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1、Stress-Induced Cardiomyopathy (Tako-tsubo syndrome) 應激性心肌病,澳門 鏡湖醫院心內科 金 椿,病情介紹,女性，70歲 (住院號：08-4361) 主訴：胸痛1小時。 AED (2008.2.28 21:45)： BP 156/84mmHg, HR 90bpm EKG ,2008.2.28 21:54,2008.2.28 23:37,2008.2.29 08:13,心肌酶譜變化,病情介紹,入院查體：BP 127/70mmHg，HR 82bpm 既往史：10多年前因右腎結石行右腎切除術，1991年曾患十二指腸潰瘍。不嗜煙酒。有上感史多天。 入院
2、診斷：ACS？,Mild stenosis at mid LAD; Mitral regurgitation.,Coronary angiogram,Left ventriculogram,Poor EF(42%) with hypokinesis of the anterior wall of LV.,Echocardiogram,One month later,住院期間,BP 100-130/60-80mmHg X-Ray：輕度肺瘀血；心影橫徑增大(c/t=0.63)，左室大。 Holter：極偶發室上性早摶部分成對出現 血生化：TG 2.0mmol/L，HDL 1.1mmol/L，血糖、
3、肝腎功能正常 出院帶藥： Betaloc-zok 12.5mg qd Acertil 2mg qd Aspirin 0.1 qd Vasteral MR 35mg bid NMR 2.5mg bid,病史小結,危險因素：絶經期後女性，血脂升高 誘因：因丈夫去世而情緒激動 表現：胸痛30min 檢查：心電圖有動態變化，血心肌酶 CAG：冠脈無明顯狹窄 Echo：心尖摶動瀰漫性減弱，各房室不大 住院期間：生命體征平穩，無心衰及心律失常,Stress-Induced Cardiomyopathy (Tako-tsubo syndrome) 應激性心肌病,In 1990 Hikaru Sato and
4、 colleagues from Japan described a novel cardiac syndrome, characterised by: transient left ventricular dysfunction with chest pain, ECG changes minimal release of myocardial enzymes mimicking an AMI Left ventriculogram revealed : left ventricle had a peculiar shape (a round bottom and narrow neck)
5、resembled a type of bottle used in Japan for trapping octopus. Sato and colleagues termed the syndrome “Tako-tsubo“ cardiomyopathy “tako” meaning octopus, and “tsubo”, bottle.,LV ventricular angiogram with typical apical ballooning.,More recently, it has also been called : acute left ventricular bal
6、looning reversible stress cardiomyopathy broken heart syndrome stress-induced myocardial stunning Apical ballooning syndrome,Stress appears to be key to the development of Tako-tsubo: can be emotional, physical or psychological in nature Studies show Tako-tsubo has occurred : after earthquakes death
7、 of a relative car accidents surprise parties fierce arguments court appearances and armed robberies,Clinical features,Chest pain is the most common symptom - up to 90% dyspnoea palpitations syncope As with AMI features of high circulating adrenaline levels (such as diaphoresis and peripheral shutdo
8、wn) are also common Requiring IABP counterpulsation and mechanical ventilation(1-5%) Other complications are rare: left ventricular thrombus formation, ventricular rupture and intractable arrhythmias,ECG changes,ECG changes on admission are often indistinguishable from acute anterior myocardial infa
9、rction ST elevation, usually in V3V6, with evolving T-wave inversion, Later in the course (after 3 days), widespread deep T-wave inversion is often seen with significant QT prolongation,Cardiac biomarker,Serial troponin and ck-MB levels only a small rise this is an important difference from AMI. A s
10、mall proportion of patients will have no troponin rise at all, and the absence of elevation does not exclude the diagnosis.,Coronary angiography,Upon admission coronary angiography revealed no or only a diffuse CAD without obstructive stenoses (50%), or spontaneous vasospasm in all patients,Left ven
11、triculography,akinesia in the anterolateral, apical, diaphragmatic, septal areas as well as base hypercontractile The median EF of the LV was 30.4% .,End-diastolic and end-systolic frames of the LV (A and B) and RV (C and D) demonstrating extent of LV and RV dysfunction (arrows).,Echocardiogram,Apic
12、al two chamber echocardiographic view showing LV apical ballooning and sigmoid septum,End-diastolic and end-systolic apical four-and-two chamber echocardiographic views demonstrating the typical apical and mid-ventricular LV wall-motion abnormalities of a patient with takotsubo cardiomyopathy,14 stu
13、dies: 2% of ST elevation infarcts, most cases in post-menopausal women. chest pain and dyspnoea in 67.8 and 17.8% Cardiogenic shock (4.2%) ventricular fibrillation (1.5%) ST-segment elevation( 81.6%) T wave abnormalities( 64.3%) Q waves( 31.8%) Cardiac biomarkers mildly elevated( 86.2%) LV dysfuncti
14、on on admission EF 20 to 49%, over a period of days to weeks. preceded by emotional (26.8%) or physical stress (37.8%). Norepinephrine concentration was elevated ( 74.3% ) excellent, with full recovery in most patients. In-hospital mortality was 1.1%. Only 3.5% of the patients experienced a recurren
15、ce.,Comparison between positron emission tomography (A, C, and E) and single-photon emission computed tomography (B, D, and F) images: metabolic image revealed severely reduced F-18 fluorodeoxyglucose uptake in the apical and mid-ventricular segments compared with perfusion abnormalities. (A and B)
