心肌缺血所导致的心肌细胞死亡。
不同类型心肌梗死的临床分类：Ⅰ型：自发性心肌梗死，与由于原发的冠状动脉事件如斑块破裂而引起的心肌缺血相关。
Ⅱ型：心肌梗死是继发于心肌的供氧和耗氧不平衡所导致的心肌缺血，如冠状动脉痉挛、贫血、冠状动脉栓塞、心律失常或低血压。
第三版心肌梗死定义英文版
Clinical BiochemistryVolume 46, Issues 1–2, January 2013, Pages 1–4Third Universal Definition of Myocardial InfarctionAllan S. Jaffe,IntroductionThe Third Universal Definition of Myocardial Infarction (MI) was recently published conjointly by the major cardiology organizations throughout the world and in the journals of the World Health Organization (WHO). This definition builds on two previous two iterations which were developed to make the diagnosis of myocardial infarction (MI) more consistent.The efforts started originally in 1999 in the conference in Nice stimulated by the innovation of Dr. Kristian Thygesen and Dr. Joseph Albert who had recognized this problem and who developed a task force jointly sponsored by the ACC (American College of Cardiology) and the ESC (European Society of Cardiology) to attempt to standardize the definition of MI [1]. This major step led to the first document which moved the field from the epidemiologically oriented definition of MI which had been developed by the WHO to track the incidence of coronary disease and therefore was oriented towards specificity to a more clinically oriented definition which relied on biomarkers as a key feature of the diagnosis. This resulted in a paradigm shift where the diagnosis required documentation of myocardial necrosis with biomarkers and especially cardiac troponin (cTn) which was emerging at the time in the proper clinical situation. A second iteration in 2007 [2] updated the guidelines and the 2012 definition refines the definition still further particularly as it relates to biomarkers [3] which have in the past decade become progressively more and more sensitive. Intrinsically, increases in sensitivity of this sort tend to result in a diminution of specificity since increasingly sensitive measurements often unmask new etiologies for in this instance, elevations of these sensitive cTn biomarkers.Areas of the 2012 definition that remains important but unchangedThe definition of MI from the pathologic circumstance obviously is not going to change. The definition mandates the finding of cardiomyocyte necrosis definedpathologically due to myocardial ischemia. However, the clinical definition since pathology is not readily available to guide clinical care relies on a surrogate marker for cardiac injury; i.e., cardiac biomarkers and particularly, cTn. As in previous iterations, cTn is the biomarker of choice and strongly preferred for the overall guidelines as well as for each specific guideline. The definition of MI from the clinical perspective has not changed substantively. It requires detection of a rise and/or afall of a cardiac biomarker, preferably cTn, with at least one value above the 99th percentile reference limit in the appropriate clinical setting (see Table 1 for criteria). There are additional types of MI which will be covered subsequently but the guidelines rely heavily on clinical signs or symptoms, a clinical situation where ischemia is suspected even if signs and symptoms are absent or imaging information suggestive of ischemia in the presence of a changing pattern of elevated biomarkers.Table 1.Criteria for acute myocardial infarction (Third Universal Definition of Myocardial Infarction).➢ Detection of a rise and/or a fall of cardiac biomarker values (preferably cardiac troponin (cTn)) with at least one value above the 99th percentile upper reference limit (URL) and at least one of the following:➢ Ischemic symptoms➢ ECG changes of new ischemia (new ST–T changes or new LBBB)➢ Development of pathologic Q waves in the ECG➢Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality➢Identification of an intracoronary thrombus by angiography or autopsy Full-size tableTable optionsThe metrics for the use of these biomarkers remain the same. One needs a value above the 99th percentile of the upper reference limit with a rising and/or a falling pattern of values. However, as cTn assay sensitivity has improved, the ability to consistently operationalize these criteria has become more problematic as will be discussed below. The document also recognizes a variety of special clinical circumstances which require unique handling. Some of these are related to cardiac procedures such as percutaneous interventions (PCI) or coronary artery bypass graft (CABG) surgery but others to novel procedures that are being developed such as transcutaneous aortic valve interventions (TAVI). The document discusses as well subsets of patients who are critically ill, those with heart failure, and those undergoing non-cardiac surgery as well. These classifications are not new from the 2007 document but are considered in greater detail.Issues related to biomarkersAs in the past, cTn is the marker of choice and a rise and/or a fall in values is necessary to define an acute event such as MI. It is recognized that there is some tension about how one defines the 99th percentile. It is assay dependent and is often defined based on convenience samples. Therefore, there is concern that perhaps they are not as reliable as if the sample populations were more intensively studied [4]. The values for these assays should be expressed in ng/L so that they are whole numbers because as assays become more complicated and more sensitive, the number