冠状动脉造影对急性下壁心肌梗塞时前侧壁导联ST段压低的分析

应用冠状动脉(冠脉)造影,对31例急性下壁心肌梗塞患者,心电图存在前壁或侧壁导联.ST段压低的情况下进行分析。结果发现冠脉双支或双支以上病变者,特别是左旋支存在病变者,易发生侧壁导联ST段压低.JP<0.05。前壁导联ST段压低者中,也以双支或双支以上病变为多。提示急性下壁心肌梗塞时,出现前侧壁导联的ST段压低,为心肌缺血扩展的标志。     

急性前壁心肌梗死患者心电图下壁导联ST段改变与其冠状动脉病变的关系

目的　探讨急性前壁心肌梗死患者心电图下壁导联 ST段改变与冠状动脉病变的关系。方法　对 81例冠状动脉左前降支 (L AD)单支病变所致急性前壁心肌梗死患者 ,依其早期心电图下壁导联 ST段改变的形态将患者分为 3组 ,即压低组、抬高组、无改变组 ,并与冠状动脉造影结果进行比较和分析。结果　下壁导联 ST段压低组中73.3%患者为 L AD非优势近端病变 ;抬高组中 6 2 .5 %患者为 L AD优势远端病变 ;无改变组中 L AD优势近端病变与 L AD非优势远端病变所占比例近似。结论　急性前壁心肌梗死患者下壁导联 ST段改变与 L AD形态及病变的部位有关。     

急性前壁心肌梗死时下壁导联ST段改变的临床价值

目的探讨急性前壁心肌梗死病人下壁导联ST段改变的临床价值.方法对93例冠状动脉左前降支(LAD)单支病变所致急性前壁心肌梗死病人,根据早期心电图下壁导联ST段改变将其分为压低组、抬高组、无改变组3组,与冠状动脉造影结果进行分析比较.结果下壁导联ST段压低组中71.4%为LAD非包绕型近端病变;抬高组中61.5%为LAD包绕型远端病变;无改变组中LAD包绕型近端病变和LAD非包绕型远端病变所占比例相近.结论急性前壁心肌梗死病人下壁导联ST段改变与LAD形态及病变部位有关.     

急性下壁心肌梗死胸导ST段压低与冠脉病变的相关性

多项研究认为急性下壁心肌梗死出现的胸前导联ST段压低可能是下壁导联ST段抬高的对应性改变,也可能为前壁心肌缺血和左冠状动脉病变所致。本组资料分析了我院51例急性下壁心肌梗死患者的心电图、冠状动脉造影结果及临床资料,探讨胸前导联ST段压低与冠脉病变的关系及临床意义,报告如下。     

肢体导联ST段改变对急性前壁心肌梗死患者冠脉闭塞部位的预测价值

目的：结合冠状动脉造影结果分析肢体导联ST段改变对判断急性前壁心肌梗死患者冠脉闭塞部位的预测价值。方法入选84例因急性前壁梗死行冠状动脉造影检查的患者,对其发病后心电图肢体导联ST段改变的情况进行分析。结果冠状动脉造影发现,前降支近端病变（伴或不伴远端病变）,肢体导联Ⅱ、Ⅲ、aVF多表现为ST段压低≥0．1 mV;前降支远端病变（不伴近端病变）,肢体导联Ⅱ、Ⅲ、aVF的ST段多表现为抬高或无明显压低。结论对于急性前壁心肌梗死患者,心电图肢体导联ST段改变可以预测冠状动脉闭塞部位,对早期诊断和治疗方案选择有一定的指导意义。     

急性下壁心肌梗塞时心前导联ST段压低:早期~(210)铊闪烁图证实病变累及邻近后侧壁或室间隔下部

心前导联 ST 段压低是急性下壁心肌梗塞心电图中常见的表现,有报道认为这是下壁导联 ST 段抬高的相应心电表现。也有报道提出心前导联 ST段压低患者,呈现整体左心室功能减退和发生率较高的后侧壁或室间隔局部左心室功能不全。为了进一步了解心前导联 ST 段压低的临床意义,本文对首次下壁心肌梗塞患者的早期心电图与~(201)铊闪烁图、冠状动脉造影间的关系进行了研究.     

