急性心肌梗死再灌注损伤的临床表现及分析

目的:对急性心肌梗死(AMI)再灌注后出现的特殊临床表现进行分析。方法:50例AMI患者经静脉溶栓后行冠状动脉造影显示TIMI血流3级。结果:再灌注后有48例胸痛迅速缓解,2例胸痛突然加重;44例出现心律失常;40例出现一过性低血压;8例出现一过性ST段抬高。结论:冠状动脉血管再通后绝大部分患者胸痛迅速缓解,且有心律失常发生,一小部分患者可出现一过性胸痛加重;一过性低血压也比较常见,可能与多种因素有关;ST段反常性抬高可能是心肌再灌注的指标;溶栓后应进行持续心电和血压监测。     

急性心肌梗死再灌注损伤临床表现及分析

目的对急性心肌梗死再灌注后出现的特殊临床表现进行分析。方法50例急性心肌梗死患者经静脉溶栓后行冠状动脉造影显示TIMI血流3级。结果再灌注后48例胸痛迅速缓解,2例患者在再灌注后胸痛突然加重;44例患者出现心律失常;40例出现一过性低血压;8例出现一过性ST段抬高。结论冠脉血管再通后绝大部分患者胸痛迅速缓解,且有心律失常发生,一部分患者可出现一过性胸痛加重;一过性低血压也比较常见,可能与多种因素有关;ST段反常性抬高可能是心肌再灌注的指标;溶栓后应进行持续心电和血压监测。     

急性心肌梗塞再灌注后室性心律失常的特征及发生过程

急性心肌梗塞(AMI)患者,缺血心肌再灌注时常出现室性心律失常。然而心律失常发生过程及特征却未曾有过研究,本文于静脉链激酶溶栓后即刻及出院前,以24小时动态心电图监测,对AMI患者进行了研究。方法:AMI 45(男35、女10)例,平均年龄59±12(32～75)岁,均符合以下条件:(1)胸痛<3小时;(2)至少2个导联ST段抬高;(3)含硝酸甘油后仍持续胸痛及ST段抬高;(4)无溶栓或抗凝禁忌。尔后所有患者均证实有AMI。于出现胸痛后2.5±1.3(1～4)小时,静脉滴注链激酶750000单位,其中未表现再灌注征象的18     

急性心肌梗死静脉溶栓冠状动脉再通指标出现的时间顺序探讨

目的探讨急性心肌梗死(AMI)病人梗死相关冠状动脉静脉溶栓再通指标出现的时间顺序。方法将67例静脉溶栓治疗的AMI病人分为再通组和未通两组,再将再通组根据AMI发病时间分为<2h、2h~6h和>6h3个亚组,观察静脉溶栓后各组再灌注心律失常时间、胸痛缓解时间、心电图ST段下降达50%时间及肌酸激酶(CK)峰时间。结果再通组从再灌注心律失常时间、胸痛缓解时间到ST段下降达50%时间呈依此延长(P<0.05或P<0.01),且前述各指标随梗死时间的延长而相应延长,未通组的CK峰时间明显长于再通组及各亚组(P<0.05)。结论AMI静脉溶栓梗死相关冠状动脉再通指标按先后顺序为再灌注心律失常、胸痛缓解、ST段下降达50%及CK峰时间,且随梗死时间延长而相应延长。     

米诺环素后处理对急性心肌梗死溶栓后早期心律失常的影响

目的观察米诺环素后处理对急性心肌梗死(AMI)溶栓治疗早期的影响,确定米诺环素能否作为后处理药物减轻心肌缺血再灌注损伤。方法 65例胸痛发作<12 h ST段抬高型AMI患者,随机分为两组。①对照组,32例,尿激酶(UK)静脉溶栓,AMI常规用药;②处理组,33例,米诺环素200 mg静脉推注后UK溶栓,与静脉溶栓同步再予米诺环素200 mg静脉点滴,AMI常规用药。CCU病房24 h观察病情变化,记录心律失常,抽血查心肌酶。结果溶栓后2 h内ST段回落≥50%和>70%的比例,冠状动脉再通的比例,处理组高于对照组(P<0.05)。再灌注心律失常的发生率,处理组低于对照组(P<0.05)。溶栓后24 h内处理组的心肌酶峰值和恶性心律失常发生率明显低于对照组(P<0.05)。结论米诺环素后处理减轻了AMI再灌注损伤,提高了UK溶栓的再通率,降低了再灌注心律失常和恶性心律失常的发生。     