of zeros could lead to clinical dysfunction. The assays should be precise and the document prefers assays that have excellent precision with a CV of 10% or less of the 99th percentile to allow detection of changing values. However, the document allows for assays with CVs up to 20% to be used [5]. It also is noted that analytic and pre-analytic problems can be problematic and lead to false-positive and false-negative values especially with more sensitive assays. It is also recommended that sex dependent values may be used with high sensitivity assays.Sampling should be done at 0, 3, and 6 h and later if additional episodes occur or if the timing of the initial symptoms is unclear. The diagnosis requires a rising and a falling pattern which is essential to differentiate elevations that are acute from those that are chronic and associated with structural heart disease such as patients with renal failure, heart failure, left ventricular hypertrophy, and the like. It is recognized that one needs to be careful because at times one could present sufficiently late asto miss an elevated value or could be near the time of peak values at which point in time one could believe that a change had not occurred when simply the values were similar on both sides of the peak.It is recognized and allowed that there may be circumstances in which cardiac injury could be present but not meet the diagnosis of MI because it is not in the appropriate setting or does not manifest a rise and a fall and there are a large number of such situations in which a diagnosis of cardiac injury may be more appropriate than the diagnosis of acute MI (see Table 2).Table 2.Elevations of cardiac troponin values because of myocardial injury (Third Universal Definition of Myocardial Infarction).➢ Injury related to primary myocardial ischemia (MI type 1; i.e., plague rupture, intraluminal coronary artery thrombus formation)➢ Injury related to supply/demand imbalance of myocardial ischemia (MI type2;i.e., tachy-/brady-arrhythmias, aortic dissection, or severe aortic valve disease, hypertrophic cardiomyopathy, cardiogenic or septicshock, severe respiratory failure, severe anemia, hypertension with or without LVH, coronary spasm, coronary embolism or vasculitis, coronary endothelial dysfunction without significant CAD)➢ Injury not related to myocardial ischemia (i.e., cardiac contusion, surgery, ablation, pacing, defibrillator shocks, rhabdomyolysis with cardiac involvement, myocarditis, cardiotoxic agents)➢ Multifactorial or indeterminate myocardial injury (i.e., heart failure, stress (takotsubo) cardiomyopathy, severe pulmonary embolism or pulmonary hypertension, sepsis and critically ill patients, renal failure, severe acute neurological (e.g., stroke) infiltrative diseases (e.g., amyloidosis), strenuous exercise)Operationalizing change in cTn values is complex and assay dependent. It should be clear that given previous ways of diagnosing infarction have often not required changes over time that as one starts to implement these changes, one will have differences in both sensitivity and specificity [6]. In fact, most of the data in this area suggests that the use of delta change criteria improves specificity but at the cost of sensitivity. There are multiple reasons why this could be the case. The first is that it may be that there are patients being diagnosed with acute infarction who do not have a rising and a falling pattern based on clinical judgment since one can have acute looking plaques even in patients with stable coronary artery disease [7]. A second potential issue relates to the situation where there is variation in coronary artery perfusion. Biomarker release is flow dependent and the consequence of that is that there may well be circumstances with closed vessels where it takes much longer for the egress of marker to reach the circulation than in others. Thus, the idea of short periods of one or two hour sampling times looking for change may be inadequate. There also are issues related to the spontaneous change that can occur. This has been termed biological variation and clearly is much more substantial than just the variability associated with the imprecision of the assays [8]. Nonetheless, it is clear there is some overlap between the values that one believes are associated with patients with MI and the values that are considered part of the spontaneous biological variation [9]. In addition, the optimal values to use with each assay are not clear. One could calculate an ROC curve which many laboratorians are enamored of doing and pick the value that classifies the most patients correctly. However, this may not be what clinicians need. Cardiologists want relatively high specificity to avoid unnecessary procedures in patients who are not at risk, whereas emergency department physicians often want more sensitive criteria so that they do not inadvertently discharge patients who are at risk [10]. The balance between these two needs to be found at each institutional level. Thus, the complexity of this issue, with high-sensitivity assays, needs to be discussed at each local site and adjudicated on a case by case by assay basis.Classification of MIsThere are multiple reasons why cTn could be elevated that need to be distinguished from MI. One could have a rising and a falling pattern of cTn due to sepsis or pulmonary embolism, or acute heart failure with myocardial