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Table of Contents
CASE REPORT  
Year : 2014  |  Volume : 17  |  Issue : 2  |  Page : 157-160
Postoperative Takotsubo cardiomyopathy


1 Department of Anaesthesiology, Breach Candy Hospital, Mumbai, Maharashtra, India
2 Department of Gynaecology, Breach Candy Hospital, Mumbai, Maharashtra, India
3 Department of Cardiology, Breach Candy Hospital, Mumbai, Maharashtra, India

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Date of Submission05-Jun-2013
Date of Acceptance05-Dec-2013
Date of Web Publication1-Apr-2014
 

   Abstract 

Takotsubo cardiomyopathy also known as transient apical ballooning syndrome or stress induced reversible cardiomyopathy is an increasingly reported syndrome generally characterized by transient systolic dysfunction of the apical and/or mid segment of the left ventricle. It is frequently precipitated by severe stress and clinically mimics an acute ST-elevation myocardial infarction, with angiographically normal coronary arteries. A high index of suspicion is needed to diagnose this syndrome. We describe a patient who developed Takotsubo cardiomyopathy in the post-operative period following vaginal hysterectomy.

Keywords: Coronary angiography; General anesthesia; Takotsubo cardiomyopathy; Vaginal hysterectomy

How to cite this article:
Bhojraj S, Sheth S, Pahlajani D. Postoperative Takotsubo cardiomyopathy. Ann Card Anaesth 2014;17:157-60

How to cite this URL:
Bhojraj S, Sheth S, Pahlajani D. Postoperative Takotsubo cardiomyopathy. Ann Card Anaesth [serial online] 2014 [cited 2020 Apr 10];17:157-60. Available from: http://www.annals.in/text.asp?2014/17/2/157/129875



   Introduction Top


Takotsubo cardiomyopathy also known as transient apical ballooning syndrome [1] or stress induced reversible cardiomyopathy [2] is an increasingly reported syndrome. It is frequently precipitated by severe stress and clinically mimics an acute ST-elevation myocardial infarction with angiographically normal coronary arteries. [3],[4] Takotsubo syndrome or broken heart or Gebrochenes-Herz syndrome [5] is defined as a combination of acute chest pain, ST segment changes and transient left ventricular (LV) apical wall motion abnormalities that mimics acute myocardial infarction (MI), related to surges in catecholamine levels. It predominantly occurs in post-menopausal women with a mean age of 58-76 years. [6] Endothelial dysfunction in the post-menopausal period probably increases the vulnerability to sympathetically mediated myocardial stunning in this cohort. Most of the patients survive the initial acute event with a very low rate of in-hospital mortality or complications. Even when ventricular systolic function is heavily compromised at presentation, it typically improves within the 1 st few days and normalizes within 8 weeks. This syndrome has been reported in the perioperative setting after both minor and major surgical procedures [7],[8],[9] and can occur following regional or general anesthesia. The authors report a patient presenting postoperatively with stress induced cardiomyopathy, which normalized over a period of 6 weeks.


