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 ::  Abstract
  ::  Introduction
  ::  Case Report
  ::  Discussion
  ::  Conclusion
 ::  References
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  Table of Contents     
Year : 2019  |  Volume : 65  |  Issue : 2  |  Page : 112-115

Recurrent Takotsubo cardiomyopathy in a postmenopausal Indian lady: Is there a pattern?

1 Department of Cardiology, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of Radiology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Submission11-Jul-2017
Date of Decision24-Dec-2017
Date of Acceptance21-Feb-2018
Date of Web Publication26-Apr-2019

Correspondence Address:
S T Chacko
Department of Cardiology, Christian Medical College, Vellore, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpgm.JPGM_383_17

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 :: Abstract 

Takotsubo cardiomyopathy (TTC) is a syndrome of acute left ventricular dysfunction with a clinical presentation often mimicking acute coronary syndrome. Without a high index of suspicion, this clinical entity often goes unrecognized. Although initially categorized as a benign completely reversible condition, it is no longer considered to be so. Recurrence of this condition, though rare, has been reported in a non-Indian population. We present a case of recurrent TTC in a postmenopausal Indian lady who had a similar clinical presentation both at the index event and at recurrence.

Keywords: Recurrent, Takotsubo cardiomyopathy, wall motion abnormality

How to cite this article:
Sharath Babu N M, Chacko S T, Chacko B R, Irodi A. Recurrent Takotsubo cardiomyopathy in a postmenopausal Indian lady: Is there a pattern?. J Postgrad Med 2019;65:112-5

How to cite this URL:
Sharath Babu N M, Chacko S T, Chacko B R, Irodi A. Recurrent Takotsubo cardiomyopathy in a postmenopausal Indian lady: Is there a pattern?. J Postgrad Med [serial online] 2019 [cited 2023 May 29];65:112-5. Available from:

 :: Introduction Top

Takotsubo cardiomyopathy (TTC) is an increasingly recognized entity of acute clinical heart failure, with significant morbidity and an in-hospital mortality of 2–5%.[1] Although described more commonly in postmenopausal women of Caucasian and Asian ethnicity, no race may be exempt. Recurrence, although rare, often adds to the morbidity of the disease. However, a second episode has been reported occurring from 3 months to even 10 years after the index event. Here, we describe Takotsubo syndrome in a postmenopausal Indian lady, who 8 months after the index event, presented with a similar clinical presentation as at the first episode, despite being on optimal medical therapy.

 :: Case Report Top

A 59-year-old postmenopausal Indian lady with no diabetes, hypertension, and prior cardiac or renal disease presented to the emergency room with episodes of giddiness and dyspnea of 4 hours duration. She reported no other symptoms. Couple of days prior to the presentation, she acknowledged a definite stressful event at home while preparing for her youngest daughter's marriage which was to be held in a few days. Clinical examination showed mild tachycardia and no features of overt heart failure.

Electrocardiogram at admission showed sinus tachycardia, J-point elevation and concave upward ST elevation in V2-V6, T wave inversion in aVL, and a QTc of 402 ms [Figure 1]a. Troponin T was elevated at 493 pg/mL (normal up to 14 pg/ml), and subsequent values showed a downward trend. NT Pro-BNP was 1348 pg/ml (normal up to 125 pg/ml). Screening for pheochromocytoma was negative (urinary metanephrines of 60 μg/24 h and normetanephrines of 311 μg/24 h). Chest radiography was noncontributory.
Figure 1: (a) Electrocardiogram on day 1. (b) Electrocardiogram on day 3

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Echocardiography performed at admission showed moderate LV systolic dysfunction, regional wall motion abnormality involving the distal LV segments in a circumferential pattern-LV segments 13–17 (hypokinesia in apical inferior, apical lateral, apical anterior, apical septal areas and apex), but not corresponding to a single coronary arterial distribution [Figure 2], and preserved contractility of basal and mid LV segments. LV ejection fraction (EF) was measured as 37%, and there were no valvular abnormalities.
Figure 2: (a) Echocardiographic image in A4C view on day 1 showing wall motion abnormality. (b) Echocardiographic image in A4C view on day 4 showing complete recovery of wall motion abnormality

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Her coronary angiography done 8 months ago was normal and hence not repeated. Considering a working diagnosis of TTC or myocarditis causing acute LV dysfunction, she was treated conservatively with beta-blockers, angiotensin converting enzyme inhibitors (ACEIs), and heparin.

