这项研究是由国家机构的资助护理研究R21 NR-011202（MMP），R21 NR-009716（MGC）。 想感谢德比Ganchan的，RN，BSN为她细心周到的数据收集。我们还要感谢圣玛丽医院的护士和医生在医院纷纷慷慨解囊，提供援助与研究的。

1。患者准备<ol><li>获得知情同意书。 </li><li>确定土地的标记准确的导管放置在胸前。为了尽量减少心电图神器和噪声梅森-Likar的电极配置，其中使用肢体引线电极被放置在躯干四肢的前端（ 图2），而不是23 </li><li>准备用酒精准备垫的躯干和皮肤干燥轻快地用纱布垫，以确保最佳的皮肤电极接触。 </li><li>如果有必要，在具体的躯干位置，以使有足够的接触与皮肤电极夹胸毛。执行此步骤谨慎，因为这名病人的人口接受抗凝治疗，因此容易出血。 </li><li>如果可能的话，使用不褪色墨水，以纪念网站，以确保皮肤电极电极返回到正确的位置，在该事件中，他们脱落或删除程序（ 即 echocardiogrAMS，胸部透视等）。 </li><li>在女性中，电极V3应被放置在顶部的乳房组织和V4和V5的电极应放在正下方下垂的乳房，使乳房位于电极的顶部上，以确保精确的安置和防止运动伪影。 </li><li>双监视用于在这项研究中，医院床边监视器和研究动态心电记录。因此，两个心电图皮肤电极被施加到躯干。 </li><li> ECG导线连接到皮肤电极之前，将病人的胸部，以防止不必要的压力的chest.Radiolucent皮肤电极上的电极施加为了避免除去射线照相程序。 </li><li>输入动态心电图设备，并开始心电监护病人的唯一的研究识别码（确定）。 </li><li>将动态心电记录在显示器袋，并通过绳绕颈或在长袍的口袋里。 </li><li>获取位置ECGs的过程中使用的心电图数据的离线分析。包括三个位置：1）仰卧，2）右侧，和3）左侧卧。 </li><li>评估病人至少每2小时时，研究人员是在医院，并在年底的一天，时移，以确保在夜间保持监测。护士，辅助人员（ 如X-射线，超声心动图，与导尿技术人员）的工作人员的教育工作，以确保皮肤更换电极如果需要拆除的过程。正确的电极放置一个的躯干图与留在床边的资源，使工作人员能够更换皮肤如果必要的，也是多余的皮肤电极的电极。 </li><li>如果病人进入心导管实验室，将透亮的引线连接到皮肤的电极，这样可以保持心电图监测在导管插入过程中，以确保连续监测。 </li><li>当监测完成，该设备具有抗菌湿巾清洁。 </li></ol> 2。心电图分析程序<ol><li>在完成监测（持续时间可能会有所不同），闪卡阅读器H-抄写员科研计算机上加载的紧凑型闪存卡的动态心电记录仪。 </li><li>准备的数据进行分析，识别和标记每个QRS波群正常，心室，室上性或工件与H-抄写心律失常分析软件。 </li><li>的心电图数据进行初步评估没有临床数据知识，以减少偏见。 </li><li>的H-抄写软件编程，使用标准的定义，识别性心肌缺血，ST的偏差（抬高或压低）≥100微伏≥2个导联（S）持续≥60秒32在这项研究中，ST段偏移过去，在60毫秒的测量J点。 </li><li>符合这些条件的ST段变化进行识别和标记的H-抄写，并表示在肛门ysis总结。人的监督，以验证是否存在缺血必须做的任何一台计算机生成的事件，以确保正确识别假阳性ST段变化。这个过程将在下面描述。 </li><li> ST段趋势变化提示急性缺血评估小时的连续获取的ECG数据（图3）的一个有效的方法进行评估。 </li><li>为了找出真正的心肌缺血，任何获得3心电图提示急性心肌缺血的评估趋势： <ol class="ualpha"><li>基线ECG之前认定为“事件前心电图的ST段变化， </li><li>心电图认定为“最大的事件心电图ST段偏移，在最高点” </li><li>认定为“事件后心电图心电图ST段偏移彻底解决，” </li></ol></li><li>评估的三个心电图的ST段改变，以确保不因假阳性的变化（ 例如 ，加速ventr要约，要约节奏，间歇性的心室起搏节奏，间歇性束支传导阻滞，或体位改变）。 </li><li>缺少的ECG数据，质量不足的和假阳性ST改变的数据从分析中排除。这些问题都可以最小化使用的一些策略。这些包括：（1）用透亮的心电电极，无需取出电极的X-射线;（2）高品质的护肤准备，由研究护士在一开始就进行监测;（3）四舍五入各地的病人每2小时天;（4）可用性的电话，回答疑虑或问题，从护理和医疗人员。此外，研究小组护理和医疗人员定期进行通信。 </li><li>一旦心电数据进行分析，用于识别病人的医疗记录日期/时间的治疗，药物治疗和症状监测期间。 </li><li>心电图分析验证，确保具有第二专家分析ECG数据使用相同的方法在一个指定的比例的样品如上所述。我们的团队这例患者的20％。 </li><li>用于研究目的，存档的心电数据，以确保适当的数据被保存到外部硬盘驱动器和/或网络驱动器上。 </li></ol>