胸前导联ST段压低范围和幅度在急性下壁心肌梗塞的意义

目的 :评价胸前导联 ST段压低对急性下壁心肌梗塞的临床意义及探讨其可能发生机理。　　方法 :回顾分析了 1992年～ 1997年期间首次住院诊断急性下壁心肌梗塞患者 183例。将患者分为 4组 :无胸前导联ST段压低组 ( 组 ,n=5 6 ) ;胸前导联 ST段 V1～ 3压低组 ( 组 ,n=31) ;胸前导联 ST段 V4～ 6 压低组 ( 组 ,n=2 3) ;胸前导联 ST段 V1～ 6 压低组 ( 组 ,n=73)。资料分析包括心电图、心肌酶谱、左心室和冠状动脉造影及心肌梗塞的并发症和病死率。　　结果 :胸前导联 ST段压低患者比无胸前导联 ST段压低患者存在较大梗塞范围 ,心肌梗塞并发症和住院病死率较高。广泛 ST段压低时更显著 ,其心律失常、心功能不全发生率和住院病死率分别为 45 .0 %、12 .3% (P<0 .0 5 )和 8.2 %(P<0 .0 1)。胸前导联 ST段广泛压低总和≥ 0 .8m V显示预后更差 ,住院病死率 9.4% ,同 ST段压低 <0 .2 m V比差异显著 (P<0 .0 5 )。 组和 组存在左前降支病变或合并多支冠状动脉病变明显高于 组 ,有统计学差异。　　结论 :胸前导联 ST段压低分布范围和压低幅度对急性下壁心肌梗塞患者的预后判断和危险分层有一定价值。可能提示心肌梗塞范围较大 ,或同时存在前降支病变和多支冠状动脉病变。     

心电图STV5V6压低在急性下壁心肌梗死中是合并前降支病变的证据

目的观察急性下壁心肌梗死心前导联ST段压低与冠状动脉病变的关系.方法对38例急性下壁心肌梗死患者均常规行冠状动脉造影检查,根据常规心电图心前导联ST段压低≥1.0mm分为STV1-4压低组(17例)与STV1-6压低组(21例),比较心电图与冠状动脉造影之间的关系.结果STV1-4段压低是下壁ST段抬高的对应性改变(P＜0.01),STV1-6段压低证实合并明显的前降支病变(P＜0.01),其灵敏度、特异度、阳性预测值、阴性预测值分别为86%、88%、90%、83%.结论急性下壁心肌梗死心电图STV     

早期甄别急性下壁心肌梗塞重症患者的新指标(文献综述)

急性透壁性下壁心肌梗塞早期,为患者进行心电图检查时,常常发现下壁导联(Ⅱ、Ⅲ、aVF)ST段抬高,有时伴心前导联(V_1-V_6)ST段下降。此种心电图改变,过去一直认为是心电图下壁导联ST段抬高在前壁导联的镜面投影,几乎无临床意义。近年来,国外一些学者注意到具有心前导联ST段下降的急性透壁性下壁心肌梗塞患者较无心前导联ST段下降者血清酶CK峰值高、左室射血分数低、并发症多、近期及远期死亡率高、下壁梗塞面积大或多合并真后壁、后侧壁和后间壁梗塞,以及伴有前壁缺血。他们认为心电图心前导联ST段的变化可作为早期甄别急性下壁心肌梗塞重症和轻型患者及多血管病变和单血管病变的有价值的非侵入性指标。然而,     