   Case Report Top


A 56-year-old female, American Society of Anesthesiologists grade I, weighing 50 kg was scheduled to undergo vaginal hysterectomy. Laboratory parameters were within the normal limits. Pre-operative electrocardiography (ECG) was normal [Figure 1]a. 2D echocardiography revealed an ejection fraction (EF) of 64%. Upon pre-operative counseling, she expressed anxiety and concern for the surgery. She was administered general anesthesia with midazolam 2 mg, fentanyl citrate 50 μg and etomidate 8 mg. Atracurium 40 mg was used to facilitate endotracheal intubation. Anesthesia was maintained with a mixture of O 2 :N 2 O (44:56), isoflurane 1-2% and boluses of fentanyl and atracurium. The hemodynamic parameters remained stable throughout the procedure. At the end of the surgical procedure, the trachea was extubated after reversal of neuromuscular blockade. The patient was conscious and post-operative pain was managed with intravenous tramadol 50 mg. At 3 h post transfer to the ward, she became hemodynamically unstable-systolic blood pressure decreased to 60 mmHg, heart rate to 60/min, and SpO 2 -76%. She was resuscitated with atropine sulfate 0.6 mg, intravenous fluids and sodium bicarbonate 25 ml. Dopamine hydrochloride and noradrenaline were started at 5 μg/kg/min and 4 μg/min, respectively. ECG revealed fresh changes with ST flattening in leads II, III and aVF and ST depression with T wave inversion in leads V2-V6 [Figure 1]b Cardiac enzymes were mildly elevated. Her white blood cell (WBC) count rose to 22,220/ul. At 5 h post-operatively her SpO 2 decreased to 70% (with 8 L of oxygen by mask), and she developed bilateral basal crepitations. Intravenous fluid intake and output showed 1775 ml and 680 ml with a positive balance of 1095 ml. The patient was immediately transferred to the intensive care unit where a central venous line was inserted through right internal jugular vein. Central venous pressure was 15 mmHg. Chest X-ray showed fluffy shadows in middle and lower zones [Figure 2]. 2D echocardiography revealed an EF of 30-35% with akinesia and ballooning of apex, anterior wall and distal septum. There was evidence of left ventricular (LV) diastolic dysfunction as well. In view of the decreased EF and high WBC counts, a differential diagnosis of acute coronary syndrome with LV failure/sepsis respectively was arrived at. Serum lactate and procalcitonin levels were normal. An urgent coronary angiography was performed after sedating and intubating her. Angiography revealed completely normal left and right coronary arteries [Figure 3]a and b. Arterial blood gases revealed; pH = 7.42, PaCO 2 = 38 mm Hg, PaO 2 = 60 mm Hg, HCO 3 = 24 mm, SpO 2 = 85%. She was extubated after a successful T-tube trial after 12 h. WBC count increased to 23,760/ul. She was started on intravenous meropenam 8 hourly. 2D echocardiography showed a further fall in EF to 25%. LV diastolic dysfunction persisted (DT = 108 ms). Chest X-ray revealed soft parenchymal opacities (She was now in a negative balance by 800 ml). In view of the ECG findings indicating myocardial ischemia, negative coronary angiography and deteriorating LV function by 2D echocardiography, she was diagnosed as a case of Takotsubo cardiomyopathy. Over the next 2-3 days, she remained stable, inotropes and vasopressors were tapered and discontinued on the fourth post-operative day. WBC count gradually decreased to 9890/ul. Repeat 2D echocardiography on 4 th day remained the same. Her total fluid intake was restricted and furosemide was ordered if urine output decreased to <0.5 ml/kg/h. She remained hemodynamically stable, was mobilized on the fifth post-operative day and discharged on the 8 th day. She was asked to follow-up at 4 weeks.
Figure 1: Pre-operative electrocardiography (ECG) (a). Post-operative ECG (b)

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Figure 2: Opacities in the chest X-ray

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Figure 3 a-b: (a) Left coronary angiogram, (b) Right coronary angiogram

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   Discussion Top


Takotsubo cardiomyopathy was first described in Japan in 1990. The hallmark of the syndrome is a transient contractile abnormality of the LV causing apical ballooning, with compensatory hyperkinesia of the basal walls. This unusual shape of the left ventricle resembles that of a Japanese pot used to trap an octopus, (tako in Japanese means octopus, tsubo means pot) hence the name Takotsubo cardiomyopathy. This can be well demonstrated by contrast echocardiography or LV angiography [Figure 4]. Onset of Takotsubo is frequently triggered by an acute medical illness or by emotional (fear, grief, anger) or physical (surgery, asthma, chemotherapy, stroke) stressors. Initial signs and symptoms resemble those of acute coronary syndrome; chest pain, dyspnea, ST segment changes on ECG and mildly elevated levels of cardiac biomarkers. [3] The most common ECG finding in Takotsubo cardiomyopathy is ST segment elevation typically in the precordial leads, [10] but the ECG can be normal or show T or Q wave abnormalities. [10] Diffuse and often deep T wave inversion involving most leads can also occur. Akashi et al. [10] reported that Takotsubo cardiomyopathy may account for 1% of all acute myocardial infarction (MI). In classic MI, size of infarct corresponds to the amount of myocardium supplied by the obstructed artery. In Takotsubo, area of affected myocardium is much larger than the normal distribution of a single coronary artery. [11] Although the exact pathogenesis of Takotsubo cardiomyopathy remains unclear, various mechanisms proposed are coronary vasospasm, microvascular dysfunction and neurogenic stunned myocardium due to increased plasma catecholamine levels. In Takotsubo cardiomyopathy catecholamine levels reaching 7-34 times as high as published normal values and 2-3 times as high as levels in patients with MI have been reported. [12] Possibility of a genetic predisposition may also exist. [13] There is emerging evidence of right ventricular affection in some cases. [14] Despite the severity of acute illness, stress induced cardiomyopathy is a transient disorder managed with supportive therapy. There are no controlled data to define the optimal medical regimen, but it is reasonable to treat these patients with standard medications for LV systolic dysfunction. These include angiotensin converting enzyme inhibitors, aspirin, clopidogrel, nitrates, glycoprotein IIb/IIIa inhibitors, beta blockers and diuretics as necessary for volume overload. [3] Patients who are hypotensive due to pump dysfunction can be treated cautiously with inotropes. Since the condition is caused by catecholamine excess, the role of sympathomimetic drugs remains to be established. Intra-aortic balloon counter pulsation is the preferred therapy when there is marked LV dysfunction associated with severe hypotension or shock. A study by Akashi et al. noted complete reversal of contractile abnormalities and recovery without any treatment. β blockers may be continued long-term to protect against catecholamine sensitivity. Warfarin may be used prophylactically to prevent LV apical thrombus, which may form due to stasis of blood in the akinetic segments.
Figure 4: Left ventricular angiogram showing apical ballooning and basal hyperkinesia