<ol>
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J., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Frequency,+duration,+magnitude,+and+consequences+of+myocardial+ischemia+during+intracoronary+ultrasonography.">Frequency, duration, magnitude, and consequences of myocardial ischemia during intracoronary ultrasonography.</a> Am. Heart J. 134, 474-478 (1997).</li><li>Drew, B. J., Pelter, M. M., Adams, M. G. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Frequency,+characteristics,+and+clinical+significance+of+transient+ST+segment+elevation+in+patients+with+acute+coronary+syndromes.">Frequency, characteristics, and clinical significance of transient ST segment elevation in patients with acute coronary syndromes.</a> Eur. Heart J. 23, 941-947 (2002).</li></ol>

作者们没有竞争的金融利益申报。

在这篇文章中描述的研究方法，使用Holter记录，捕捉连续12导联心电图记录。虽然计算机辅助软件工程ST段短暂性脑缺血检测，准确分析，需要仔细，专家的监督。在分析过程中考虑的重要因素包括：（1）神器，（2）的一致性和准确性放置电极，（3）身体姿势的变化，（4）药物的影响，以及（5）突然波形的变化。 总之，连续12导联心电图监测，这是既便宜又非侵入性，可识别短暂的心肌缺血发作的前兆MI，即使在无症状。10,12,33,34，12导联心电图监测医院的做法是不常见的，相反，只有两条引线，通常被监控。 12导联心电图监测获得的信息可能会提供有用的信息，决定与ACS患者的最佳治疗。然而，随机临床试验评估缺血的临床反应，以确定需要的价值，这种技术识别高风险的患者可能受益于更积极的管理策略，在ACS。