stretch; none of which would be associated, nor should be considered the same as MI. In addition, there are types of MIs as well and it may well be of some importance to distinguish the types as the care of these individuals may be different. The task force recognized multiple types of acute MI [3]. They define type 1 which many have called the so called “wild” type as an episode associated with plaque rupture and spontaneous in nature. Thus, these patients most often present after an episode of chest discomfort often with ECG changes, elevated biomarkers, and in the studies of such patients it is clear that having an elevated cTn indicates a beneficial response to an aggressive strategy with anticoagulation and the use of IIb/IIIa agents and early invasive strategy [11]. So called type 2 MIs are less typical. They often occur in patients who have fixed atherosclerotic disease who developed tachycardia, hyper- or hypotension, or in individuals who have abnormalities in coronary vasomotion such that they do not improve increased coronary blood flow in response to stress or have overt vasospasm. Such events can even occur in some individuals whose coronary arteries are totally normal but who have such severe supply demand imbalance due to extreme tachycardia, hyper- or hypotension. These scenarios can become complex. One could suggest that there is a continuum between myocardial injury which might be diagnosed, for example, in a young person with tachycardia who had an elevated cTn than who was totally asymptomatic, to a similar patient who might have more typical chest pain who might be called a type 1 MI, to an individual who might have vague symptoms that are difficult to classify in whom a diagnosis of type 2 MI might be made. This is an area where clinical judgment will be important for clinicians but it should be clear that solitary elevation of cTn even with a rising and a falling pattern does not mandate a diagnosis of MI. These distinctions are made more difficult by the fact that in certain circumstances such as the elderly, the diabetic, and patients who are postoperative classic findings may not be observed.Type 3 MI subsumes that circumstance where there is a patient with a classic MI documented either by electrocardiography or angiography where the biomarkers have not been obtained or have not had sufficient time to be elevated. This is rarely a problem except in those patients who succumb at a very early time during the process.There also are myocardial infarctions associated with revascularization procedures such as PCI or CABG. These are complex and will be covered below. Electrocardiographic changesThe electrocardiographic changes that should be observed for did not change markedly but looking for evidence of circumflex coronary artery ischemia is emphasized. Posterior leads (V7–V9) should be recorded in patients who may havecircumflex involvement. This may be suspected if there is ST segment depression in V1–V3. The ECG criteria for acute MI and common ECG pitfalls in diagnosing infarction are detailed in the Third Universal Definition of Myocardial Infarction [3].Periprocedural myocardial infarctionsThis is an area of intense controversy. It is clear that myocardial injury can occur after percutaneous procedures. This can be due to emboli, whether they are a clot of atherosclerotic, occlusion of a side branch, or simply prolonged ischemia. What has been problematic has been the ability to know for sure that these events are associated with an adverse prognosis [12]. The criteria provided do not attempt to make that distinction since such a distinction requires outcome data. The thought with that is that for many such elevations, elevations prior to the procedure are present but have been ignored [12]. Indeed in recent meta-analysis, not one study that claimed to have a normal baseline had such a baseline. Therefore, the proponents of this particular point of view would argue that there is rarely prognostic significance. If so, the question arises as to whether or not diagnosing these patients with acute MI is of value. The opposing view is that prior studies, particularly done with less sensitive markers where one could ignore the baseline changes because markers like CK-MB were insensitive and did not detect very many such elevations suggested that there was prognostic significance to these events. Given the task force has moved strongly toward a cTn oriented structure and did not have to, nor did, dwell on the issue of prognostic significance, the question then was viewed as how to define a distinction between the cardiac injury that might have led to the procedure and some sort of additional insult caused by the procedure itself. The task force then decided to mandate the need for a normal cTn value or documentation of a stable or a falling pattern at baseline and then to rely on a 5 fold elevation of cTn when there was a clear cut abnormality induced by the procedure itself or marked symptoms occurred. The criteria uses previously of a threefold was increased to fivefold along with these ancillary criteria given the increase in assay sensitivity that has occurred since 2007 but it should be clear that given the heterogeneity of present day cardiac troponin assays that this will be a moving target depending upon the assay that one utilizes in any given situation.A similar statement can be made for