特殊STEMI协和病例讨论明

1、case sharing: broken heart syndrome北京协和医院 杨 明病例1高某，女，高某，女，67岁，岁，病案号：病案号：c767493 入院日期：入院日期：2011-3-30主诉：主诉： 心悸、胸闷心悸、胸闷3h 入院情况2011-3-30 10:00am “胆总管多发结石胆总管多发结石” 行行ercp 术术1：30pm 心悸、胸闷，无发热、腹痛、皮肤巩膜黄染、胸痛、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、尿少等不适意识障碍、四肢冰凉、尿少等不适 心肌酶：心肌酶：ck：60u/l，ck-mb：7.4ug/l，ctni：3.66ug/l心电图既往

2、史既往史 高血压病高血压病2年，血压最高年，血压最高180/100mmhg雅施达雅施达4mg qd 血压可控血压可控制在制在130/80mmhg2011-3-15因反复恶心呕吐，查腹部超声、因反复恶心呕吐，查腹部超声、ct及及mrcp提示胆管结提示胆管结石石3-15行第一次行第一次ercp取石术，术后患者焦虑、烦躁、常怀疑自己患取石术，术后患者焦虑、烦躁、常怀疑自己患有肿瘤、拒绝进食。有肿瘤、拒绝进食。因胆管结石较多，此次为二次因胆管结石较多，此次为二次ercp取石。取石。个人史、月经婚育史、家族史无殊入院查体 t 36.8、hr 117bpm、bp110/80mmhg， spo2 100%（

3、3l/min） 精神烦躁，时间及空间定向力准确，对答切题，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。及脑膜刺激征阴性。 入院诊断入院诊断冠状动脉粥样硬化性心脏病冠状动脉粥样硬化性心脏病 急性急性st段抬高型心肌梗死（前壁）段抬高型心肌梗死（前壁） 心功能心功能1级（级（killip）精神烦躁原因待查精神烦躁原因待查高

4、血压病高血压病3级（极高危）级（极高危）左肾结石碎石术后左肾结石碎石术后胆管结石胆管结石 ercp术后术后子宫切除术后子宫切除术后stemi !急诊冠脉造影病例1冠脉造影病例1冠脉造影病例1冠脉造影病例1冠脉造影病例1冠脉造影心脏超声(入院当天3-30)： 心尖部心肌运动明显减弱，ef 41%心脏超声(入院当天3-30)：入院后治疗可达龙 艾司洛尔 2d倍他乐克至今心肌酶变化表心电图变化入院一周后一周后心脏超声：心尖部及左室余室壁运动未见异常, ef 73% 入院当天一周后心脏超声入院当天一周后心脏超声病例2韩某某，女，72岁病案号 1681545主诉：胸闷10小时入院日期：2010-11-3

5、0 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。卵巢癌手术前ecg胸痛时ecgii，iii，avf，v2,v3,v4导联st段抬高我院急诊抢救室（发病4h）i，avl，v2-4导联st抬高，v2呈qs型，v3 rs型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

6、50%既往史既往史：否认高血压、糖尿病、高血脂病史。个人史、月经婚育史、家族史个人史、月经婚育史、家族史无特殊，不嗜烟酒。入院查体入院查体：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。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

7、!病例2冠脉造影病例2冠脉造影病例2冠脉造影病例2冠脉造影病例2冠脉造影病例2冠脉造影病例2冠脉造影病例2冠脉造影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血脂:tc:3.57mmol/l, tg:1.24mmol/lldl:1.83mmol/l, hdl:1.18mmol/l发病24hi，avl st段抬高，v2-4 st段抬高，v3 r波恢复12月6日（发病7天）v2-4 t波双向，r波恢复正常入院echo1周后echo入院echo1周后echo2个病

8、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心肌酶升的不像其他stemi那么那么“高高”左室射血功能和左室射血功能和ecg在短时间内恢复正常在短时间内恢复正常stemi？myocardial infarction with normal coronary arteriespathogenetic mechanisms正向重构正向重构负向重构负向重构ivus纤维帽破口纤维帽破口oct能敏锐发现斑块破裂octmisdiagnosestako-tsubo-like syndro

9、metako-tsubo-like syndromethis rare syndrome, first described in japanese patients in 1991 , consists of transient left ventricular dysfunction with chest symptoms, electrocardiographic changes and minimal myocardial enzyme release mimicking ami, but without significant cad.stress cardiomyopathy“amp

10、ulla” cardiomyopathytransient left ventricular apical ballooning syndrome“broken heart syndrome”neurogenic myocardial stunning in 2006, under the name “stress cardiomyopathy”, it was classified within the group of acquired cardiomyopathiesit was named tako-tsubo-like syndrome because of the end-syst

11、olic shape of the left ventricle at ventriculography, with apical ballooning, which resembles a tako-tsubo, i.e., the japanese device used for trapping octopuses . epidemiologythe prevalence of the disease is unknown. in japan it is estimated to be as high as 1-2% of hospital admissions for chest pa

12、in and acute dynamic st-segment electrocardiographic changes.in the united states 2-2.2% of the patients presenting with the clinical picture of an st-segment elevation acute myocardial infarction (stemi) or unstable angina are ultimately diagnosed with ttc.epidemiologystudies in specific population

13、s have shown a much higher incidence. 1/3 of the patients they studied, who were admitted to a 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 bron

14、chial asthma was found by hertting et al in 32 patients diagnosed retrospectively with ttc. all these findings offer some evidence supporting the hypothesis that catecholamine surge may play an important role in the pathogenesis of the syndrome.triggering conditions：psychological trigger：unexpected

15、loss of a close relative, confrontation with another person, devastating financial loss, fear prior to a medical procedure, etc. physical stress ：pulmonary disease, sepsis, trauma, cerebrovascular accident pathogenesisunknownseveral theories catecholamine surge occult coronary atherosclerosis with p

16、laque rupturecoronary spasmmicrovascular dysfunction and spasmclinical characteristicschest pain（100%）ecg：56% st-segment elevation17% 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 differ

17、ential diagnosis between ttc and an acs in everyday 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 weeksminimally elevated card

18、iac markerscardiac imaging studies usually 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, s

19、uggesting that myocardial stunning rather than necrosis is the underlying mechanism of the acute left ventricular dysfunction. 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 i

20、n some patients with the use of intravascular ultrasound. whether this finding is of any pathophysiologic relevance remains currently unknown. 左室造影mritreatmentthe optimal treatment for ttc remains unknown. initial management should be the treatment of myocardial ischemia（ aspirin, clopidogrel, nitra

21、tes, intravenous heparin and -blockers ）send the patient immediately to the catheterization laboratory close monitoring for the development of heart failure, cardiogenic shock or malignant arrhythmiasafter the diagnosis of ttc has been established, antiplatelet agents and nitrates should be disconti

22、nued. 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. prognosisttc usually has a