<html>根据最近的美国心脏协会的统计数据，冠状动脉疾病（CAD）， ​​估计是负责120万的住院治疗，治疗是最昂贵的医疗条件。1超过半数的医院停留CAD患者之间谁也逗留期间接受经皮冠状动脉介入治疗（PCI）或冠状动脉旁路移植术（CABG）。由于CAD的患病率，在医院工作的医生有可能经常会遇到这些病人。这篇稿子的目的是描述的ECG应用程序和分析方法的比较研究（电Çardiographic中为例缺血中号 IA COM P O N环进行投资，以PHAŕmacological TRËatment的一个西伯;（R21 NR-011202） ，这可能被利用的其他研究，探索这个临床问题。 T“每年近70万美国人将有一个新的冠心病发作，或急性冠脉综合征（ACS）。1 ACS的病理生理涉及动脉粥样硬化斑块破裂，因此，治疗的目的是稳定斑块，以防止细胞死亡然而，有相当大的临床医生的辩论中，哪些是最好的治疗途径：早期浸润性经皮冠状动脉介入治疗（PCI /支架）时表示，一个保守的方法（ 即药物治疗或PCI /支架如果出现复发症状）。 -5 在三种类型的ACS有三种类型：ST段抬高心肌梗死（STEMI），非ST段抬高心肌梗死（NSTEMI）和不稳定型心绞痛（UA）。6，NSTEMI / UA是近四倍，作为共同的STEMI。7 ，8 NSTEMI / UA的处理决定主要是根据症状和休息或运动心电图（ECG）。然而，因为动态的和不可预知的Natu重新动脉粥样硬化斑块，这些方法往往是在检测心肌缺血，因为症状是不可靠的，和/或持续心电监护，尚未动用。 NSTEMI / UA的表现形式包括：（1）症状（胸部，手臂，下巴或颈部疼痛，出汗，恶心），（2）释放NSTEMI的情况下，心脏生物标志物（肌钙蛋白I，肌钙蛋白T，或creatnine的激酶MB）和（3）心电图（ECG）的变化（间歇性ST段抬高/抑郁，或T波倒置）。虽然症状可能发生在ACS，这是有据可查的，短暂的心电图检测缺血发作是在70％以上的患者无临床症状。9-12重要的是，许多研究都发现，患者的心电图检测心肌缺血，患者相比，没有这样的事件，因此在短期内11-13和长期不利结果 ​​的风险较高。14-16，症状是在NSTEMI / UA，这是一个不可靠的指标缺血治疗早期侵入性策略或服药初期战略决策问题，因为病人的症状往往是2-5此外，生物标志物识别NSTEMI / UA的患者为时已晚，因为他们的存在表明，血清中细胞死亡已经发生。 表示缺血的心电图变化发生在几秒钟内冠状动脉的血流量减少。10,17复杂的心电图变化在急性缺血性ST段的三个点之一，这是衡量的部分，（1）J点， （2）J点，加上60毫秒（msec）的，或（3）J点加80（毫秒）（ 图1）。 12导联心电图识别MI，它是非侵入性的，廉价的，如果持续保持可识别短暂性脑缺血，甚至当它是无临床症状症状和生物标志物的重要优势。虽然12导联心电图监测是理想的，因为亩ltiple地区的心脏进行评估，典型的医院实践结合的监测，只有两个导联。两个心电图导联的护士在医院环境中最常用的监控V1和II。不幸的是，这两根导线用于检测在许多ACS患者短暂性脑缺血是不敏感的。10,19因此，缺血外发生的这两个监控线索将被错过。 使用12导联心电图监测比较研究的目的是评估的频率和过性心肌缺血的临床后果，NSTEMI / UA患者早期侵入性的初始保守的方法，其中包括药物单独管理的PCI /支架治疗，过渡到PCI /支架以下症状反复发作。在我们的研究中，连续12导动态心电记录仪是用来捕捉缺血。本描述性研究的目的是评估的频度和临床后果的反刻度心肌缺血，NSTEMI / UA患者的治疗无论是早期介入治疗PCI /支架或保守治疗（药物治疗或PCI /支架后，症状反复发作）。 方法上的挑战虽然计算机辅助软件工程ST段短暂性脑缺血检测，准确分析，需要仔细，专家的监督。在分析过程中考虑的重要因素包括：（1）神器，（2）的一致性和准确性放置电极，（3）身体姿势的变化，（4）药物的影响，和（5）突然波形的变化。这些因素都将在下面讨论。 工件：由于临床显着的ST段变化小为100微伏（一个小盒子上的心电图纸），噪声信号的肌肉刺激可显着阻碍分析。大部分文物是皮肤准备不当有关。的问题CAN是很容易解决病人的躯干与细致的皮肤准备在一开始监测，并根据需要在整个监测期间21日至23日的皮肤准备应包括在网站电极去除毛发，大力清除皮肤油/碎片，使用醇制备焊盘和/或毛巾。23,24 电极位置的一致性和准确性假阳性ST段电极移动或删除时，在监控过程中可能发生的变化。20这种可管理的网站监测，以确保电极在一开始就用不褪色墨水标记每个电极都将重新应用到正确的位置，如果他们脱落或删除程序（ 例如 ，超声心动图，X-射线）。25我们建议的评估，以确保病人的躯干，至少每4小时皮肤电极在胸前。 体位的变化：udies使用连续ST段监测表明，一些患者可在体位改变（ 即 ，左，右侧卧），可被误诊为心肌缺血的表现伴随QRS波群和ST段振幅的变化。26,27我们的研究小组发现，假阳性ST段报警，体位改变是最常见的原因。使用超声心动图，Feldman和同事28发现，当患者从仰卧到左侧卧位，左心室移近侧胸壁。这有一个直接的影响从胸部电极的左心室的距离上，并导致在心电图中的R波的振幅的增加导致移到该心肌领土。这些变化已经证实了别人。26,27一般情况下，位置心电图变化怀疑时，心电波形的幅度增加，同时ST段变化。一个有用的策略是获得“位置的模板心电图假设与患者仰卧，左，右侧卧的位置时，开始监测，为以后进行比较分析。 药理作用：即使在治疗剂量的药物可影响心电波形。药物改变ST段是特别重要的，因为它们会导致误诊为心肌缺血。29这些药物包括洋地黄，抗心律失常药，吩噻嗪类。 “洋地黄效应”是用来描述特征的ST段和T波改变可能出现的这种药物，包括“拱形”ST段压低，扁平的T-波和短QT间期的时间间隔。等30个其他药物，作为抗心律失常药物（ 如奎尼丁，索他洛尔和胺碘酮）30，吩噻嗪，用于治疗精神分裂症/精神障碍，增加QT间期，减少T波振幅31 Ňevertheless，服用这些药物的患者可以监视可能表明急性心肌缺血急性ST段变化。项目的基线异常的药物是慢性看到，因此任何ST段偏移（压低或抬高），应评估患者的基线ST段电平发生急性心肌缺血。 突然波形变化：瞬态条件，如心律失常，右或左束支传导阻滞（BBB），以及间歇性的心室节奏的节拍，可以扭曲的ST段和导致假阳性缺血诊断。20 总之，连续ST段监测识别性心肌缺血疑似ACS患者是一个很好的工具。然而，这种方法要求仔细的电极中的应用，并导致电线进行在开始和整个监测。这种方法也需要认真的人监督为了消除假阳性ST段的改变。 步骤分步方法在比较研究中，数字动态心电图记录仪（H12 +，莫仪器，密尔沃基，威斯康星州），它记录了在4毫秒的间隔超过10秒采样，以确定中位数拍的电势。全部12导联（I，II，III，AVR，AVL，aVF导联V1-V6），同时获得一个数字采样速率为每秒1000个样本每通道存储到一个紧凑的闪存卡。此外，H12 +电极阻抗测量，以确保正常的皮肤前的准备工作开始动态心电图记录。的显示器指示如果一个心电导联线已成为分离的，还提供了一个用于记录日记事件的内部时钟。从动态心电图监测烧录卡的数据被下载到H-抄写员，脱线动态心电分析系统（莫仪器，密尔沃基，威斯康星州）。该软件允许连续心电图记录分析INGS来确定的信号的质量，心律失常的存在下，和局部缺血。 研究助理工作经验的心脏病患者人口的动态心电数据收集。会议在研究开始的培训计划，以确保研究方案的质量和一致性。一个培训课程，包括心电监护程序，包括如何应用心电监护设备，启动/保持科研计算机上的心电监护，并下载动态心电数据。回示威活动进行间信度完成整个研究过程中，通过随机评估10％，目前在读的科目。双周研究小组会议的招聘目标，面临的挑战进行了讨论，并间信度测试的结果可以共享。 在比较研究的研究方法有两个重要的步骤，病人准备和立东北心电图分析。这两种方法都将在随后的部分中的一步一步的方式解释。

<table border="1"><tbody><tr><td> 的试剂/材料名称 </td><td> 公司 </td><td> 目录编号 </td><td> 评论 </td></tr><tr><td> 皮肤电极：生物PROTECH的泡沫Radiotranslucent电极</td><td>心脏直接</td><td> SKU：T716C </td><td></td></tr><tr><td> 透亮导联线 </td><td>优势医疗电缆</td><td> LW-3090R48/5A </td><td></td></tr><tr><td> 动态心电记录：H12 +版本3.12，12导联动态心电图记录仪，24小时Compact Flash卡，美国心脏协会10线LeadForm病人电缆</td><td>莫仪器，威斯康星州密尔沃基</td><td> H12PLUS-AAA-XXXXX </td><td></td></tr><tr><td> H-抄写动态心电分析系统 ，版本3.71 </td><td>莫仪器，威斯康星州密尔沃基</td><td> ĤSCRIBE - 咩 - AACXX的</td><td></td></tr></tbody></table>

a research method for detecting transient myocardial ischemia in patients with suspected acute coronary syndrome using continuous st-segment analysis