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Most complications occur during the acute phase of illness. Heart failure and pulmonary edema occur in 3-46% of patients. LV outflow tract obstruction can occur due to basal hyperkinesia. Mortality rates of 1-3% have been reported. In approximately 5% of patients, a second or third stress induced event may occur. However, since the syndrome has been documented for a relatively short time, its natural history remains largely unknown. The syndrome must be differentiated from myocarditis and pheochromocytoma. The cardiac biomarkers levels are very high in myocarditis. Pheochromocytoma present with pre-operative hypertension. Complications such as cardiogenic shock, acute renal failure, arrhythmias are higher in none of the patients presenting with Takotsubo due to pheochromocytoma. [15] Our patient exhibited most of the characteristics of Takotsubo cardiomyopathy that have been described in literature.

We continued inotropes and vasopressors in our case to maintain hemodynamic stability. Fluids were restricted in view of the pulmonary edema. She maintained a good diuresis without the need for systemic diuretics. Since she went into pulmonary edema we did not start her on β blockers. Antiplatelet agents were withheld in view of her post-surgical status. Recovery of the patient was uneventful and she was discharged without any cardiac medications. Upon follow-up at 6 weeks, her LV systolic function had normalized, left ventricular ejection fraction (LVEF) was 60%, with no evidence of diastolic dysfunction or pulmonary hypertension.

To summarize, the clinical presentation of Takotsubo cardiomyopathy mimics that of acute coronary syndrome and has important implications. Demonstration of normal coronary arteries clinches the diagnosis in favor of Takotsubo cardiomyopathy.

 
   References Top

1.Eshtehardi P, Koestner SC, Adorjan P, Windecker S, Meier B, Hess OM, et al. Transient apical ballooning syndrome - Clinical characteristics, ballooning pattern, and long-term follow-up in a Swiss population. Int J Cardiol 2009;135:370-5.  Back to cited text no. 1
    
2.Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008;118:397-409.  Back to cited text no. 2
    
3.Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review: Transient left ventricular apical ballooning: A syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858-65.  Back to cited text no. 3
    
4.Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: A novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11-8.  Back to cited text no. 4
    
5.Sharkey SW, Lesser JR, Maron MS, Maron BJ. Why not just call it tako-tsubo cardiomyopathy: A discussion of nomenclature. J Am Coll Cardiol 2011;57:1496-7.  Back to cited text no. 5
    
6.Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472-9.  Back to cited text no. 6
    
7.Tiwari AK, D'Attellis N. Intraoperative left ventricular apical ballooning: Transient Takotsubo cardiomyopathy during orthotopic liver transplantation. J Cardiothorac Vasc Anesth 2008;22:442-5.  Back to cited text no. 7
    
8.Gavish D, Rozenman Y, Hafner R, Bartov E, Ezri T. Takotsubo cardiomyopathy after general anesthesia for eye surgery. Anesthesiology 2006;105:621-3.  Back to cited text no. 8
    
9.Crimi E, Baggish A, Leffert L, Pian-Smith MC, Januzzi JL, Jiang Y. Images in cardiovascular medicine. Acute reversible stress-induced cardiomyopathy associated with cesarean delivery under spinal anesthesia. Circulation 2008;117:3052-3.  Back to cited text no. 9
    
10.Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Koike H, Sasaka K. The clinical features of takotsubo cardiomyopathy. QJM 2003;96:563-73.  Back to cited text no. 10
    
11.Ito K, Sugihara H, Katoh S, Azuma A, Nakagawa M. Assessment of Takotsubo (ampulla) cardiomyopathy using 99mTc-tetrofosmin myocardial SPECT - Comparison with acute coronary syndrome. Ann Nucl Med 2003;17:115-22.  Back to cited text no. 11
    
12.Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539-48.  Back to cited text no. 12
    
13.Kumar G, Holmes DR Jr, Prasad A. "Familial" apical ballooning syndrome (Takotsubo cardiomyopathy). Int J Cardiol 2010;144:444-5.  Back to cited text no. 13
    
14.Elesber AA, Prasad A, Bybee KA, Valeti U, Motiei A, Lerman A, et al. Transient cardiac apical ballooning syndrome: Prevalence and clinical implications of right ventricular involvement. J Am Coll Cardiol 2006;47:1082-3.  Back to cited text no. 14
    
15.Agarwal V, Kant G, Hans N, Messerli FH. Takotsubo-like cardiomyopathy in pheochromocytoma. Int J Cardiol 2011;153:241-8.  Back to cited text no. 15
    

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Correspondence Address:
Shilpa Bhojraj
Department of Anaesthesiology, Breach Candy Hospital, Bhullabhai Desai Road, Mumbai - 400 026, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.129875

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