1、Case Sharing: Broken Heart Syndrome北京協和醫院 楊 明病例1高某，女，高某，女，67歲，歲，病案號：病案號：C767493 入院日期：入院日期：2019-3-30主訴：主訴： 心悸、胸悶心悸、胸悶3h 入院情況2019-3-30 10:00am “膽總管多發結石 行ERCP 術1：30pm 心悸、胸悶，無發熱、腹痛、皮膚鞏膜黃染、胸痛、認識妨礙、四肢冰涼、尿少等不適 心肌酶：CK：60U/L，CK-MB：7.4ug/L，CTnI：3.66ug/L心電圖既往史既往史 高血壓病高血壓病2年，血壓最高年，血壓最高180/100mmHg雅施達雅施達4mg qd 血壓

2、可控血壓可控制在制在130/80mmHg2019-3-15因反復惡心嘔吐，查腹部超聲、因反復惡心嘔吐，查腹部超聲、CT及及MRCP提示膽管結提示膽管結石石3-15行第一次行第一次ERCP取石術，術后患者焦慮、焦躁、常疑心本人患取石術，術后患者焦慮、焦躁、常疑心本人患有腫瘤、回絕進食。有腫瘤、回絕進食。因膽管結石較多，此次為二次因膽管結石較多，此次為二次ERCP取石。取石。個人史、月經婚育史、家族史無殊入院查體 T 36.8、HR 117bpm、BP110/80mmHg， SpO2 100%3L/min 精神焦躁，時間及空間定向力準確，對答切題，言語欠清，雙側瞳孔等大，對光反射靈敏，鼻膽管引流通

3、暢、可見墨綠色膽汁、無異常臭味，心肺腹未見明顯異常，四肢肌力肌張力正常，雙側病理征及腦膜刺激征陰性。 入院診斷入院診斷冠狀動脈粥樣硬化性心臟病冠狀動脈粥樣硬化性心臟病 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級級Killip精神焦躁緣由待查精神焦躁緣由待查高血壓病高血壓病3級極高危級極高危左腎結石碎石術后左腎結石碎石術后膽管結石膽管結石 ERCP術后術后子宮切除術后子宮切除術后急診冠脈造影病例1冠脈造影病例1冠脈造影病例1冠脈造影病例1冠脈造影病例1冠脈造影心臟超聲(入院當天3-30)： 心尖部心肌運動明顯減弱，EF 41%心臟超聲(入院當天3-30)：入院后治療可

4、達龍 艾司洛爾 2d倍他樂克至今心肌酶變化表心電圖變化入院一周后一周后心臟超聲：心尖部及左室余室壁運動未見異常, EF 73% 入院當天一周后心臟超聲入院當天一周后心臟超聲病例2韓某某，女，72歲病案號 1681545主訴：胸悶10小時入院日期：2019-11-30 入院情況入院情況11-30日8am:外院擬行“卵巢癌剖腹探查術，麻醉前平臥位時突發胸悶、憋氣，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 口服后病癥減輕，轉至我院急診。卵巢癌手術前ECG胸痛時ECGII，III，AVF，V2,V3,V4導聯ST段抬高我院急

5、診搶救室發病4hI，AVL，V2-4導聯ST抬高，V2呈QS型，V3 rS型1：15pm起病5h：我院急診查心肌酶： CK97U/l、CKMB 9.5ug/l、cTnI 2.51ug/l。 床旁UCG：室間隔中下段無運動、心尖部、前壁運動減低，EF單平面50%既往史：否認高血壓、糖尿病、高血脂病史。既往史：否認高血壓、糖尿病、高血脂病史。個人史、月經婚育史、家族史無特殊，不嗜煙酒。個人史、月經婚育史、家族史無特殊，不嗜煙酒。入院查體：入院查體：HR 100bpm，BP 108/63mmHg，雙肺呼吸音低，雙下肺，雙肺呼吸音低，雙下肺可及細濕羅音，左肺為著。心律齊，全腹韌，叩診實音，中下腹可及可

6、及細濕羅音，左肺為著。心律齊，全腹韌，叩診實音，中下腹可及不規那么包塊，質韌，壓痛不規那么包塊，質韌，壓痛+，無反跳痛、肌緊張，肝脾肋下未，無反跳痛、肌緊張，肝脾肋下未及，肝脾區無叩痛，挪動性濁音及，肝脾區無叩痛，挪動性濁音+，腸鳴音正常。雙下肢無水腫，腸鳴音正常。雙下肢無水腫，雙足背動脈正常。左胸可見穿刺引流管通暢。，雙足背動脈正常。左胸可見穿刺引流管通暢。入院診斷：入院診斷： 冠狀動脈粥樣硬化性心臟病 急性ST段抬高性心肌梗死前壁 心功能1級Killip 盆腔占位 卵巢癌能夠性大 雙側胸腔積液 腹腔積液 病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病例2冠脈造影病

7、例2冠脈造影病例2冠脈造影診治經過診治經過心肌酶發病12h達峰：cTnI 4.87ug/l，CKMB 28.1ug/l，CK239U/l，之后逐漸回落至正常床旁心臟超聲：室壁運動及左室收縮功能逐漸恢復正常血脂:TC:3.57mmol/l, TG:1.24mmol/lLDL:1.83mmol/l, HDL:1.18mmol/l發病24hI，AVL ST段抬高，V2-4 ST段抬高，V3 R波恢復12月6日發病7天V2-4 T波雙向，R波恢復正常入院ECHO1周后ECHO入院ECHO1周后ECHO2個病例與常見的個病例與常見的STEMI不同：不同：冠心病危險要素很少冠心病危險要素很少發病于手術或操

8、作前后高度緊張形狀下發病于手術或操作前后高度緊張形狀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在短時間內恢復正常在短時間內恢復正常STEMI？Myocardial infarction with normal coronary arteriesPathogenetic mechanisms正向重構正向重構負向重構負向重構IVUS纖維帽破口纖維帽破口OCT能敏銳發現斑塊破裂OCTMisdiagnosesTako-tsubo-like syndromeTako-tsubo-like syndromeThis rare syndrome, fir

9、st 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“ampulla cardiomyopathytransient left ventricular api

10、cal ballooning syndrome“broken heart syndromeneurogenic myocardial stunning In 2019, under the name “stress cardiomyopathy, it was classified within the group of acquired cardiomyopathiesIt was named Tako-tsubo-like syndrome because of the end-systolic shape of the left ventricle at ventriculography

11、, 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 pain and acute dynamic ST-segment electrocardiographic

12、 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 populations have shown a much higher incidence. 1/3 of the pat

13、ients 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 bronchial asthma was found by Hertting et al in 32 patie

14、nts 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 loss of a close relative, confrontation with another

15、 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 plaque rupturecoronary spasmMicrovascular dysfunction

16、 and spasmClinical characteristicsChest pain100%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 differential diagnosis between TTC and an ACS in everyday cl

17、inical 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 cardiac markersCardiac imaging studies usually reveal exte

18、nsive 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 rather than necrosi

19、s is the underlying mechanism of the acute left ventricular dysfunction. 冠脈造影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 use of intravascular ultrasou

20、nd. 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, nitrates, intravenous heparin and -blockers send the patient

21、 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 discontinued. On the other hand, since this is catecholamine-ind

22、uced 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 beni