每年，估计有785,000美国人将有一个新的冠心病发作，或急性冠脉综合征（ACS）。 ACS的病理生理涉及动脉粥样硬化斑块的破裂，因此，稳定斑块的治疗的目的是为了防止细胞死亡。然而，有相当多的临床医生的辩论中，哪些是最好的治疗途径：经皮冠状动脉介入治疗（PCI /支架）时表示，保守的方法（ 即的药物只与PCI /支架如果出现复发症状）早期浸润性。 有三种类型的ACS：ST段抬高心肌梗死（STEMI），非ST段抬高心肌梗死（NSTEMI）和不稳定型心绞痛（UA）。在这三种类型中，NSTEMI / UA是常见的STEMI近4倍，。 NSTEMI / UA的处理决定主要是根据症状和休息或运动心电图（ECG）。然而，因为动态和不可预测性的atherosclerotiÇ斑块，这些方法往往是在检测心肌缺血，因为症状是不可靠的，和/或持续心电监护，尚未动用。 连续12导联心电图监测，这是既便宜又非侵入性的，短暂的心肌缺血发作的前兆MI，即使无症状。然而，连续12导联心电图监测是不平凡的医院的做法，而是只有两条引线，通常监测。 12导联心电图监测获得的信息可能会提供有用的信息，以决定最好的ACS治疗。 目的，因此，利用12导联心电图监测，比较研究（电Çardiographic中为例缺血中号 IA COM P O N账单INV 一个西伯PHAŕmacological数Ëatment）的目的是评估的频度和临床后果的瞬态NSTEMI / UA患者的心肌缺血，无论是早期介入治疗PCI /支架或那些管理保守治疗（药物治疗或PCI /支架以下症状反复发作）。这篇稿子的目的是描述所使用的方法的比较研究。 方法。进行这项研究的医院和大学的机构审查委员会的权限。研究护士识别疑似ACS住院的病人从急诊科和遥测单元。一旦同意，12导联心电图动态心电图监测，病人的整个住院过程中仍然存在。患者也维持在每家医院协议的常规床边心电监护系统。离线心电图进行分析，使用先进的软件和仔细的人的监督。