心电图改变对急性下壁心肌梗死相关血管的预测价值

目的:对急性下壁心肌梗死患者的心电图资料进行回顾性研究,分析和比较心电图改变与冠状动脉造影及临床特点的对应性关系。探讨体表心电图改变对急性下壁心肌梗死患者的临床价值。方法:选取86例急性下壁心肌梗死患者,根据冠状动脉造影结果分为右冠状动脉(RCA)病变组和左冠状动脉(LCA)病变组。对比分析其心电图改变与冠状动脉造影结果及临床特点。结果:Ⅰ、Ⅱ、Ⅲ、aVR导联ST段及aVL导联波形改变对诊断梗死相关血管具有重要价值;V3与Ⅲ导联ST段改变比值预测梗死相关血管部位具有重要价值;伴aVR导联ST段压低患者病情重;伴胸前导联ST段压低者病情重、并发症发生率明显增高。结论:心电图对诊断下壁急性心肌梗死相关血管及其临床特点具有重要的预测价值。     

急性心肌梗死对应导联ST段变化与冠状动脉病变的关系

目的 用冠状动脉造影技术研究急性心肌梗死(AMI)对应导联ST段变化与冠状动脉病变的关系。方法136例急性心肌梗死共分五组:①组,前壁梗死(V1-6)伴有Ⅱ,Ⅲ,aVF导联ST段下移。②组,下壁梗死(Ⅱ,Ⅲ,aVF)同时伴有V1-6导联ST段下移。③组,下壁梗死(Ⅱ,Ⅲ,aVF)同时伴有I,aVL导联ST段下移。④组,前壁梗死(V1-6)未伴有其它导联的ST段变化。⑤组,下壁梗死(Ⅱ,Ⅲ,aVF)未伴有其它导联的ST段变化。所有患者均进行冠状动脉造影。结果 前壁心肌梗死伴有Ⅱ,Ⅲ,aVF导联ST段下移25例中有88%为左冠状动脉前降支病变,其中90.9%为左冠状动脉近端病变。前壁心肌梗死未伴有Ⅱ,Ⅲ,aVF导联ST段下移的36例患者中有94.4%为左冠状动脉前降支病变,两者统计无显著性差异。在下壁心肌梗死伴有V1-6导联ST段下移组22例中有81.8%为右冠状动脉病变,但同时伴有前降支病变的却有77.3%,其中单支病变仅18.2%。下壁心肌梗死未伴有V1-6导联ST段下移34例有91.2%为右冠状动脉病变,但同时伴有前降支病变的仅有32.4%,其中单支病变达52.9%。两组统计分别为P<0.001和P相似文献   

Occurrence of anterior ST depression in inferior myocardial infarction and relation to clinical outcome

In 229 patients admitted to the coronary care unit (CCU) at Sahlgren's Hospital developing inferior myocardial infarction, and with no previous myocardial infarction, the clinical outcome was related to the presence of ST-segment depression in 16 anterior chest leads. In all, 64% had anterior ST-segment depression. These patients differed from those not having ST depression in several aspects. They had larger infarcts, as assessed by serum enzyme activity and ECG recording. They were more prone to congestive heart failure and required more treatment for this complication. Their intensity and duration of pain during the first 4 days appeared to be more substantial. During a 5-year follow-up, patients with anterior ST depression tended to have a higher mortality. We conclude that among patients with inferior myocardial infarction and no previous infarction, those with anterior ST-segment depression form a subgroup with a more severe clinical course.     

Characteristics and mechanism of reciprocal ST-segment depression in acute ST segment elevation myocardial infarction: Reciprocal ST-segment depression and ST segment elevation myocardial infarction

At present, the mechanism of reciprocal ST-segment depression (RSTD) is unclear. ST-segment changes may be caused by the potential difference between the positive and negative electrodes, although this requires further investigation. The characteristics of RSTD and their relationship with ST-segment elevation in acute ST segment elevation myocardial infarction (STEMI) patients were analyzed. We replaced the negative electrode of the precordial leads of an inferior wall myocardial infarction patient and observed the changes in the ST-segment of the precordial leads. A total of 85 patients were included, of which 75 were patients with RSTD. All 45 patients with inferior myocardial infarction had limb lead RSTD, and 37 had anterior lead ST-segment depression. All ST-segment changes in STEMI can be explained by the proposed mechanism, and the value of ST segment depression in limb leads can be calculated by the value of ST segment elevation. In summary, the mechanism of RSTD in acute myocardial infarction may be that the action potential (AP) of the negative electrode of the lead weakens or disappears and the AP of the positive electrode may not be completely offset, resulting in ST-segment depression. Animal experimental studies are needed for further confirmation. When the negative electrode of the precordial lead is changed in acute inferior wall myocardial infarction patient, the ST-segment of the precordial lead changes accordingly. All the changes are consistent with our analysis.     

