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EDITORIAL
Year : 2016  |  Volume : 60  |  Issue : 3  |  Page : 155-156  

'Broken-heart syndrome'… Be aware..


Department of Anaesthesiology, SRMC, Porur, Chennai, Tamil Nadu, India

Date of Web Publication2-Mar-2016

Correspondence Address:
Mahesh Vakamudi
Department of Anaesthesiology, SRMC, Porur, Chennai, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5049.177863

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How to cite this article:
Vakamudi M. 'Broken-heart syndrome'… Be aware.. Indian J Anaesth 2016;60:155-6

How to cite this URL:
Vakamudi M. 'Broken-heart syndrome'… Be aware.. Indian J Anaesth [serial online] 2016 [cited 2020 Sep 26];60:155-6. Available from: http://www.ijaweb.org/text.asp?2016/60/3/155/177863

Takotsubo cardiomyopathy (TCM), also known by various other names such as broken-heart syndrome, stress-induced cardiomyopathy and apical ballooning syndrome, is an acute, reversible, transient left ventricular dysfunction that was first described by a Japanese cardiologist in 22 patients in the year 1990. The Japanese word 'takotsubo' means an octopus trap, used to describe the shape of the left ventricle in this condition during systole. Since its original publication, there have been several case reports describing its occurrence in patients in the periprocedural and perioperative periods, underscoring the importance of the need for awareness about this rare syndrome among anaesthesiologists. There are several case reports published from India too. In this issue of the Indian Journal of Anaesthesia, a case of this entity is reported after thyroidectomy and also one describing its occurrence in a young patient who developed anaphylaxis to cephalosporin intraoperatively during limb salvage surgery for osteosarcoma of the tibia.[1],[2]

TCM is more common in elderly postmenopausal women, although presentations have been reported in young men and women also. A systematic review of this syndrome has recently been published by Ono and Falcão.[3] The triggering factor for this cardiomyopathy seems to be the elevated levels of plasma catecholamines due to physical or emotional stress, which leads to coronary spasm, direct myocardial toxicity or microvascular impairment. Iatrogenic administration of catecholamines can also be a trigger of this syndrome.[4] Lyon et al. have described a novel pathophysiological hypothesis to explain the myocardial stunning due to catecholamine excess.[5] It has been proposed that apical ballooning could be due to the abundance of beta receptors in this region that can lead to negative inotropy due to change in the intracellular signal trafficking. The Heart Failure Association of the European Society of Cardiology has recently published a position statement on takotsubo syndrome that includes a diagnostic algorithm comprising seven criteria including anatomic features, electrocardiogram (ECG) changes, cardiac biomarkers and reversibility of the ventricular dysfunction.[6]


   What Is the Dilemma: Steps in Diagnosis Top


The dilemma posed to an anaesthesiologist with the presentation of this syndrome is that it closely resembles acute coronary syndrome (ACS). Patients may present with symptoms of chest pain, breathlessness, syncope or with complications such as cardiogenic shock, ventricular arrhythmias, pulmonary oedema, left ventricular outflow tract obstruction and cardiac arrest. The similarities of this syndrome with ACS are marked in terms of the clinical presentation, ECG changes and elevation in biomarker profiles. However, the crucial difference is that the epicardial coronaries are normal and the wall motion abnormalities are not restricted to a single coronary vascular bed.

Looi et al.[7] in a recent study from Australia observed the evolution of ECG changes in TCM compared to myocardial infarction (MI). They found that though ST elevation occurs in TCM, it is less prominent and is not accompanied by reciprocal ST depression or pathological Q waves. Deep T-wave inversion and significant QT prolongation are seen after 24–48 h that can lead to torsades de pointes. The biomarker elevation is also only moderate in TCM, as compared to ACS. B-type natriuretic peptide (BNP) levels are much more elevated in TCM, compared to acute MI (AMI), and Scantlebury and Prasad[8] have showed that the ratio of BNP to Trop T could help in distinguishing between the two conditions. Wittstein et al.[9] have shown that serum catecholamine levels are much more exaggerated in TCM, compared with MI. It may not be possible to differentiate TCM from AMI based on systolic and diastolic function of the heart, although on echocardiography (ECHO), basal segments are usually spared in TCM. Coronary angiography is essential to distinguish the two. Pathak et al. have also reported only a mild elevation in biomarkers, CP-MBand Trop T, although there is no mention of BNP levels. Demonstration of elevated levels of BNP would have made their diagnosis of TCM more conclusive along with absent occlusive findings on a coronary angiogram. Their recommendation to use intraoperative transoesophageal ECHO for the diagnosis is a very useful suggestion.


