特殊STEMI协和病例讨论杨明PPT课件

1、病例病例1 高某，女，67岁， 病案号：C767493 入院日期：2011-3-30 主诉： 心悸、胸闷3h 第1页/共76页入院情况入院情况 2011-3-30 10:00am “胆总管多发结石” 行ERCP 术 1：30pm 心悸、胸闷，无发热、腹痛、皮肤巩膜黄染、胸痛、意识障碍、四肢冰凉、尿少等不适 心肌酶：CK：60U/L，CK-MB：7.4ug/L，CTnI：3.66ug/L第2页/共76页心电图心电图第3页/共76页既往史既往史 高血压病2年，血压最高180/100mmHg雅施达4mg qd 血压可控制在130/80mmHg2011-3-15因反复恶心呕吐，查腹部超声、CT及MRC

2、P提示胆管结石 3-15行第一次ERCP取石术，术后患者焦虑、烦躁、常怀疑自己患有肿瘤、拒绝进食。 因胆管结石较多，此次为二次ERCP取石。个人史、月经婚育史、家族史无殊第4页/共76页入院查体入院查体 T 36.8、HR 117bpm、BP110/80mmHg， SpO2 100%（3L/min） 精神烦躁，时间及空间定向力准确，对答切题，言语欠清，双侧瞳孔等大，对光反射灵敏，鼻胆管引流通畅、可见墨绿色胆汁、无异常臭味，心肺腹未见明显异常，四肢肌力肌张力正常，双侧病理征及脑膜刺激征阴性。 第5页/共76页入院诊断入院诊断冠状动脉粥样硬化性心脏病 急性ST段抬高型心肌梗死（前壁） 心功能1级（

3、Killip）精神烦躁原因待查高血压病3级（极高危）左肾结石碎石术后胆管结石 ERCP术后子宫切除术后STEMI !第6页/共76页急诊冠脉造影急诊冠脉造影第7页/共76页病例1冠脉造影第8页/共76页病例1冠脉造影第9页/共76页病例1冠脉造影第10页/共76页病例1冠脉造影第11页/共76页病例1冠脉造影第12页/共76页心脏超声心脏超声(入院当天3-30)： 心尖部心肌运动明显减弱，EF 41%第13页/共76页心脏超声(入院当天3-30)：第14页/共76页入院后治疗入院后治疗可达龙 艾司洛尔 2d倍他乐克至今第15页/共76页心肌酶变化表心肌酶变化表第16页/共76页心电图变化心电图

4、变化入院一周后第17页/共76页一周后心脏超声：心尖部及左室余室壁运动未见异常, EF 73% 第18页/共76页入院当天入院当天一周后心脏超声第19页/共76页入院当天一周后心脏超声第20页/共76页病例病例2韩某某，女，72岁病案号 1681545主诉：胸闷10小时入院日期：2010-11-30 第21页/共76页入院情况入院情况 11-30日8am:外院拟行“卵巢癌剖腹探查术”，麻醉前平卧位时突发胸闷、憋气，ECG：II、III、avF ST上抬0.05-0.1mv，V2-4 ST 抬高0.3mv，予三硝及阿司匹林200mg 口服后症状减轻，转至我院急诊。第22页/共76页卵巢癌手术前卵

5、巢癌手术前ECG第23页/共76页胸痛时胸痛时ECGII，III，AVF，V2,V3,V4导联导联ST段抬高段抬高第24页/共76页我院急诊抢救室（发病我院急诊抢救室（发病4h）I，AVL，V2-4导联导联ST抬高，抬高，V2呈呈QS型，型，V3 rS型型第25页/共76页 1：15pm（起病5h）： 我院急诊查心肌酶： CK97U/l、CKMB 9.5ug/l、cTnI 2.51ug/l。 床旁UCG：室间隔中下段无运动、心尖部、前壁运动减低，EF单平面50%第26页/共76页第27页/共76页 既往史：否认高血压、糖尿病、高血脂病史。 个人史、月经婚育史、家族史无特殊，不嗜烟酒。 入院查体

6、：HR 100bpm，BP 108/63mmHg，双肺呼吸音低，双下肺可及细湿罗音，左肺为著。心律齐，全腹韧，叩诊实音，中下腹可及不规则包块，质韧，压痛（+），无反跳痛、肌紧张，肝脾肋下未及，肝脾区无叩痛，移动性浊音（+），肠鸣音正常。双下肢无水肿，双足背动脉正常。左胸可见穿刺引流管通畅。第28页/共76页入院诊断：入院诊断： 冠状动脉粥样硬化性心脏病 急性ST段抬高性心肌梗死（前壁） 心功能1级（Killip） 盆腔占位 卵巢癌可能性大 双侧胸腔积液 腹腔积液 STEMI !第29页/共76页病例病例2冠脉造影冠脉造影第30页/共76页病例2冠脉造影第31页/共76页病例2冠脉造影第32页/

7、共76页病例2冠脉造影第33页/共76页病例2冠脉造影第34页/共76页病例2冠脉造影第35页/共76页病例2冠脉造影第36页/共76页病例2冠脉造影第37页/共76页诊治经过诊治经过 心肌酶发病12h达峰：cTnI 4.87ug/l，CKMB 28.1ug/l，CK239U/l，之后逐渐回落至正常 床旁心脏超声：室壁运动及左室收缩功能逐渐恢复正常 血脂: TC:3.57mmol/l, TG:1.24mmol/l LDL:1.83mmol/l, HDL:1.18mmol/l第38页/共76页发病发病24hI，AVL ST段抬高，段抬高，V2-4 ST段抬高，段抬高，V3 R波波恢复恢复第39页