Significance of precordial ST segment depressions in acute inferior infarct--correlation with coronary angiography and ventriculography findings in the acute infarct phase

Thirty-two patients presenting with acute transmural inferior wall myocardial infarction underwent cardiac catheterization and angiography within 12 hours of onset of symptoms. Twelve lead electrocardiograms performed within 11/2 hours of catheterization revealed the following: Seventeen patients exhibited ST-segment depression in the anterior precordial leads in addition to inferior wall changes (group A). Fifteen patients did not manifest any ST-segment changes in the anterior precordial leads (group B). Clinical, arteriographic, and ventriculographic variables were compared between the two groups. No significant differences were observed with regard to age, sex, risk factors for coronary disease, duration of symptoms prior to angiography, Killip class, number of inferior leads with ST-segment elevation, or initial creatine kinase. The extent of coronary artery disease as well as the prevalence of severe disease in the left anterior descending artery were similar for both groups. Biplane left ventriculography revealed no significant differences between the two groups with regard to global or local left ventricular function.     

急性前壁心肌梗死并下壁导联ST段压低与冠状动脉病变的关系

目的：观察急性前壁心肌梗死下壁导联ＳＴ段压低与冠状动脉病变的关系。方法：对６６例急性前壁心肌梗死患者均常规行冠状动脉造影术,根据常规心电图下壁导联ＳＴ段压低＞１ｍｍ分为ＳＴ段压低组（４８例）与ＳＴ段正常组（１８例）,比较分析心电图与冠状动脉造影之间的关系。结果：急性前壁心肌梗死患者２７．３％有下壁导联ＳＴ段压低,ＳＴ段压低组中冠状动脉病变支数与正常组无显著性差异（Ｐ＞０．０５）,７３．２％为左前降支（ＬＡＤ）近端病变,显著高于ＳＴ段正常组（４５．８％）。ＳＴ段压低组５５．６％伴有心电图ＳＴＩ,ａＶＬ抬高,显著高于ＳＴ段正常组（４．２％）（Ｐ＜０．０１）。结论：急性前壁心肌梗死并下壁导联ＳＴ段压低与冠状动脉病变支数无关,而与ＬＡＤ近端病变有关,可能反映高侧壁心肌缺血时的心电图对应性改变。     

Precordial ST-segment depression in acute inferior myocardial infarction: innocent bystander or a high risk indicator?

ST-segment depression in the anterior precordial leads is seen in roughly one-half of patients with first acute inferior myocardial infarction. Concomitant stenosis of the left anterior descending artery can be detected angiographically in approximately 50% of all patients with inferior infarction whether or not precordial ST-segment depression is present. The presence of precordial ST-segment depression identifies a subgroup of patients with inferior myocardial infarction who have a lower left ventricular ejection fraction and quantitatively more severe abnormalities involving the posterolateral and inferoseptal segments. The contribution of anterior wall ischemia to the genesis of the precordial pattern remains problematic; although most studies to date have not supported this viewpoint, careful quantitative thallium perfusion studies have not been done. Short-term mortality and morbidity seem less favorable in the presence of precordial ST-segment depression, but this has not been substantiated by all authors.     

前壁导联ST段压低与急性下壁心肌梗死冠脉病变状况及预后的关系

目的探讨前壁导联ST段压低与急性下壁心肌梗死（MI）冠脉病变程度及预后的关系。方法根据MI初期是否并发前壁导联ST段压低将96例急性下壁MI分为两组即前壁导联ST段压低组（A组,56例）和前壁导联ST段无压低组（B组,40例）,将两组冠脉造影结果、梗死部位及预后进行比较分析。结果A组多支血管病变（52%）、梗死相关血管近端病变（82%）,下后壁MI（88%）、下后壁+右室MI（90%）,心力衰竭（16%）、心源性休克（14%）、室速（21%）。B组多支血管病变（30%）、梗死相关血管近端病变（22%）,下后壁MI（12%）、下后壁+右室MI（10%）,心力衰竭（2%）、心源性休克（2%）、室速（8%）。两组分项比较差异均显著（均P<0.05）。结论并发胸前导联ST段压低的急性下壁MI多为多支血管病变,梗死相关血管多为近端病变,梗死部位多,预后不良。     