急性心肌梗死溶栓治疗后ST段再抬高的临床分析

目的 :观察急性心肌梗死 (AMI)静脉溶栓治疗后ST段再抬高的临床特点。方法 :回顾性分析符合静脉溶栓标准的AMI患者 1 0 7例 ,根据溶栓后有无ST段再抬高而分为ST段抬高组 (A组 )和ST段未抬高组 (B组 ) ,比较两组间发病年龄、伴发疾病、梗死相关血管、再通率、梗死后开始溶栓时间、再灌注心律失常、心功能变化 (Kil lip分级)。结果 :A组伴发糖尿病、高血压、高脂血症、梗死血管多支病变、心功能不全、再灌注心律失常发生率均高于B组 ,而冠状动脉再通率明显低于B组。结论 :溶栓治疗后ST段再抬高与患者并发糖尿病、高血压、高脂血症密切相关 ,梗死相关冠状动脉存在多支病变。该类患者再通率低 ,心肌受损重 ,易并发心功能不全 ,再灌注心律失常发生率高     

肌酸激酶峰值早期出现通常不是急性前壁心肌梗死患者成功再灌注后心肌被挽救的标志

很多研究证明急性心肌梗死 ( AMI)患者 ,接受再灌注治疗时胸痛会迅速缓解 ,出现再灌注心律失常和抬高的 ST段也会迅速下降 ,是冠脉灌注成功的临床和心电图标志 ,磷酸肌酸激酶 ( PCK)峰值提前出现也被认为是可靠的生化指标。然而 PCK早期出现是否是再灌注成功后“濒死”心肌能被挽救尚不清楚。因此作者研究了再灌注治疗 PCK出现时间与左室功能的关系。5 5 4例急性前壁心肌梗死患者达到如下标准者纳入本研究 :( 1)典型胸痛持续时间≥ 3 0分钟 ,( 2 )≥两个胸前导联 ST段抬高≥ 2 .0 mm ,( 3 )血浆 CK活性≥正常上限 2倍 ,( 4 )无 MI史…     

急性心肌梗死静脉溶栓与再灌注性心律失常

为进—步了解急性心肌梗死溶栓治疗中再灌注心律失常的主要形式及特点,观察尿激酶静脉溶栓治疗43例急性心肌梗死患者,其中27例临床判定再通,再通率62.79％,再灌注心律失常发生率以室性期前收缩(48.50％)和加速性心室自主节律(44.44％)为高,且后者与梗死组相比意义显著(P<0.01)。其特点为一过性,可自行终止,不转为恶性室性心动过速;且与胸痛缓解、ST段回降及酶峰前移的符合率明显高于未通组。认为加速性心室自主节律是溶栓后再灌注心律失常的特殊形式,可作为判定再通可靠的无创性指标之一。     

抬高的ST段恢复程度对溶栓治疗后心肌灌注的影响

为了进一步明确急性心肌梗死(AMI)患者溶栓治疗后ST段变化对心肌再灌注的影响，对我院68例AMI患者溶栓后ST段变化及心肌灌注情况进行检测分析。     

左旋卡尼汀对急性心肌梗死经皮冠状动脉介入治疗患者的心肌保护作用

目的在急性心肌梗死(AMI)接受直接经皮冠状动脉介入(PCI)治疗的患者中,评价国产左旋卡尼汀(L-carnitine,L-CN)对缺血-再灌注损伤心肌的保护作用。方法连续入选发病12h内ST段抬高AMI接受PCI的患者42例,随机分L-CN治疗组22例和对照组20例。观察肌酸磷酸激酶同工酶(CK-MB)、心肌TMP分级、术中再灌注心律失常、低血压、心电图ST段回落>50%、左心室舒张末期内径(LVEDD)和射血分数(LVEF)的改变。结果与对照组比较,L-CN治疗组CK-MB峰值明显减低,达峰时间提前;术中出现再灌注心律失常、低血压的比例明显减少;术后1h ST段回落>50%的患者比例明显增多;术后3个月时LVEDD仅轻度增大,LVEF显著升高。结论左旋卡尼汀对AMI直接PCI治疗患者的心肌具有抑制再灌注损伤、缩小梗死面积、改善心室重构等多重保护作用。     

