Transcript 入院情况

Case Sharing:
Broken Heart Syndrome
北京协和医院
杨明
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
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
心电图
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130/80mmHg
 2011-3-15因反复恶心呕吐，查腹部超声、CT及MRCP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
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。
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（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 !
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
心率、心肌酶监测表
50
40
30
20
10
0
HR（10bpm）
可达龙 艾司洛尔 2d
倍他乐克至今
NT-BNP
（ng/ml）
CK（10U/L）
CTnI（ug/L）
1
2
3
4
5
入院天数
6
7
8
CK-MB（ug/L）
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
心脏超声
一周后
入院当天
心脏超声
一周后
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
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ECG
II，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50%
 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：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：
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 !
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
 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
发病24h
I，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ECHO
1周后ECHO
入院ECHO
1周后ECHO
2个病例与常见的STEMI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？
Myocardial infarction with
normal coronary arteries
Pathogenetic mechanisms
正向重构
负向重构
IVUS
OCT
纤维帽破口
OCT能敏锐发现斑块破裂
OCT能敏锐发现内膜撕裂
Misdiagnoses
Tako-tsubo-like syndrome
Tako-tsubo-like syndrome
 This 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
 “ampulla” cardiomyopathy
 transient 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 cardiomyopathies
 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 trapping 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 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.
Epidemiology
 Studies in specific 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 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.
 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
person, devastating financial loss, fear prior
to a medical procedure, etc.
 physical stress ：pulmonary disease, sepsis,
trauma, cerebrovascular accident
Pathogenesis
 Unknown
 Several theories
 Catecholamine surge
 occult coronary atherosclerosis with plaque
rupture
 coronary spasm
 Microvascular dysfunction and spasm
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 everyday
clinical practice.
 The time course of these ECG changes in TTC seems similar
to that observed in patients with early reperfused STelevation acute myocardial infarction, with T-wave
inversion persisting for at least 2-3 weeks
 Minimally elevated cardiac markers
 Cardiac 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, suggesting 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 in some
patients with the use of intravascular ultrasound.
 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 ischemia（ 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 malignant
arrhythmias
 After the diagnosis of TTC has been established,
antiplatelet agents and nitrates should be
discontinued.
 On the other hand, since this is catecholamineinduced clinical syndrome, β-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.
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 majority 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 syndrome
（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 the apex；
(5) normal coronary arteries at angiography;
(6) rapid improvement within few weeks
Myocardial infarction with normal
coronary arteries------- Multiple aetiologies and Variable prognosis
Thank you！