特殊stemi協(xié)和病例討論楊明

1、Case Sharing: Broken Heart Syndrome,北京協(xié)和醫(yī)院 楊 明,病例1,高某，女，67歲，病案號(hào)：C767493 入院日期：2011-3-30主訴： 心悸、胸悶3h,入院情況,2011-3-30 10:00am “膽總管多發(fā)結(jié)石” 行ERCP 術(shù)1：30pm 心悸、胸悶，無發(fā)熱、腹痛、皮膚鞏膜黃染、胸痛、意識(shí)障礙、四肢冰涼、尿少等不適 心肌酶：CK：60U/L，CK-M

2、B：7.4ug/L，CTnI：3.66ug/L,心電圖,既往史,高血壓病2年，血壓最高180/100mmHg雅施達(dá)4mg qd 血壓可控制在130/80mmHg2011-3-15因反復(fù)惡心嘔吐，查腹部超聲、CT及MRCP提示膽管結(jié)石3-15行第一次ERCP取石術(shù)，術(shù)后患者焦慮、煩躁、常懷疑自己患有腫瘤、拒絕進(jìn)食。因膽管結(jié)石較多，此次為二次ERCP取石。,個(gè)人史、月經(jīng)婚育史、家族史無殊,入院查體,T 36.8℃、HR 117b

3、pm、BP110/80mmHg， SpO2 100%（3L/min） 精神煩躁，時(shí)間及空間定向力準(zhǔn)確，對(duì)答切題，言語欠清，雙側(cè)瞳孔等大，對(duì)光反射靈敏，鼻膽管引流通暢、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(cè)病理征及腦膜刺激征陰性。,入院診斷,冠狀動(dòng)脈粥樣硬化性心臟病 急性ST段抬高型心肌梗死（前壁） 心功能1級(jí)（Killip）精神煩躁原因待查

4、高血壓病3級(jí)（極高危）左腎結(jié)石碎石術(shù)后膽管結(jié)石 ERCP術(shù)后子宮切除術(shù)后,STEMI !,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(dāng)天3-30)：,心尖部心肌運(yùn)動(dòng)明顯減弱，EF 41%,心臟超聲(入院當(dāng)天3-30)：,入院后治療,,,可達(dá)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

5、聲：心尖部及左室余室壁運(yùn)動(dòng)未見異常, EF 73%,入院當(dāng)天,一周后,心臟超聲,入院當(dāng)天,一周后,心臟超聲,病例2,韓某某，女，72歲病案號(hào) 1681545主訴：胸悶10小時(shí)入院日期：2010-11-30,入院情況,11-30日8am:外院擬行“卵巢癌剖腹探查術(shù)”，麻醉前平臥位時(shí)突發(fā)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 口服后癥狀

6、減輕，轉(zhuǎn)至我院急診。,卵巢癌手術(shù)前ECG,胸痛時(shí)ECGII，III，AVF，V2,V3,V4導(dǎo)聯(lián)ST段抬高,我院急診搶救室（發(fā)病4h）I，AVL，V2-4導(dǎo)聯(lián)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(yùn)動(dòng)、心尖部、前壁運(yùn)動(dòng)減低，EF單平面50%,,既往史：否認(rèn)高血壓、糖尿病、高血脂病史。

7、個(gè)人史、月經(jīng)婚育史、家族史無特殊，不嗜煙酒。入院查體：HR 100bpm，BP 108/63mmHg，雙肺呼吸音低，雙下肺可及細(xì)濕羅音，左肺為著。心律齊，全腹韌，叩診實(shí)音，中下腹可及不規(guī)則包塊，質(zhì)韌，壓痛（+），無反跳痛、肌緊張，肝脾肋下未及，肝脾區(qū)無叩痛，移動(dòng)性濁音（+），腸鳴音正常。雙下肢無水腫，雙足背動(dòng)脈正常。左胸可見穿刺引流管通暢。,入院診斷：,冠狀動(dòng)脈粥樣硬化性心臟病 急性

8、ST段抬高性心肌梗死（前壁） 心功能1級(jí)（Killip） 盆腔占位 卵巢癌可能性大 雙側(cè)胸腔積液 腹腔積液,STEMI !,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