Cardiac magnetic resonance imaging (CMRI) performed on day 2 showed preserved contractility of basal and mid LV segments, a kinetic apical segments, and apex of left ventricle with patchy edema and no myocardial late gadolinium enhancement. LV EF was 35% on CMRI. Classical MRI findings seen in myocarditis of mid myocardial late gadolinium enhancement was evidently absent. The absence of myocardial scar also ruled out myocardial infarction. Cardiac MRI favored a diagnosis of TTC [Figure 3].[2]
Figure 3: Two chamber end-diastolic (a), two chamber end-systolic (b) and four chamber end-systolic (c) steady state free precession images show apical ballooning with akinesis of the apical segments and apex of left ventricle (short arrows). (d) No enhancement (long arrows) seen on late gadolinium imaging

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Electrocardiograms done on subsequent days showed deepening T wave inversions and prolonging QTc which peaked at a QTc of 642.25 ms by day 3 [Figure 1]b. On day 4, repeat echocardiography showed normal biventricular function with no wall motion abnormalities [Figure 2], further reiterating the diagnosis. By day 6, QTc interval normalized and T inversions decreased in amplitude, nevertheless, persisted. However, her in-hospital stay was free of significant arrhythmias. She was then discharged on ACEI and beta-blockers.

Eight months before, she was admitted with similar complaints of dyspnea and giddiness. Prior to that episode, she had to go through the tragic death of a close family member. On evaluation for the same, she was noted to have dynamic ECG changes similar to the present one and mild LV dysfunction with wall motion abnormalities involving the LV apical segments. She then underwent a coronary angiogram, which showed normal epicardial coronaries. She was initiated on regular medications and advised follow-up. Echocardiogram repeated 1 month later showed normal LV function with no wall motion abnormalities.

 :: Discussion Top

Takotsubo is seen more commonly in postmenopausal women and is often precipitated by emotional or physical stress. However, a triggering event may not be identified in all. The incidence of this apical ballooning syndrome is 1.5–2.2%.[3],[4]

Diagnosis is traditionally made using the modified Mayo Clinic criteria,[5] which require all the following criteria to be met: (a) transient wall motion abnormalities of LV which extend beyond a single epicardial vascular distribution; a stressful trigger is often seen but not always present; (b) absence of obstructive coronary disease or angiographic evidence of acute plaque rupture; (c) new electrocardiographic abnormalities (either ST-segment elevation and/or T wave inversion) or modest elevation in cardiac troponin; and (d) absence of pheochromocytoma or myocarditis. Our patient satisfied these criteria and also the European Heart Failure Association diagnostic criteria for TTC.[1]

Although prognosis is often considered good, especially if they survive the initial 48 h, it is no longer considered to be benign. In the initial 24–48 h of presentation, patients have a higher incidence of cardiogenic shock and cardiac arrhythmias, especially TdP (torsades de pointes) with grossly prolonged QTc, thus contributing to the mortality. The high catecholamine levels in TTC and the myocardial dysfunction mediated by it precludes the safe use of inotropes when they develop cardiogenic shock.

ECGs in TTC, although mimics acute coronary syndrome (ACS), demonstrate two distinct patterns – patients presenting with ST elevation ECG and those presenting with just T wave inversions. These ST elevations are often diffuse and concave upwards with no reciprocal changes. In this group of patients, T inversions appear when ST elevation subsides. In the second more common form, T inversions occurr from the beginning and persist without ST elevations.[6] Our patient had the former variety. The T inversion also has a specific pattern of evolution. Deepening T waves and progressively prolonged QTc intervals are often characteristic. Gradually, the QTc begins to normalize in 48–96 h.

Going by biomarkers, there often is a disproportionate rise in BNP/NT-proBNP compared to cardiac troponins. Contrary to ACS, the coronary arteries are typically open and the wall motion abnormality does not match that of any epicardial coronary artery territory.

Complete normalization of LV function and wall motion abnormalities generally takes approximately 4–8 weeks.[7] Sharkey et al. have demonstrated that in 5% of the cases normalization of LV EF can take 2.5–12 months.[8] However, in our case the ventricular function recovered by day 4.