   How Do We Manage? What Are the Controversies? Top


Prognosis in this syndrome is favourable, with the mortality ranging from 0 to 10%, which emphasises the importance of timely diagnosis and appropriate management. The Heart Failure Association of the European Society of Cardiology stratifies patients into high-risk and low-risk groups based on major and minor risk factors. The aim of treatment should be supportive to maintain cardiac function and prevent complications. Although in the case report by Pathak et al., ephedrine and adrenaline were used to manage hypotension, suggested acute therapy involves the management of myocardial ischaemia with oxygen, intravenous heparin, antiplatelet agents and β blockers along with cessation of any sympathomimetics. The role of β blockers has been a controversy with some concerns that their use can lead to cardiogenic shock. A recent retrospective cohort study in Japan by Isogai et al.[10] found no significant association between the use of β blockers early in the course of the syndrome and in-hospital mortality. Anticoagulants should be initiated early, provided there is no contraindication to reduce the risk of thromboembolism from the apical thrombosis. Cardiogenic shock should be managed with mechanical supports such as left ventricular assist devices or extracorporeal membrane oxygenation or with levosimendan, and the use of inotropes is regarded as a contraindication. Continuous monitoring of ECG, haemodynamics and regular ECHO is essential. A team approach is important with the involvement of the cardiologist, the anaesthesiologist and the primary physician when this condition presents perioperatively.

In summary, although many case reports have been published in the literature, several questions remain unanswered regarding the exact pathophysiology of the syndrome; it is much important for all the perioperative physicians to be aware of the existence of this rare syndrome and lay focus on its timely diagnosis and appropriate management to prevent mortality.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Bharathi KS, Kulkarni S, Sadananda KS, Gurudatt CL. Takotsubo cardiomyopathy precipitated by negative pressure pulmonary oedema following total thyroidectomy. Indian J Anaesth 2016;60:202-5.  Back to cited text no. 1
  Medknow Journal  
2.
Pathak S, Dubey M, Goel N. Takotsubo cardiomyopathy due to cephalosporin anaphylaxis under general anaesthesia. Indian J Anaesth 2016;60:215-6.  Back to cited text no. 2
  Medknow Journal  
3.
Ono R, Falcão LM. Takotsubo cardiomyopathy systematic review: Pathophysiologic process, clinical presentation and diagnostic approach to takotsubo cardiomyopathy. Int J Cardiol 2016;209:196-205.  Back to cited text no. 3
    
4.
Abraham J, Mudd JO, Kapur NK, Klein K, Champion HC, Wittstein IS. Stress cardiomyopathy after intravenous administration of catecholamines and beta-receptor agonists. J Am Coll Cardiol 2009;53:1320-5.  Back to cited text no. 4
    
5.
Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy – a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008;5:22-9.  Back to cited text no. 5
    
6.
Lyon AR, Bossone E, Schneider B, Sechtem U, Citro R, Underwood SR, et al. Current state of knowledge on takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail 2016;18:8-27.  Back to cited text no. 6
    
7.
Looi JL, Wong CW, Lee M, Khan A, Webster M, Kerr AJ. Usefulness of ECG to differentiate takotsubo cardiomyopathy from acute coronary syndrome. Int J Cardiol 2015;199:132-40.  Back to cited text no. 7
    
8.
Scantlebury DC, Prasad A. Diagnosis of takotsubo cardiomyopathy. Circ J 2014;78:2129-39.  Back to cited text no. 8
    
9.
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. 9
    
10.
Isogai T, Matsui H, Tanaka H, Fushimi K, Yasunaga H. Early ß-blocker use and in-hospital mortality in patients with takotsubo cardiomyopathy. Heart 2016. pii: heartjnl-2015-308712.  Back to cited text no. 10
    




 

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