16、Horizontal long-axis; (C and D) vertical long-axis; (E and F) short-axis.,Light microscopy,Endomyocardial biopsy specimen: contraction-band necrosis (arrows) and small amounts of mononuclear cell infiltration (haematoxylin and eosin stain). (A) Original magnification x100; (B) original magnification
17、 x200.,PAS staining (arrows) shows remarkable intracellular accumulation of glycogen (A). After functional recovery only small amounts of glycogen particularly around the nuclei of myocytes (arrows) were documented (B).,Electron microscopy,Electron microscopy of acute biopsies showing numerous vacuo
18、les of different sizes and contents (myelin bodies, residual cellular products), loss of contractile material, and areas of non-specified cytoplasm (A). The interstitial space was widened containing formation of cellular debris (B). In the acute phase, formation of myelin bodies could be documented
19、(C). In TTC contraction bands of sarcomeres were found (D). Recovered biopsies showed a nearly complete rearrangement of contractile material with regularly distributed sarcomeres, normal nuclei, and mitochondria (E, F). vac, vacuole; svac, small vacuoles; N, nucleus; cyt, cytoplasm; mit, mitochondr
20、ia; cd, cellular debris; mb, myelies bodies; sarc, sarcomeres; cb, contraction band.,Immunohistochemistry,Immunohistochemistry of intracellular proteins (specific labelling green, phalloidin red, nuclei blue). -actinin was detected only in the border zone during TTC (A). After functional recovery a
21、regular distribution was found (B). N-terminal dystrophin showed a decrease in TTC verifying a loss of protein-to-protein interaction (C) in comparison with biopsies after functional recovery (D). C-terminal dystrophin was unaltered in TTC suggesting that integrity of the sarcolemma is maintained (E
22、, F). Connexin-43 showed a reduced cellcell connection in TTC (G), whereas a myocardial integrity was documented after functional recovery (H).,Immunolabelling for titin was performed using T12 (A, B) and Tz1/Z2 (C, D). F-actin (red) was visualized with TRITCconjugated phalloidin and nuclei (blue) w
23、ere counterstained with Draq-5. Note that titin in the acute stage (A, C) is either absent in the central parts of the myocytes or shows a punctuated pattern as compared with a clear cross-striated pattern of labelling and higher expression levels in the recovery phase (B, D).,Immunohistochemistry o
24、f extracellular proteins (specific labelling green, phalloidin red, nuclei blue). The ECM stained by fibronectin (A, B) and collagen-1 (C, D) was increased and the myocardial syncytium was separated. After functional recovery, a decrease of extracellular proteins was observed. Macrophages (arrows) s
25、howing inflammatory response were regionally accumulated in TTC (E, F). Slight increase of T-lymphocytes (arrows) was regionally observed in TTC (G, H).,Pathophysiology,precise mechanisms are unknown catecholamine-mediated mechanisms with likely mediation via cardiac sympathetic nerves. Sudden surgi
26、ng catecholamine levels, can be precipitated by emotional or physical stress Catecholamine levels are characteristically far higher than in matched patients,catecholamine-mediated multivessel epicardial spasm, microvascular coronary spasm, or possible direct catecholamine-mediated myocyte injury.,Pa
27、thophysiology,Pathophysiology,On myocardial biopsy, the histological appearances are very similar to contraction band necrosis seen in phaeochromocytoma In a rodent model, TTC can be prevented with - or -blockade The more dense distribution of adrenoceptors at the apex might explain why the apex is
28、affected while the base is spared In addition, oestrogen downregulates cardiac adrenoceptors and attenuates their response to activation, providing a plausible reason why the condition is largely confined to postmenopausal women,Mayo Clinic criteria for tako-tsubo cardiomyopathy,1,Transient,reversib
29、le akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments with regional wall motion abnormalities . 2,Absence of obstructive coronary artery stenosis 50% of the luminal diameter or angiographic evidence of acute plaque rupture. 3,New ECG abnormalities consisting of ST-seg
30、ment elevation or T-wave inversion.,Absence of: recent head trauma intracranial bleeding phaeochromocytoma obstructive epicardial coronary artery disease myocarditis hypertrophic cardiomyopathy,Treatment and prognosis,inotropic support to maintain adequate blood pressure -blockade The wall motion abnormality returns to normal in many patients within days, and certainly within the first month excellent prognosis with no long-term sequelae,Thank you！ Q & A,