CABG. Unfortunately, given the heterogeneity of assays, there is no single cutoff value that can be utilized. However, it is clear that individuals who start with an elevated cTn preoperatively elaborate more cTn [3]. Thus, a normal baseline value is important for comparative information. It is also clear that the more cTn that is elaborated, the more adverse the prognosis; thus, making many more comfortable with this diagnosis than with the post-PCI diagnosis [13]. However, there also is an obligatory amount of injury that is indigenous to the cardiac surgical procedure and the question is how much should be or should not be included. An arbitrary decision was made to suggest that above a tenfold increase from the URL value for any given cTn assay should be considered abnormal and leadto investigation looking to see if the additional criteria were present. These could be provided by imaging or by the electrocardiogram.Novel circumstancesSeveral other circumstances are recognized in the guidelines that are of relevance. For example, any procedure done on the heart is likely to cause elevations of cTn. Therefore, transcatheter aortic valve implantations, the so called TAVI or mitral clip procedures are likely to cause such cardiac injury. The task force suggested that the criteria for CABG be applied in that circumstance. In non-cardiac surgical procedures, there often are cTn elevations. Many of these appear to be the so called type 2 events although definitive information in this area is lacking and it is not clear that we have defined well enough the appropriate clinical criteria to distinguish type 1 and type 2 MI [3]. Nonetheless, it appears that at least based on an earlier data and vascular surgery patients that patients often have abnormalities in the supply and demand that can be documented. It has been shown [14] that tachycardia, hypotension, or hypertension post operatively is often associated with ST–T wave changes and subsequent elevation in cTn and the adverse prognosis are known to be associated to such elevations. However, the pathologic literature would suggest, and this is why one needs to be cautious in this area, that those events that lead to mortality often are associated with plaque rupture and may be more type 1 events [15]. Thus, there is still ambiguity about exactly what types of infarctions might exist and therefore the criteria are highly nuanced in that regard. Similar statements can be made about patients who are critically ill who may have elevations for a variety of reasons, some of which have nothing to do with the supply demand imbalance and some of which do. Some of the elevations in cTn could be related to the toxic effects of the disease (sepsis and heat shock proteins and/or TNF) or of medications that are being used therapeutically [16]. What is suggested by the task force is that the clinician needs to develop his or her own sense of when these elevations are due to ischemia and an imbalance between myocardial oxygen supply and demand and then one can diagnose that episode as a type 2 MI. In the absence of such a diagnosis, one would suggest the presence of cardiac injury due to whatever pathophysiology is thought to be present. Heart failure perhaps is one of those more common situations where this issue may arise. Many patients have heart failure due to ischemic heart disease. However, there also are non-ischemic mechanisms for the cTn release including acute myocardial stretch [17] so the task force took a very careful look and suggested that although some elevations could be due to acute ischemia, that the vast majority might well be considered not to be due to acute infarction. Again, this is an area where clinical judgment is likely to be essential. Clinical trials and societal issuesIt was acknowledged in the guidelines that the implementation of the criteria suggested for the diagnosis of MI could cause substantial difficulties both for patients and for those who are doing clinical trials. The diagnosis of MI carries with it substantial negative consequences and clinicians should be aware and sensitive to that issue when they are making this diagnosis. In addition, clinical trial groups may have difficulty at times collecting the ideal information to employ the criteria proposed. Their ability to come as close as possible however to more clearly mimic the real world of clinical cardiology will be important if those trials are to have real applicability to the everyday patient. Nonetheless, it is clear that there may be times when resource limitations and/or circumstance make total adherence impossible. ConclusionThe 2012 guidelines expand on the criteria previously established and amplify on the criteria. However, it is clear that as additional data are developed, these guidelines are apt to change still further.DisclosuresDr. Jaffe has or presently consults for most of the major diagnostic companies. 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全球心肌梗死第三版(英文)
Criteria for prior myocardial infarction
Universal classification of MI
Type 1: Spontaneous myocardial infarction Type 2: Myocardial infarction secondary to an ischaemic
Pathological characteristics
Pathological characteristics of
myocardial ischaemia and infarction MI is defined in pathology as myocardial cell death due to prolonged ischaemia
Global perspectives
Cardiovascular disease is a global health problem.