Recurrence of TTC has been reported in literature at varying frequency, ranging from 2.7% to 11% over a 4-year period.[3],[9] Singh et al.[10] reported a recurrence rate of 5% at 6 years (cumulative). Patients with severe TTC at index admission were noted to have higher recurrences. However, Parodi et al.[11] inferred that the severity of initial LV dysfunction does not impact long-term event rates. A retrospective analysis of 114 patients with recurrent TTC demonstrated that the pattern of clinical presentation is often similar to the index event,[12] but the pattern of LV involvement often may not be so. Brunetti et al.[13] and Singh et al.[10] documented that ACEI may be more effective than beta-blockers in preventing a recurrence of TTC. However, randomized controlled trials are lacking.

Our patient, even while on ACEIs since the first episode, had a recurrence of TTC with identical clinical pattern and similar echocardiographic form as at the first presentation. Although this may raise the possibility of genetic predisposition in developing a recurrence, there has been no conclusive evidence for the same.[14]

 :: Conclusion Top

Recurrence of TTC, although rare, often follows similar clinical pattern of presentation as at the index event. Hence, with a high degree of suspicion and a careful history and clinical evaluation, the diagnosis can be established early. The predisposing factors and strategies to prevent a recurrence, however, need to be carefully studied.

Declaration of patient consent

The authors certify that appropriate patient consent was obtained.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

 :: References Top

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. 1
Kohan AA, Levy Yeyati E, De Stefano L, Dragonetti L, Pietrani M, Perez de Arenaza D, et al. Usefulness of MRI in Takotsubo cardiomyopathy: A review of the literature. Cardiovasc Diagn Ther 2014;4:138-46.  Back to cited text no. 2
Elian D, Osherov A, Matetzky S, Hod H, Guetta V, Feinberg MS, et al. Left ventricular apical ballooning: Not an uncommon variant of acute myocardial infarction in women. Clin Cardiol 2006;29:9-12.  Back to cited text no. 3
Parodi G, Del Pace S, Carrabba N, Salvadori C, Memisha G, Simonetti I, et al. Incidence, clinical findings, and outcome of women with left ventricular apical ballooning syndrome. Am J Cardiol 2007;99:182-5.  Back to cited text no. 4
Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): A mimic of acute myocardial infarction. Am Heart J 2008;155:408-17.  Back to cited text no. 5
Namgung J. Electrocardiographic findings in Takotsubo cardiomyopathy: ECG evolution and its difference from the ECG of acute coronary syndrome. Clin Med Insights Cardiol 2014;8:29-34.  Back to cited text no. 6
Ghadri JR, Ruschitzka F, Lüscher TF, Templin C. Takotsubo cardiomyopathy: Still much more to learn. Heart Br Card Soc 2014;100:1804-12.  Back to cited text no. 7
Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG, Lesser JN, et al. Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol 2010;55:333-41.  Back to cited text no. 8
Elesber AA, Prasad A, Lennon RJ, Wright RS, Lerman A, Rihal CS. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol 2007;50:448-52.  Back to cited text no. 9
Singh K, Carson K, Usmani Z, Sawhney G, Shah R, Horowitz J. Systematic review and meta-analysis of incidence and correlates of recurrence of Takotsubo cardiomyopathy. Int J Cardiol 2014;174:696-701.  Back to cited text no. 10
Parodi G, Bellandi B, Del Pace S, Barchielli A, Zampini L, Velluzzi S, et al. Natural history of Takotsubo cardiomyopathy. Chest 2011;139:887-92.  Back to cited text no. 11
El-Battrawy I, Ansari U, Behnes M, Hillenbrand D, Schramm K, Haghi D, et al. Clinical and echocardiographic analysis of patients suffering from recurrent Takotsubo cardiomyopathy. J Geriatr Cardiol 2016;13:888-93.  Back to cited text no. 12
Brunetti ND, Santoro F, De Gennaro L, Correale M, Gaglione A, Di Biase M. Drug treatment rates with beta-blockers and ACE-inhibitors/angiotensin receptor blockers and recurrences in takotsubo cardiomyopathy: A meta-regression analysis. Int J Cardiol 2016;214(Supplement C):340-2.  Back to cited text no. 13
Limongelli G, Masarone D, Maddaloni V, Rubino M, Fratta F, Cirillo A, et al. Genetics of Takotsubo Syndrome. Heart Fail Clin 2016;12:499-506.  Back to cited text no. 14


  [Figure 1], [Figure 2], [Figure 3]


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