8、/共76页12月月6日（发病日（发病7天）天）V2-4 T波双向，波双向，R波恢复正常波恢复正常第40页/共76页入院入院ECHO1周后ECHO第41页/共76页入院ECHO1周后ECHO第42页/共76页2个病例与常见的个病例与常见的STEMI不同：不同： 冠心病危险因素很少 发病于手术或操作前后高度紧张状态下 心肌酶升的不像其他STEMI那么“高” 左室射血功能和ECG在短时间内恢复正常STEMI？第43页/共76页Myocardial infarction with normal coronary arteries第44页/共76页Pathogenetic mechanisms第45页/

9、共76页第46页/共76页正向重构负向重构第47页/共76页第48页/共76页IVUS纤维帽破口OCT能敏锐发现斑块破裂OCT第49页/共76页第50页/共76页第51页/共76页第52页/共76页第53页/共76页Misdiagnoses第54页/共76页Tako-tsubo-like syndrome第55页/共76页Tako-tsubo-like syndrome This rare syndrome, first described in Japanese patients in 1991 , consists of transient left ventricular dysfunc

10、tion with chest symptoms, electrocardiographic changes and minimal myocardial enzyme release mimicking AMI, but without significant CAD.第56页/共76页 stress cardiomyopathy “ampulla” cardiomyopathy transient left ventricular apical ballooning syndrome “broken heart syndrome” neurogenic myocardial stunnin

11、g In 2006, under the name “stress cardiomyopathy”, it was classified within the group of acquired cardiomyopathies第57页/共76页 It was named Tako-tsubo-like syndrome because of the end-systolic shape of the left ventricle at ventriculography, with apical ballooning, which resembles a tako-tsubo, i.e., t

12、he Japanese device used for trapping octopuses . 第58页/共76页Epidemiology The prevalence of the disease is unknown. In Japan it is estimated to be as high as 1-2% of hospital admissions for chest pain and acute dynamic ST-segment electrocardiographic changes. In the United States 2-2.2% of the patients

13、 presenting with the clinical picture of an ST-segment elevation acute myocardial infarction (STEMI) or unstable angina are ultimately diagnosed with TTC.第59页/共76页Epidemiology Studies in specific populations have shown a much higher incidence. 1/3 of the patients they studied, who were admitted to a

14、 medical ICU with a non-cardiac diagnosis (respiratory failure or sepsis), suffered from transient left ventricular apical ballooning. An increased incidence of chronic obstructive pulmonary disease or bronchial asthma was found by Hertting et al in 32 patients diagnosed retrospectively with TTC. Al

15、l these findings offer some evidence supporting the hypothesis that catecholamine surge may play an important role in the pathogenesis of the syndrome.第60页/共76页Triggering conditions： psychological trigger：unexpected loss of a close relative, confrontation with another person, devastating financial l

16、oss, fear prior to a medical procedure, etc. physical stress ：pulmonary disease, sepsis, trauma, cerebrovascular accident 第61页/共76页Pathogenesis Unknown Several theories Catecholamine surge occult coronary atherosclerosis with plaque rupture coronary spasm Microvascular dysfunction and spasm第62页/共76页

17、第63页/共76页Clinical characteristics Chest pain（100%） ECG： 56% ST-segment elevation 17% T-wave inversions 10% Q-waves or abnormal R-wave progression. 17% non-specific changes or no changes at all. ECG difference are too subtle to be helpful in the differential diagnosis between TTC and an ACS in everyd

18、ay clinical practice. The time course of these ECG changes in TTC seems similar to that observed in patients with early reperfused ST-elevation acute myocardial infarction, with T-wave inversion persisting for at least 2-3 weeks第64页/共76页 Minimally elevated cardiac markers Cardiac imaging studies usu

19、ally reveal extensive apical and/or mid-ventricular akinesis or hypokinesis with basal sparing, discordant with the minimally increased cardiac enzymes. These wall motion abnormalities typically extend beyond the vascular territory of a single coronary artery, suggesting that myocardial stunning rat

20、her than necrosis is the underlying mechanism of the acute left ventricular dysfunction. 第65页/共76页冠脉造影冠脉造影 The typical finding is the absence of obstructive coronary artery disease. However, Ibanez et al were able to describe the presence of ruptured atherosclerotic plaques in some patients with the

21、 use of intravascular ultrasound. Whether this finding is of any pathophysiologic relevance remains currently unknown. 第66页/共76页左室造影左室造影第67页/共76页MRI第68页/共76页Treatment The optimal treatment for TTC remains unknown. Initial management should be the treatment of myocardial ischemia（ aspirin, clopidogre

22、l, nitrates, intravenous heparin and -blockers ） send the patient immediately to the catheterization laboratory Close monitoring for the development of heart failure, cardiogenic shock or malignant arrhythmias第69页/共76页 After the diagnosis of TTC has been established, antiplatelet agents and nitrates

23、 should be discontinued. On the other hand, since this is catecholamine-induced clinical syndrome, -blockers should be kept on board and ACEI should also be started until the recovery of cardiac function. Diuretics are appropriate in the case that congestive heart failure develops. Anticoagulation should also be considered in the case of severe systolic dysfunction to reduce the risk of thromboembolism. 第70页/共76页Prognosis TTC usually has a benign course with full recover