Understanding the burden and effects of CAD in populations is of critical importance.Changing clinical definitions, criteria and biomarkers add challenges to our understanding and ability to improve the health of the public. The definition of MI for clinicians has important and immediate therapeutic implications.
Definition of myocardial infarction Criteria for acute myocardial infarction Criteria for prior myocardial infarction
最新全球心梗统一定义 英文翻译版
心肌梗死的定义急性心肌梗死的标准当临床上发现急性心肌缺血伴有心肌坏死的证据时，就应当使用心肌梗死这一术语。
因此，只要符合下列任何一条标准，就应诊断心肌梗死：·检测到心肌标志物（尤其是肌钙蛋白[cTn]）升高和/或下降，至少有一次超出正常参考值上限（URL）的第99%百分位值，并且至少伴有下列一项证据：·心肌缺血的症状·新发的或推测新发的显著ST-T改变或新出现的左束支传导阻滞(LBBB)·心电图出现病理性Q波·影像学检查发现新发的心肌丢失或新发的节段性室壁运动异常·冠脉造影或尸检发现冠脉内存在新鲜血栓·心源性死亡，伴有心肌缺血的症状，并伴有推定为新发的心肌缺血ECG改变或新出现的LBBB，但死亡之前未能获取血液标本或血液中心肌标志物尚未开始升高。
·经皮冠脉介入治疗（PCI）相关MI定义为：基线cTn值正常（≤99% URL）的患者，PCI术后升高超过99% URL的5倍；若基线水平升高且保持稳定或处于下降期，则术后cTn较基线值升高>20%。
此外，尚需具备以下任何一项：（i）心肌缺血的症状，（ii）新发现的心肌缺血ECG 改变，（iii）血管造影结果与PCI并发症相吻合，（iv）影像学检查显示新发的心肌丢失或新发的节段性室壁运动异常。
·在心肌缺血时冠脉造影或尸检发现支架血栓形成，并伴有心肌标志物升高和/或下降，至少有一次数值超过99% URL，即可界定为支架内血栓相关性MI。
·冠脉搭桥（CABG）相关性MI定义为：基线cTn值正常（≤99% URL）的患者，手术后心肌标志物超过99% URL的10倍。
此外，尚需有以下任何一项表现：（i）新出现的病理性Q波或新出现的LBBB，（ii）冠脉造影发现新的桥血管或自身冠脉闭塞，（iii）影像学检查显示新出现的心肌丢失或新发的节段性室壁运动异常。
陈旧性心肌梗死的标准符合下列任何一条标准，即可诊断陈旧性心肌梗死：·伴或不伴症状的病理性Q波，同时排除了非缺血性病因。
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心肌梗死的定义急性心肌梗死的标准当临床上发现急性心肌缺血伴有心肌坏死的证据时，就应当使用心肌梗死这一术语。