9、,,,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,診治經(jīng)過,心肌酶發(fā)病12h達(dá)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(yùn)動(dòng)及左室收縮功能逐漸恢復(fù)正常血脂:TC:3.57mmol/l, TG:1.24mmol/lLDL:1.83mmol/l, HDL:1.18mmol/l,發(fā)病24hI，AVL ST段抬高，V2-4 ST段抬

10、高，V3 R波恢復(fù),12月6日（發(fā)病7天）V2-4 T波雙向，R波恢復(fù)正常,,入院ECHO,1周后ECHO,入院ECHO,1周后ECHO,2個(gè)病例與常見的STEMI不同：,冠心病危險(xiǎn)因素很少發(fā)病于手術(shù)或操作前后高度緊張狀態(tài)下心肌酶升的不像其他STEMI那么“高”左室射血功能和ECG在短時(shí)間內(nèi)恢復(fù)正常,,STEMI？,Myocardial infarction with normal coronary arteries,Patho

11、genetic mechanisms,,,正向重構(gòu),負(fù)向重構(gòu),,IVUS,,,纖維帽破口,OCT能敏銳發(fā)現(xiàn)斑塊破裂,OCT,OCT能敏銳發(fā)現(xiàn)內(nèi)膜撕裂,,,,,Misdiagnoses,Tako-tsubo-like syndrome,Tako-tsubo-like syndrome,This rare syndrome, ?rst described in Japanese patients in 1991 , consists of

12、transient left ventricular dysfunction with chest symptoms, electrocardiographic changes and minimal myocardial enzyme release mimicking AMI, but without signi?cant CAD.,,stress cardiomyopathy“ampulla” cardiomyopathytr

13、ansient 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 cardio

14、myopathies,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., the Japanese device used for trapp

15、ing octopuses .,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 t

16、he 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.,Epidemiology,Studies in sp

17、ecific populations 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 vent

18、ricular 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. All these findings offer som

19、e 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, confrontatio

20、n with another person, devastating financial loss, fear prior to a medical procedure, etc. physical stress ：pulmonary disease, sepsis, trauma, cerebrovascular accident,Pathogenesis,UnknownSeveral theories Catecholamin

21、e surge occult coronary atherosclerosis with plaque rupturecoronary spasmMicrovascular dysfunction and spasm,,Clinical characteristics,Chest pain（100%）ECG：56% ST-segment elevation17% T-wave inversions 10% Q-waves

22、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 clinical practice. The time

23、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,,Minimally elevated ca

24、rdiac 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 abnorma

25、lities typically extend beyond the vascular territory of a single coronary artery, suggesting that myocardial stunning rather than necrosis is the underlying mechanism of the acute left ventricular dysfunction.,冠脈造影,The

26、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

27、nd. Whether this finding is of any pathophysiologic relevance remains currently unknown.,左室造影,MRI,Treatment,The optimal treatment for TTC remains unknown. Initial management should be the treatment of myocardial ischem

28、ia（ aspirin, clopidogrel, nitrates, intravenous heparin and β-blockers ）send the patient immediately to the catheterization laboratory Close monitoring for the development of heart failure, cardiogenic shock or maligna

29、nt arrhythmias,,After the diagnosis of TTC has been established, antiplatelet agents and nitrates should be discontinued. On the other hand, since this is catecholamine-induced clinical syndrome, β-blockers should be ke

30、pt 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

31、 severe systolic dysfunction to reduce the risk of thromboembolism.,Prognosis,TTC usually has a benign course with full recovery of left ventricular function within 2-4 weeks from the onset of symptoms in the great major

32、ity of the cases. Complications : cardiogenic shock 6.5%,congestive heart failure 3.8%, ventricular tachycardia 1.6%, and death 3.2%.Recurrences, although rare, have also been reported.,病例1左室造影：,Tako-tsubo-like synd

33、rome（broken heart syndrome）,(1) elderly (>60 years old) women; (2) symptoms similar to an AMI; (3) Emotionnal or physical stress as trigger(4) a left ventricular wall hypokinesia extending from the mid segments to