急性前壁心肌梗死R波、Q波和ST段演变速度的观察

目的 通过心电图对急性心肌梗死的诊断提供更多的信息。方法 对21例急性前壁心肌梗死患者进行R波、Q波和ST段变化进行同步12导联心电图动态观察。将开始到结束的7次标测分成6个时间间隔．分别计算各个时间间隔的∑R、∑Q、和∑ST的平均值和标准差。结果∑R于胸痛发作后12h内迅速下降；∑Q逐渐增大，24h内变化最显著；EST 12h内迅速下降，48h后渐趋稳定。12例（57％）R波消失，Q波在发病后12h内形成；另9例（43％）于24h内形成。结论心肌梗死后ST段抬高、R波下降和Q波形成在快速型和慢速型心肌梗死患者中不同。     

急性心肌梗死墓碑形ST段抬高的临床意义

目的探讨急性心肌梗死（acute myocardial infarction，AMI）墓碑形ST段抬高的临床意义。方法将86例AMI患者以ST段抬高的特征分为两组，墓碑形抬高组36例、其他形抬高组50例。观察两组的一般临床资料（年龄、有否合并糖尿病），并比较两组AMI的发生部位、PCI前心梗后心绞痛、并发症及死亡的发生率、首次CK值、各项心电指标及PCI后心肌缺血再灌注损伤的发生率。结果两组各项临床指标及心电图指标差异均有统计学意义；墓碑形ST段抬高组PCI后心肌缺血再灌注损伤的发生率亦明显高于其他形ST段抬高组。结论墓碑形ST段抬高患者梗死部位特殊而广泛、并发症多、死亡率高、易出现心肌缺血再灌注损伤，对此类患者应高度重视并积极预防心肌缺血再灌注损伤的发生。     

Identification of the optimal electrocardiographic leads for detecting acute epicardial injury in acute myocardial infarction

Current coronary care electrocardiographic (ECG) monitoring techniques are aimed at detection of cardiac arrhythmias rather than myocardial ischemia. However, in patients with acute myocardial infarction (AMI) who undergo reperfusion therapy, monitoring ST-segment deviation could provide an early noninvasive indicator of coronary artery reocclusion. In this study, the admission 12-lead ECGs of patients with initial AMI were used to propose optimal lead locations for ST-segment monitoring. The study population was selected from consecutive Duke University Medical Center admissions during 1965 to 1981 who met the following inclusion criteria: chest pain for no more than 8 hours, initial AMI documented by ECG and 3 of 4 enzyme criteria, greater than or equal to 0.1 mV (1 mV = 10 mm) of ST elevation in at least 1 of the standard 12 leads (not aVR) on admission ECG, and no ECG evidence of conduction disturbances, ventricular hypertrophy or tachycardia. ST-segment deviation was quantified; AMI location was assigned based on the lead with maximal deviation. Of the 80 patients who had an inferior AMI, lead III was both the most frequent location for ST elevation (94%) and the most common site with maximal ST deviation. Lead V2 had the highest incidence of ST-segment depression (60%). In the 68 patients who had an anterior AMI, lead V2 had the highest frequency of ST elevation (99%). Leads V2 and V3 were the most common sites of maximal elevation. Thus, for monitoring ST deviation, leads III and V2 may be superior to leads II and V1, which are commonly used in arrhythmia monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reperfusion phenomenon is a strong predictor of left ventricular remodeling after acute myocardial infarction.

BACKGROUND:Many clinicians have seen the reperfusion phenomenon, a paradoxical response that includes a transient increase of chest pain, additional ST-segment elevation or ventricular arrhythmias immediately after coronary reperfusion, in patients with acute myocardial infarction (AMI). The aim of the present study was to investigate the impact of this phenomenon during coronary reperfusion on left ventricular (LV) remodeling in patients with AMI. METHODS AND RESULTS: One hundred and thirty-eight consecutive patients with a first anterior-wall AMI, undergoing coronary reperfusion treatment within 24 h of onset were prospectively evaluated for reperfusion phenomenon and followed up with scheduled evaluations of LV function and morphology with left ventriculography for 1 year. Of the 138 enrolled patients, 77 underwent serial left ventriculography at the acute, subacute and 1-year phases. Of these 77 patients, 39 demonstrated the reperfusion phenomenon. The LV end-diastolic volume index significantly increased from the acute to subacute phase and to the 1-year phase, but was unchanged in the 38 patients without reperfusion phenomenon. In multivariate analysis, reperfusion phenomenon was the only determinant of LV dilatation after AMI. CONCLUSIONS: Reperfusion phenomenon was a strong predictor of LV remodeling after reperfusion therapy for AMI.     