因此，只要符合下列任何一条标准，就应诊断心肌梗死：·检测到心肌标志物（尤其是肌钙蛋白[cTn]）升高和/或下降，至少有一次超出正常参考值上限（URL）的第99%百分位值，并且至少伴有下列一项证据：·心肌缺血的症状·新发的或推测新发的显著ST-T改变或新出现的左束支传导阻滞(LBBB)·心电图出现病理性Q波·影像学检查发现新发的心肌丢失或新发的节段性室壁运动异常·冠脉造影或尸检发现冠脉内存在新鲜血栓·心源性死亡，伴有心肌缺血的症状，并伴有推定为新发的心肌缺血ECG改变或新出现的LBBB，但死亡之前未能获取血液标本或血液中心肌标志物尚未开始升高。
·经皮冠脉介入治疗（PCI）相关MI定义为：基线cTn值正常（≤99% URL）的患者，PCI术后升高超过99% URL的5倍；若基线水平升高且保持稳定或处于下降期，则术后cTn较基线值升高>20%。
此外，尚需具备以下任何一项：（i）心肌缺血的症状，（ii）新发现的心肌缺血ECG 改变，（iii）血管造影结果与PCI并发症相吻合，（iv）影像学检查显示新发的心肌丢失或新发的节段性室壁运动异常。
·在心肌缺血时冠脉造影或尸检发现支架血栓形成，并伴有心肌标志物升高和/或下降，至少有一次数值超过99% URL，即可界定为支架内血栓相关性MI。
·冠脉搭桥（CABG）相关性MI定义为：基线cTn值正常（≤99% URL）的患者，手术后心肌标志物超过99% URL的10倍。
此外，尚需有以下任何一项表现：（i）新出现的病理性Q波或新出现的LBBB，（ii）冠脉造影发现新的桥血管或自身冠脉闭塞，（iii）影像学检查显示新出现的心肌丢失或新发的节段性室壁运动异常。
陈旧性心肌梗死的标准符合下列任何一条标准，即可诊断陈旧性心肌梗死：·伴或不伴症状的病理性Q波，同时排除了非缺血性病因。
·影像学检查发现局部心肌丢失的表现如室壁变薄并丧失收缩功能，同时排除非缺血性病因。
·病理检查发现陈旧性心肌梗死。
引言心肌梗死的诊断可根据其临床特征表现，包括心电图改变、升高的心肌坏死生物标志物和影像学改变，或通过病理检查而确诊。
它是世界范围内一个主要的致死、致残病因。
心肌梗死可能是冠心病的首发表现，也可能在已确诊冠心病的患者反复发生。
人群中心肌梗死发生率的有关资料，尤其是区分发生率和复发事件率的标准资料，可以帮助了解人群中和不同人群间的冠心病负担。
从流行病学的观点看，特定人群中心肌梗死的发生率可以反映该人群中冠心病的患病率。
心肌梗死这一术语无论对个人还是社会都有重要的心理和法律上的意义。
心肌梗死是一个标志反映全世界一个重要的健康问题，也是临床试验、观察研究和质量控制的一个结果指标。
这些研究和项目均需要精确、统一的心肌梗死定义。
过去，对心肌梗死这个临床综合征有一个基本共识。
在流行病学研究中，世界卫生组织（WHO）从症状、心电图异常和心肌酶学三个方面界定心肌梗死。
然而，随着敏感性和特异性更高的血清心肌生物标志物以及更敏感的影像学技术的临床应用，现已经可以检出更少量的心肌损伤或坏死。
此外，尽管有相似的临床表现，心肌梗死患者的治疗已经得到显著的改进，从而减少了心肌损伤和坏死。
再者，有必要区分导致心肌梗死的不同原因，例如“自发性”和“操作相关性”心肌梗死。
因此，内科医生、其他医务人员及患者需要最新的心肌梗死定义。
2000年，第一次全球心肌梗死工作组发表了新的心肌梗死定义，认为心肌缺血情况下的任何心肌坏死应当视为心肌梗死（1）。
这些原则又被第二次全球心肌梗死工作组重新定义，形成了2007年心肌梗死全球统一定义，其强调了可导致心肌梗死的不同原因（2）。