心电数据的初步分析，包括使用H-抄写软件的11导联ST段趋势的评估。值得注意的是，aVR导联不上显示的趋势，因为它是一个倒置的铅和不被视为可用于趋势分析，然而，这的铅是可见的12导联心电图打印输出。这种方法是一种快速简便的评估，用于评估小时的心电数据可能存在短暂的心肌缺血。印刷12导联心电图的ST段趋势的改变需要进一步的深入分析之前，期间和之后的趋势变化，将在下面解释。 <img alt="图1" src="/files/ftp_upload/50124/50124fig1.jpg" /> 图1。图 A显示了一个正常的ST段，PR段相比持平;的乙 showsST段抬高，通常显示总的冠状动脉闭塞;C显示ST段压低，通常表示部分冠状动脉闭塞。 ST段偏移也可测得的J点，J点+ 60 + 80毫秒毫秒，或J点。 （来源：M.骤降，M.＆凯里，在AACN重症监护程序手册 （ED韦根林恩·麦克海尔DJ）511-518（爱思唯尔·桑德斯，2011年许可）。 <img alt="图2" src="/files/ftp_upload/50124/50124fig2.jpg" /> 图2的躯干说明使用的的梅森- Likar电极配置的领先位置。右臂（RA）到右肩锁骨下窝，左臂（LA）的左肩锁骨下​​窝，右腿（RL）右下腹部肚脐下方，左腿（LL）左下腹部脐下; V1第四肋间胸骨边境的权利; V2第4肋间左胸骨边境V3之间的中间V2和V4，V4第五，我锁骨中线ntercostal空间; V5 V4腋前线直线距离; V6 V4腋直线。 （来源：M.骤降，M.＆凯里，在AACN重症监护程序手册 （ED韦根林恩·麦克海尔DJ）511-518（爱思唯尔·桑德斯，2011年许可）。 <img alt="图3" fo:content-width="5in" fo:src="/files/ftp_upload/50124/50124fig3highres.jpg" src="/files/ftp_upload/50124/50124fig3.jpg" /> 图3说明 “正常”，或者非缺血性ST段趋势的病人有23个半小时的ST段监测。在Y-轴，11个导联，V1导联显示在顶部和底部，导致III。 0.0在Y-轴表示一个正常的或等电ST段。的X-轴显示一个24小时的时间周期。在这个例子中，心电监护开始就在0900和0800第二天早上结束。在这名病人的ST段保持在0.0点整个监视时段期间（实线），表示有表示瞬态心肌缺血的没有ST段移位。可以从任何时间点在监测期间，通过简单的选择一个特定的时间和打印心电图12导联心电图。它可以保存在任何ECG（S）的研究报告格式文档文件。 <a href="https://www.jove.com/files/ftp_upload/50124/50124fig3large.jpg" target="_blank">点击此处查看大图</a> 。 <img alt="图4" fo:content-width="6in" fo:src="/files/ftp_upload/50124/50124fig4highres.jpg" src="/files/ftp_upload/50124/50124fig4.jpg" /> 图4，在这个例子中示出，一个短暂的ST段抬高事件。监测启动之前1200和连续地被保持，直到1000的第二天（X-轴）。在1230中，小于1小时开始监测后，ST段高程被认为是在导 ​​致II，aVF导联和三（见底部3 ST段的趋势）。4A，4B，和4C是12导联心电图的印刷前的事件，在最大的ST段变化，和事后并显示突然ST段抬高Ⅱ导联，aVF导联III暗示的完整的冠状动脉闭塞，1小时后解决。值得注意的是，这名病人是无症状的ST段改变医院的工作人员均未检出。 ST段趋势也显示了两个额外的小，但短暂的ST段变化，这些线索在1500，只是1800年之前的。由于这些ST段的改变不超过100微伏ST的事件，他们不能算作短暂性脑缺血事件的阈值。第二天早上，在0800这个病人的心脏导管插入术实验室，根据他的症状和肌钙蛋白（2.5微克/升）。发现90％病变在右冠状动脉，支架被放置。 ST段抬高结束时的监测期occurred在经皮冠状动脉介入治疗的程序，包括支架置入术，并按照以下步骤解决。4A事件前的短暂性脑缺血事件的心电图。4B。最大ST段抬高的缺血性事件。注ST段抬高的200毫伏中导致II，III，aVF导联。4C，12导联心电图的缺血性事件。需要注意的是ST段抬高的解决线索II，III，aVF导联（箭头）。 <a href="https://www.jove.com/files/ftp_upload/50124/50124fig4large.jpg" target="_blank">点击这里查看大图</a> 。 <img alt="图5" fo:content-width="6in" fo:src="/files/ftp_upload/50124/50124fig5highres.jpg" src="/files/ftp_upload/50124/50124fig5.jpg" /> （1）分离的导线或皮肤ELECTR 图5。这个数字说明了两个问题，可以发生在动态心电图监测，中断由于连续监测;诗，和（2）运动伪影。在这两种情况下，心电图数据是不是可用于分析。到1400之前，在所有的引线时，右腿电极（接地电极）脱落ST段趋势消失。当导线被替换了在1600监控恢复。不幸的是，同样的问题发生后的0100，并一直持续到年底的记录。 <a href="https://www.jove.com/files/ftp_upload/50124/50124fig5large.jpg" target="_blank">点击此处查看大图</a> 。 在该图中还示出了监控时恢复之前至1600是对ST-趋势的急剧变化。看到了类似的不规则的ST段趋势的变化在约1200，和2030至00年。5A显示了运动伪影的ST段变化的来源，也是源的其他不规则的趋势变化。在一般情况下，突然的或不稳定的ST段趋势的变化往往表示运动伪影或体位改变而变化，而不是心肌缺血。然而，从之前的心电图，期间和之后，ST段趋势的变化，应打印并仔细评估可能的缺血。 <img alt="图6" fo:content-width="6in" fo:src="/files/ftp_upload/50124/50124fig6highres.jpg" src="/files/ftp_upload/50124/50124fig6.jpg" /> 图6。ST段趋势显示假阳性ST段的变化，由于间歇性的心室定速器。之前0100 ST段趋势的变化，V3导联的ST段抬高，V4，V5，II，aVF导联和第三。6A是在0点51分○二秒的12导联心电图之前的趋势变化。值得注意的是，心房的步行者的尖峰可见在过去的4次10秒的节奏条中的铅II（见底部图）。注ST段压低，导致II，III，AVF，V5和V6可能是由于洋地黄类药物，病人服用。这些变化是慢性和本整个监测期间，6B示出了得到的心电图在1点二十○分39秒心室起搏现在本，心房起搏是可见的，以及。心室起搏的结果是从主要负为主阳性，导致V3，V4，V5，II，aVF导联ST段抬高的ST段改变。然而，这些变化是由于缺血，但相当异常的去极化和复与心室步行者的。 <a href="https://www.jove.com/files/ftp_upload/50124/50124fig6large.jpg" target="_blank">点击这里查看大图</a> 。

Watch this Scientific Journal Video about A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis at JoVE.

A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis

连续12导联心电图（ECG）监控可识别性心肌缺血，即使无症状，其中疑似急性冠状动脉综合征（ACS）患者。在这篇文章中，我们描述的方法启动病人监护仪，动态心电图设备，下载的心电图数据进行离线分析，以及如何利用ECG软件，以确定短暂性脑缺血。

研究方法检测疑似急性冠脉综合征患者短暂心肌缺血的连续ST段分析

Each year, an estimated 785,000 Americans will have a new coronary attack, or acute coronary syndrome (ACS). The pathophysiology of ACS involves rupture ...