A new ECG criterion to identify takotsubo cardiomyopathy from anterior myocardial infarction: role of inferior leads

With the exception of contrast-enhanced cardiovascular magnetic resonance imaging, clear distinction of takotsubo cardiomyopathy from anterior wall myocardial infarction cannot be achieved currently by simple and noninvasive tests. The aim of this study was to examine the role of inferior ECG leads in distinguishing these two conditions. From January 2004 to June 2006, eight female patients suffering from takotsubo cardiomyopathy were identified by the Mayo Clinic criteria. The clinical and ECG features were compared with 27 consecutive sex- and age-matched patients with anterior wall myocardial infarction admitted to the Coronary Care Unit within the same period. The observed ECG features were then verified with that of 62 published cases of takotsubo cardiomyopathy. Takotsubo cardiomyopathy patients had similar left ventricular ejection fraction (35.0% ± 5.7% vs 38.2% ± 6.4%, P = 0.829), lower peak creatinine kinase level (461 ± 330 U/l vs 2723 ± 1826 U/l, P = 0.020), more ST-segment elevation in the inferior leads (50% vs 7.4%, P = 0.016), and virtually no ST-segment depression in inferior leads (0% vs 48.2%, P = 0.015) compared with patients who had anterior wall myocardial infarction. ST-segment elevation of ≥1.0 mm in lead II had 62.5% sensitivity and 92.6% specificity in detecting takotsubo cardiomyopathy. The observed ECG characteristics were comparable with those in the literature. In patients who present with anterior wall myocardial infarction, the absence of ST-segment depression or ST-segment elevation in inferior leads, especially if the ST-segment in lead II ≥ III, is highly suggestive of takotsubo cardiomyopathy.     

Extent of ST-segment depression and cardiac events in non-ST-segment elevation acute coronary syndromes.

AIMS: We sought to determine whether the extent of myocardial ischaemia on the admission electrocardiogram (ECG) has independent predictive value for short-term risk stratification of patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS). Although the presence of ischaemic ECG changes on admission has been shown to predict outcome, the relationship between the extent of ECG changes and the risk of cardiac events is still ill defined. METHODS AND RESULTS: We analysed the admission ECGs of 5192 ACS patients enrolled in the GUSTO-IIb trial, without an ECG indication for thrombolysis. ECG tracings showing one or more of the following were eligible: ST-segment depression >0.5 mm, T-wave inversion >1 mm, and ST-segment elevation >0.5 mm but <1 mm. ECG variables associated with unfavourable 30 day outcomes in a univariable analysis were further assessed in a multivariable logistic regression model including independent clinical predictors. In the multivariable clinical, enzymatic, and ECG model, the sum of ST-segment depression (in millimetres) in all leads was a powerful independent predictor of 30 day death (P<0.0001), with a continuous increase in risk with the extent of ST-segment depression. The sum of ST-segment depression (P<0.0001) and the presence of minimal inferior ST-segment elevation (P<0.0001) or anterior ST-segment elevation (P=0.0182) were also independent predictors of the composite of death and myocardial infarction or reinfarction. The extent of ST-segment depression showed a highly significant correlation with the prevalence of three-vessel (P<0.0001) or left main coronary disease (P<0.0001), and also with the peak levels of creatine kinase (P<0.0001) during the index episode of ACS. CONCLUSION: In patients with NSTE ACS, the sum of ST-segment depression in all ECG leads is a powerful predictor of all-cause mortality at 30 days, independent of clinical variables and correlates with the extent and severity of coronary artery disease. The presence of even minimal (<1 mm) ST-segment elevation in anterior or inferior leads is independently associated with adverse outcomes.