这份由欧洲心脏病协会（ESC），美国心脏病学会基金会（ACCF）、美国心脏协会（AHA）和世界心脏联盟（WHF）发布的共识，得到了医学团体的认可并被WHO所采纳（3）。
然而，敏感性更高的心肌坏死标志物检测方法的发展要求进一步修订其定义，尤其是心肌坏死发生在危重症的情况下、冠脉介入术后或冠脉搭桥术后。
第三次全球心肌梗死工作组延续了ESC/ACCF/AHA/WHF的努力,将新的见解和最新数据整合进这份文件，目前认为极少量的心肌损伤或坏死能被心肌生物标志物或影像学检测到。
心肌缺血和梗死的病理特征从病理的角度说，心肌梗死是指长时间心肌缺血引起的心肌细胞死亡。
心肌缺血开始后，组织学的细胞死亡并不是立即发生，而是在一定的时期（至少20min，有些动物模型时间更短）后出现（4）。
尸检发现通常需几个小时以后才能在肉眼或显微镜下鉴别心肌坏死。
心肌细胞的完全坏死至少需要2~4小时或者更久，这取决于通向缺血区的侧枝循环是否开通、持续性或间歇性冠脉闭塞、心肌细胞对缺血的敏感性、缺血预适应和/或心肌对氧和营养需求的个体差异（2）。
心肌梗死愈合的整个过程至少需要5~6周时间。
再灌注可以改变坏死区域的大体观和镜下观。
心肌坏死损伤的生物标志物检测血液中敏感而特异的生物标志物如心肌肌钙蛋白（cTn）和肌酸激酶同工酶CKMB的浓度增高提示心肌损伤（2）。
心肌肌钙蛋白I和T是心肌细胞收缩装置的组成部分，几乎专一性表达于心脏。
虽然血液中这些生物标志物的升高反映心肌细胞坏死损伤，但并不揭示其潜在机制（5）。
多种可能性可导致心肌结构蛋白释放，包括心肌细胞正常更新、凋亡、肌钙蛋白降解产物释放、细胞膜通透性增加、膜泡的形成并释放和心肌坏死（6）。
尽管病理机制不同，心肌缺血导致的心肌坏死统称为心肌梗死。
在主要为非缺血性心肌损伤的临床情况下也可能发现心肌坏死的组织学证据。
心衰、肾衰、心肌炎、心律失常、肺栓塞、经皮介入或外科冠脉手术时可能发现小量的心肌坏死损伤。
如图1所示，这些应称为心肌损伤，不能称为心肌梗死或操作的并发症。
现在认识到，临床情况的复杂性使得有时很难确定个体病例可能位于椭圆形的哪一部分（图1）。
这种情况下，鉴别cTn是急性还是慢性升高很重要，前者需要有cTn值升高和/或下降的动态变化，后者通常不会有cTn浓度急剧变化。
表1列举了引起cTn增高的临床情况。
在患者病程记录中应描述导致心肌损伤的多方面因素。
图 1 本图说明了各种临床状况，例如肾功衰，心衰，快速或缓慢型心律失常，心脏或非心脏手术可能导致心肌细胞死亡的心肌损伤，检测到肌钙蛋白升高。
然而，假如出现急性心肌缺血的临床表现和肌钙蛋白的升高和/或下降，这些临床状况也可能与心肌梗死有关。
较理想的心肌标志物是心肌肌钙蛋白，无论是整体的或是各种特殊类型的心梗，它都具有高度心肌组织特异性及高度临床敏感性。
cTn升高和/或降低的动态变化对于诊断急性心肌梗死是必需的（7）。
心肌肌钙蛋白浓度增高是指其检测值超过正常参考上限（upper reference limit，URL）的第99百分位值。
第99百分位值是诊断心肌梗死的决定水平，针对所使用的特定检测方法每个实验室都应当确定该数值，且必须有适当的质量控制（8,9）。
制造商确定的正常上限第99百分位值（99% URL），包括那些正在发展中的高敏感检测方法，可以在产品说明或近期的文献中找到（10-12）。