Massive hemorrhagic myocardial infarction after coronary thrombolysis

A 53-year-old man with occlusion of the proximal left anterior descending coronary artery received intravenous tissue plasminogen activator, and reperfusion was achieved within four and a half hours from the onset of chest pain. Recurrence of electrocardiographic ST segment elevation without attendant chest pain heralded reocclusion in the first hour after thrombolysis, which was successfully treated. After a stable course, post-infarction refractory cardiogenic shock developed on day 4, and autopsy demonstrated a massive (more than 100 cm2) hemorrhagic infarct. Several features of this case underscore the potential of coronary thrombolysis to cause significant reperfusion injury.     

Time-dependent predictors of primary cardiac arrest in patients with acute myocardial infarction

To understand predictors of cardiac arrest early in acute myocardial infarction (AMI), for the Thrombolytic Predictive Instrument, we developed a multivariable regression model predicting primary cardiac arrest using time-dependent variables based on a case-control study of emergency department (ED) patients with AMI: 65 cases with sudden cardiac arrest and 258 without cardiac arrest. Within the first hour of AMI symptom onset, adjusting for age, systolic blood pressure, serum potassium, and infarct size, increased risk of cardiac arrest was associated with electrocardiographic prolonged QTc interval and a greater sum of ST-segment elevation. After 1 hour, the effect of ST-segment elevation was much reduced and the effect of the QTc interval was reversed, so prolonged QTc appeared protective. Accordingly, for patients presenting 30 minutes after chest pain onset, compared with a QTc of 0.44, the risk for cardiac arrest for patients with QTc of 0.50 was more than doubled (odds ratio [OR] 2.20, 95% confidence intervals [CI] 1.17 to 4.13), whereas for those presenting after an hour, it was much lower (e.g., at 1.5 hours, OR 0.21, 95% CI 0.06 to 0.73). Patients presenting 30 minutes after chest pain onset with a sum of ST elevation of 20 mm had a threefold higher risk than patients with a sum of ST elevation of 5 mm (OR 3.37, 95% CI 1.83 to 6.20). However, if presenting 1.5 hours after chest pain onset, the risk was barely elevated (OR 1.18; 95% CI 1.09 to 1.29). Thrombolytic therapy was protective, halving the odds of cardiac arrest (OR 0.51, 95% CI 0.27 to 0.93). Thus, the relation of prolonged QTc interval and substantial ST segment elevation to cardiac arrest in AMI may be obscured because patients with these risks are more likely to die soon after AMI onset, before ED presentation, and are thereby unavailable for study. Those with prolonged QTc or substantial ST elevation who survive the initial 1.5-hour period are those less susceptible to these risks.     

Chest pain in the emergency room. Importance of a systematic approach

OBJECTIVE: To evaluate the efficiency of a systematic diagnostic approach in patients with chest pain in the emergency room in relation to the diagnosis of acute coronary syndrome (ACS) and the rate of hospitalization in high-cost units. METHODS: One thousand and three consecutive patients with chest pain were screened according to a pre-established process of diagnostic investigation based on the pre-test probability of ACS determinate by chest pain type and ECG changes. RESULTS: Of the 1003 patients, 224 were immediately discharged home because of no suspicion of ACS (route 5) and 119 were immediately transferred to the coronary care united because of ST elevation or left bundle-branch block (LBBB) (route 1) (74% of these had a final diagnosis of acute myocardial infarction [AMI]). Of the 660 patients that remained in the emergency room under observation, 77 (12%) had AMI without ST segment elevation and 202 (31%) had unstable angina (UA). In route 2 (high probability of ACS) 17% of patients had AMI and 43% had UA, whereas in route 3 (low probability) 2% had AMI and 7 % had UA. The admission ECG has been confirmed as a poor sensitivity test for the diagnosis of AMI ( 49%), with a positive predictive value considered only satisfactory (79%). CONCLUSION: A systematic diagnostic strategy, as used in this study, is essential in managing patients with chest pain in the emergency room in order to obtain high diagnostic accuracy, lower cost, and optimization of the use of coronary care unit beds.