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Research

JoVE Journal

Medicine

24.1K 次观看.  University of Nevada, Reno. 连续12导联心电图（ECG）监控可识别性心肌缺血，即使无症状，其中疑似急性冠状动脉综合征（ACS）患者。在这篇文章中，我们描述的方法启动病人监护仪，动态心电图设备，下载的心电图数据进行离线分析，以及如何利用ECG软件，以确定短暂性脑缺血。

视频: A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis

Acute Myocardial Infarction in Rats

With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular diseases. Animal models that mimic human cardiac disease, such as myocardial infarction (MI) and ischemia-reperfusion (IR) that induces heart failure as well as pressure-overload (transverse aortic constriction) that induces cardiac hypertrophy and heart failure (Goldman and Tarnavski), are useful models to study cardiovascular disease. In particular, myocardial ischemia (MI) is a leading cause for cardiovascular morbidity and mortality despite controlling certain risk factors such as arteriosclerosis and treatments via surgical intervention (Thygesen). Furthermore, an acute loss of the myocardium following myocardial ischemia (MI) results in increased loading conditions that induces ventricular remodeling of the infarcted border zone and the remote non-infarcted myocardium. Myocyte apoptosis, necrosis and the resultant increased hemodynamic load activate multiple biochemical intracellular signaling that initiates LV dilatation, hypertrophy, ventricular shape distortion, and collagen scar formation. This pathological remodeling and failure to normalize the increased wall stresses results in progressive dilatation, recruitment of the border zone myocardium into the scar, and eventually deterioration in myocardial contractile function (i.e. heart failure). The progression of LV dysfunction and heart failure in rats is similar to that observed in patients who sustain a large myocardial infarction, survive and subsequently develops heart failure (Goldman). The acute myocardial infarction (AMI) model in rats has been used to mimic human cardiovascular disease; specifically used to study cardiac signaling mechanisms associated with heart failure as well as to assess the contribution of therapeutic strategies for the treatment of heart failure. The method described in this report is the rat model of acute myocardial infarction (AMI). This model is also referred to as an acute ischemic cardiomyopathy or ischemia followed by reperfusion (IR); which is induced by an acute 30-minute period of ischemia by ligation of the left anterior descending artery (LAD) followed by reperfusion of the tissue by releasing the LAD ligation (Vasilyev and McConnell). This protocol will focus on assessment of the infarct size and the area-at-risk (AAR) by Evan's blue dye and triphenyl tetrazolium chloride (TTC) following 4-hours of reperfusion; additional comments toward the evaluation of cardiac function and remodeling by modifying the duration of reperfusion, is also presented. Overall, this AMI rat animal model is useful for studying the consequence of a myocardial infarction on cardiac pathophysiological and physiological function.

The rat model of acute myocardial infarction (AMI) is useful to study the consequence of a MI on cardiac pathophysiological and physiological function.

大鼠急性心肌梗死

With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular ...

科研

医学

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload

Children with sickle cell anemia (SCA) may be at risk of cerebral vasculopathy and strokes, which can be prevented by chronic transfusion programs. Repeated transfusions of packed red blood cells (PRBCs) is currently the simplest and most used technique for chronic transfusion programs. However, iron overload is one of the major side effects of this therapy. More developed methods exist, notably the apheresis of RBC (erythrapheresis), which is currently the safest and most efficient method. However, it is costly, complicated, and cannot be implemented everywhere, nor is it suitable for all patients. Manual exchange transfusions combine one or more manual phlebotomies with a PRBC transfusion.
At the Reference Center of Sickle Cell Disease, we set up a continuous method of manual exchange transfusion that is feasible for all hospital settings, demands no specific equipment, and is widely applicable. In terms of HbS decrease, stroke prevention, and iron overload prevention, this method showed comparable efficiency to erythrapheresis. In cases where erythrapheresis is not available, this method can be a good alternative for patients and care centers.

We have outlined a method of continuous manual exchange transfusion for the treatment of sickle cell disease in patients. This safe protocol was designed to effectively limit iron overload in patients in need of chronic transfusions and can be used extensively without any special equipment.

与镰状细胞疾病患者连续手动换血：的有效方法避免铁超负荷

Children with sickle cell anemia (SCA) may be at risk of cerebral vasculopathy and strokes, which can be prevented by chronic transfusion programs. ...

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any potential therapeutic approach directed against acute left ventricular (LV) dysfunction. Current imaging modalities (e.g., echocardiography and magnetic resonance imaging) have several limitations since data on LV pressure cannot directly be measured. LV catheterization in mice undergoing coronary artery occlusion could serve as a novel method for a real-time evaluation of LV function.
At the beginning of the procedure, mice were anesthetized followed by endotracheal intubation. For LV catheterization, the right carotid artery was exposed via middle-neck incision. The catheter was introduced and placed into the LV cavity. Left thoracotomy was conducted and the left main coronary artery (LCA) was ligated. To induce reperfusion, the suture was released after 45 min. Pressure-volume data was recorded at all times.
Ligation of the LCA caused a decrease in LV systolic function as evidenced by a 30% reduction in stroke volume, LV ejection fraction (EF), and cardiac output. Maximum dP/dt as a parameter for LV contractility was also significantly reduced and diastolic function was severely impaired (minimum dP/dt -40%). Reperfusion over a period of 20 min did not lead to a complete recovery of LV function.
Real-time pressure-volume analysis served as a valid procedure for monitoring cardiac function during acute myocardial infarction in mice. Maintaining stable anesthesia and a standardized surgical approach was crucial to ensure valid results. As the early phase of acute myocardial infarction is critical for morbidity and mortality, the delineated method could be beneficial for preclinical evaluation of new strategies for cardioprotection.

Acute myocardial infarction in mice induces acute but incompletely characterized changes in left ventricular (LV) function. LV catheterization in mice undergoing coronary artery occlusion serves as a novel method for a real-time evaluation of LV function.

小鼠急性心肌梗死的实时压力容积分析

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any ...

Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats

Coronary artery disease is the leading cause of death worldwide. After an acute myocardial infarction, early and successful myocardial intervention via recanalization of the coronary artery is the most effective strategy for reducing the size of ischemic myocardium. The coronary microvasculature cannot be visualized and imaged&#160;in vivo, but there are several invasive and noninvasive techniques that can be used to assess parameters which depend directly on coronary microvascular function. The endothelial function after ischemia reperfusion can be assessed also at the level of the coronary circulation via the coronary flow reserve (CFR).&#160;In this study, peak velocity of left anterior descending (LAD) coronary arteries was measured in rats in vivo via Transthoracic Doppler Echocardiography during resting and stress challenge (induced by Dobutamine). A normal heart can increase its coronary blood flow up to four times above the resting values during stress induction. Following ischemia reperfusion, we found a significantly diminished CFR, which can be used as a marker of coronary microvascular dysfunction. CFR has opened a window on the importance of microvascular dysfunction and has been shown to predict cardiovascular risk independent of whether the severe obstructive disease is present.

Coronary flow reserve (CFR), is defined as the ratio of maximal coronary blood flow to the resting coronary blood flow. We present a protocol for evaluating CFR in rats via ultrasound, which offers the opportunity to predict cardiovascular risk factors in the absence of obstructive coronary disease.

大鼠心肌缺血再灌注后冠状动脉流动储备评价

Coronary artery disease is the leading cause of death worldwide. After an acute myocardial infarction, early and successful myocardial intervention via ...

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

The beneficial effects of reperfusion therapy for ST-segment elevation myocardial infarction (STEMI) is attenuated by reperfusion injury. No approach has been proven successful in preventing this injury in the clinical setting to date. Meanwhile, a novel approach for cardioprotection in patients with STEMI, i.e., postconditioning with lactate-enriched blood (PCLeB), has recently been reported. PCLeB is a modification of the original protocol of postconditioning, aimed at increasing the delay in the recovery from tissue acidosis produced during ischemia. This was sought to achieve controlled reperfusion with tissue oxygenation and minimal lactate washout. In this modified postconditioning protocol, the duration of each brief reperfusion is gradually increased in a stepwise manner from 10 to 60 s. Each brief ischemic period lasts for 60 s. At the end of each brief reperfusion, injection of lactated Ringer&#39;s solution (20&#8211;30 mL) is performed directly into the culprit coronary artery immediately before the balloon inflation and the balloon is quickly inflated at the lesion site, so that the lactate is trapped inside the ischemic myocardium during each brief repetitive ischemic period. After seven cycles of balloon inflation and deflation, full reperfusion is performed. Stenting is performed thereafter, and the percutaneous coronary intervention is completed. Excellent in-hospital and 6 month outcomes in a limited number of patients with STEMI treated using PCLeB have already been reported. This method article provides a detailed description of each step of the PCLeB procedures.

Herein, we present a protocol for postconditioning with lactate-enriched blood, which is a novel approach for cardioprotection. This protocol comprises&#160;intermittent reperfusion and timely coronary injections of lactated Ringer&#39;s solution. This can be applied to ST-segment elevation myocardial infarction patients who undergo primary percutaneous coronary intervention.

在ST段高心肌梗死中,用乳酸富血进行心脏保护的后调节

The beneficial effects of reperfusion therapy for ST-segment elevation myocardial infarction (STEMI) is attenuated by reperfusion injury. No approach has ...

Predicting Amputation using Local Circulating Mononuclear Progenitor Cells in Angioplasty-treated Patients with Critical Limb Ischemia

Critical limb ischemia (CLI) represents an advanced stage of the peripheral arterial disease. Angioplasty improves the blood flow to the lower limb; however, some patients irreversibly progress to limb amputation. The extent of vascular damage and the mechanisms of vascular repair are factors affecting post-angioplasty outcome. Mononuclear Progenitor Cells (MPCs) are reactive to vascular damage and repair, with the ability to reflect vascular diseases. The present protocol describes quantification of MPCs obtained from blood circulation from vessel close to the angioplasty site, as well as its relationship with endothelial dysfunction and its predictive ability for limb amputation in the next 30 days after angioplasty in patients with CLI.

Lower limb amputation may occur even after angioplasty of obstructed vessels in Critical Limb Ischemia (CLI). Mononuclear Progenitor Cells (MPCs) reflect vascular repair. The present protocol describes the quantification of MPCs from circulation close to angioplasty, and its relationship with endothelial dysfunction and prediction of lower limb amputation.

预测使用局部循环单核祖细胞在血管成形术治疗的危肢缺血患者截肢

Critical limb ischemia (CLI) represents an advanced stage of the peripheral arterial disease. Angioplasty improves the blood flow to the lower limb; ...

Operating Transverse Aortic Constriction with Absorbable Suture to Obtain Transient Myocardial Hypertrophy

Based on twice transverse aortic constrictions (TACs) in mice, it is proved that myocardial hypertrophic preconditioning (MHP) could attenuate cardiomyocyte hypertrophy and slow down progression to heart failure. For novices, however, the MHP model is usually quite difficult to establish because of the technical obstacles in ventilator operation, opening the chest repeatedly, and bleeding caused by debanding. To facilitate this model, to increase the surgical success rate and to reduce the incidence of bleeding, we switched to absorbable sutures for the first TAC combing with a ventilator-free technique. Using a 2-week absorbable suture, we demonstrated that this procedure could cause significant myocardial hypertrophy in 2 weeks; and 4 weeks after surgery, myocardial hypertrophy was almost completely regressed to the baseline. Using this protocol, the operators could master the MHP model easily with a lower operation mortality.

This protocol presents an improved method to obtain transient myocardial hypertrophy with absorbable suture, simulating left ventricular hypertrophy decrease after removing pressure overload. It could be valuable for the studies on myocardial hypertrophic preconditioning.