检测结果的单位为ng/L或pg/mL，心肌肌钙蛋白检测值升高的判断标准取决于检测方法，可以根据不同检测方法的精密度性能来确定，那些高敏感检测方法也同样如此。
理想的精密度，也即每种检测方法在99% URL的变异系数（CV）应小于10%；更好的精密度（CV<10%）能够得到更好的灵敏度，并有利于发现心肌肌钙蛋白的浓度变化（13）。
检测方法的精密度不理想（在99% URL 的CV>10%）将难以发现有意义的改变，但不会导致假阳性结果。
不应当使用在99% URL 的CV超过20%的检测方法（13）。
业已认识到分析前和分析中的问题可导致cTn值的增高或降低（10,11）。
初次评估时应采血检测cTn，3-6小时后复测。
如果有进一步的缺血事件发生，或是初始症状发生的时间不清，还需继续采血检测（14）。
cTn升高和/或下降，至少有一次超出正常上限值，对于诊断心梗是必需的，并伴有高患病可能性。
鉴别cTn浓度是急性而非慢性增高，需要有cTn升高和/或下降的动态变化，cTn慢性增高多与结构性心脏疾病相关（10,11,15-19）。
例如，肾衰或心衰患者可能发生明显的慢性cTn增高。
这种增高可能非常明显，就如许多心梗病人中所见，但不会发生急剧变化（7）。
然而，如果患者有高患病风险并在心梗症状出现后，cTn升高和/或下降的动态变化模式对于诊断心梗并不是绝对必需的，例如，靠近cTn时间-浓度曲线的峰值，或在曲线的缓慢下降期，不一定能检测到这种动态变化。
心肌细胞坏死后，cTn检测值的增高可持续2周或更长（10）。
对于高敏感检测方法，推荐依据性别使用不同的参考值（20,21）。
cTn增高超过正常参考上限第99百分位值，伴有或不伴有cTn的动态变化，或是缺乏心肌缺血的临床证据，应当进一步探究其他与心肌损伤有关的诊断，如心肌炎、主动脉夹层、肺栓塞或心衰。
肾衰及其他可能导致cTn水平增高的非缺血性慢性疾病，见表1（10,11）。
如果不能检测cTn，最好的替代项目是CKMB（采用质量法测定）。
与肌钙蛋白一样，CKMB超过正常参考上限第99百分位值为诊断心梗的决定水平（22）。
应当采用性别差异的参考值（22）。
表1 心肌损伤导致的心肌肌钙蛋白增高与原发性心肌缺血有关的损伤斑块破裂腔内冠状动脉血栓形成与供需失衡导致心肌缺血有关的损伤快速/缓慢型心律失常主动脉夹层或重度主动脉瓣病变肥厚性心肌病心源性、低血容量性或感染性休克严重呼吸衰竭严重贫血高血压伴或不伴左室肥厚冠状动脉痉挛冠状动脉栓塞或血管炎冠状动脉内皮功能障碍不伴有显著冠状动脉疾病与心肌缺血无关的损伤心脏挫伤、手术、消融、起搏或除颤器电击横纹肌溶解症累及心脏心肌炎心脏毒性制剂，如蒽环类药物、赫赛汀多因素或不确定性心肌损伤心衰Takotsubo心肌病（压力诱导的心肌病）严重肺栓塞或肺动脉高压败血症和危重病人肾功能衰竭严重的急性神经系统疾病，如中风、蛛网膜下腔出血浸润性疾病，如淀粉样变、结节病剧烈运动心肌缺血和梗死的临床表现心肌缺血的发生源于供氧和需氧的失衡，是心肌梗死的初始步骤。
临床上，心肌缺血可从患者的病史及心电图上认定。
心肌缺血症状是劳力或静息状态下胸部、上肢、下颌或上腹部各种组合的不适感，或者缺血等同症状，如呼吸困难或乏力。
急性心肌梗死的症状通常要持续至少20min以上。
一般来说，这种不适感部位是弥散的，非局限的，不随体位的变化而变化，也不受局部运动的影响。