操作横向主动脉收缩与可吸收的缝合获得瞬时心肌萎缩

Based on twice transverse aortic constrictions (TACs) in mice, it is proved that myocardial hypertrophic preconditioning (MHP) could attenuate ...

Induction of Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury in Mice

Acute myocardial infarction is a common cardiovascular disease with high mortality. Myocardial reperfusion injury can counteract the beneficial effects of heart reflow and induce secondary myocardial injury. A simple and reproducible model of myocardial infarction and myocardial ischemia-reperfusion injury is a good tool for researchers. Here, a customizable method to create a myocardial infarction (MI) model and MIRI by precision ligation of the left anterior descending coronary artery (LAD) through micromanipulation is described. Accurate and reproducible ligature positioning of the LAD helps obtain consistent results for heart injury. ST-segment changes can help to identify model accuracy. The serum level of cardiac troponin T (cTnT) is used to assess the myocardial injury, cardiac ultrasound is employed to evaluate the myocardial systolic function, and Evans-Blue/triphenyl tetrazolium chloride staining is used to measure infarct size. In general, this protocol reduces procedure duration, ensures controllable infarct size, and improves mouse survival.

Here we describe a simple and reproducible method that can induce myocardial infarction or myocardial ischemia-reperfusion injury in mice by precision ligation of the left anterior descending coronary artery through micromanipulation.

小鼠心肌梗死和心肌缺血再灌注损伤的诱导

Acute myocardial infarction is a common cardiovascular disease with high mortality. Myocardial reperfusion injury can counteract the beneficial effects of ...

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence suggests that thrombolytic therapy or primary percutaneous coronary intervention (PPCI) does not prevent reperfusion injury. There is still no ideal animal model for MIRI. This study aims to improve the MIRI model in rats to make surgery easier and more feasible. A unique method for establishing MIRI is developed by using a soft tube during a key step of the ischemic period. To explore this method, thirty rats were randomly divided into three groups: sham group (n = 10); experimental model group (n = 10); and existing model group (n = 10). Findings of triphenyltetrazolium chloride staining, electrocardiography, and percent survival are compared to determine the accuracies and survival rates of the operations. Based on the study results, it has been concluded that the improved surgery method is associated with a higher survival rate, elevated ST-T segment, and larger infarct size, which is expected to mimic the pathology of MIRI better.

Myocardial ischemia-reperfusion model of rat heart is improved by using a self-made retractor, polyvinyl chloride tube, and a unique knotting method. Electrocardiogram, triphenyltetrazolium chloride and histological staining, and percent survival analysis results showed that the improved model group has higher success and survival rates than the already existing model group.

心肌缺血再灌注损伤的改进啮齿动物模型

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence ...

辅助外泌体治疗：促进 CABG 手术后的心肌恢复

Surgical Porcine Model of Chronic Myocardial Ischemia Treated by Exosome-laden Collagen Patch and Off-pump Coronary Artery Bypass Graft

Chronic myocardial ischemia resulting from progressive coronary artery stenosis leads to hibernating myocardium (HIB), defined as myocardium that adapts to reduced oxygen availability by reducing metabolic activity, thereby preventing irreversible cardiomyocyte injury and infarction. This is distinct from myocardial infarction, as HIB has the potential for recovery with revascularization. Patients with significant coronary artery disease (CAD) experience chronic ischemia, which puts them at risk for heart failure and sudden death. The standard surgical intervention for severe CAD is coronary artery bypass graft surgery (CABG), but it has been shown to be an imperfect therapy, yet no adjunctive therapies exist to recover myocytes adapted to chronic ischemia. To address this gap, a surgical model of HIB using porcine that is amenable to CABG and mimics the clinical scenario was used. The model involves two surgeries. The first operation involves implanting a 1.5 mm rigid constrictor on the left anterior descending (LAD) artery. As the animal grows, the constrictor gradually causes significant stenosis resulting in reduced regional systolic function. Once the stenosis reaches 80%, the myocardial flow and function are impaired, creating HIB. An off-pump CABG is then performed with the left internal mammary artery (LIMA) to revascularize the ischemic region. The animal recovers for one month to allow for optimal myocardial improvement prior to sacrifice. This allows for physiologic and tissue studies of different treatment groups. This animal model demonstrates that cardiac function remains impaired despite CABG, suggesting the need for novel adjunctive interventions. In this study, a collagen patch embedded with mesenchymal stem cell (MSC)-derived exosomes was developed, which can be surgically applied to the epicardial surface distal to LIMA anastomosis. The material conforms to the epicardium, is absorbable, and provides the scaffold for the sustained release of signaling factors. This regenerative therapy can stimulate myocardial recovery that does not respond to revascularization alone. This model translates to the clinical arena by providing means of physiological and mechanistic explorations regarding recovery in HIB.

作者聚焦：增强冠状动脉血运重建

This study presents a surgical porcine model of chronic myocardial ischemia due to progressive coronary artery stenosis, resulting in impaired cardiac function without infarction. Following ischemia, animals undergo off-pump coronary artery bypass graft with epicardial placement of stem cells-derived exosomes-laden collagen patch. This adjunctive therapy improves myocardial function and recovery.

外泌体胶原贴片和体外循环冠状动脉旁路移植术治疗慢性心肌缺血的外科猪模型

Chronic myocardial ischemia resulting from progressive coronary artery stenosis leads to hibernating myocardium (HIB), defined as myocardium that adapts ...