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LETTER TO EDITOR
Year : 2022  |  Volume : 32  |  Issue : 3  |  Page : 185-186

Beware of making the diagnosis of hypertrophic cardiomyopathy in patients with takotsubo syndrome based on early imaging


Icahn School of Medicine at Mount Sinai, New York; Division of Cardiology, Elmhurst Hospital Center, Broadway, Elmhurst, NY, USA

Date of Submission17-Mar-2022
Date of Decision09-May-2022
Date of Acceptance12-Jul-2022
Date of Web Publication16-Nov-2022

Correspondence Address:
John E Madias
Division of Cardiology, Elmhurst Hospital Center, Broadway, Elmhurst, NY 11373
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcecho.jcecho_16_22

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How to cite this article:
Madias JE. Beware of making the diagnosis of hypertrophic cardiomyopathy in patients with takotsubo syndrome based on early imaging. J Cardiovasc Echography 2022;32:185-6

How to cite this URL:
Madias JE. Beware of making the diagnosis of hypertrophic cardiomyopathy in patients with takotsubo syndrome based on early imaging. J Cardiovasc Echography [serial online] 2022 [cited 2022 Dec 6];32:185-6. Available from: https://www.jcecho.org/text.asp?2022/32/3/185/361210



To the Editor,

I enjoyed reading the report by Schlossbauer et al.[1] about their interesting case of a 66-year-old woman who had suffered a typical apical ballooning variant of takotsubo syndrome (TTS), and who was initially thought of having a concomitant hypertrophic cardiomyopathy (HCM). The latter diagnosis was based on the persisting apical thickening detected at cardiac magnetic resonance imaging (CMR). This thickening was present in “the absence of significant elevated edema-sensitive T2 values at CMR,”[1] at 1 month after the illness onset, in spite of the normalization of left ventricular ejection fraction. This patient, at a follow-up transthoracic echocardiography and CMR, 6 months later, had complete resolution of apical wall thickening, resulting in the correct diagnosis of TTS-induced “pseudohypertrophy.”[1] Such “pseudohypertrophy,” indeed masquerading as apical (“Japanese” variety or “Yamaguchi”) HCM, has been repeatedly encountered and commented upon in the setting of TTS, and has been attributed by this author to underlying myocardial edema (ME).[2],[3],[4],[5] Moreover, this “pseudohypertrophy” has been erroneously attributed by others to myocarditis, HCM (both the apical variety and the midventricular obstructive variant, with left ventricular outflow tract obstruction), or transient catecholamine-induced left ventricular hypertrophy. What is new in this report is that the “pseudohypertrophy” encountered in the setting of TTS can be diagnosed by CMR in the absence of significant ME (elevated T2 values) or delayed gadolinium enhancement indicative of mild fibrosis (T1 values), or very mild such alterations. In other words, ME could still be present without significant CMR T2 values. This TTS/”pseudohypertrophy” phenotype may be much more frequent than is currently appreciated.[1],[5] Furthermore, ME has been linked to changes in the electrocardiogram (ECG), which reveals low QRS voltage, or transient attenuation of the QRS complexes, in the limb, precordial, or all 12 ECG leads. ECG lead aVR is particularly suited to represent ECG changes occurring in the left ventricular apex in TTS (Madias JE: Transient attenuation of the amplitude of the QRS complexes in the diagnosis of Takotsubo syndrome. Eur Heart J Acute Cardiovasc Care 2014; 3:28-36; Madias JE: Reversible attenuation of the amplitude of the electrocardiogram QRS complexes in a patient with Takotsubo syndrome: A quantitative analysis. Int J Cardiol. 2014;176:1107-9). Accordingly, I would appreciate the kind consideration of the authors in providing the readers with information about all the leads of the three ECGs (admission, 1 month, and 6 months) of their patients. Indeed, the two ECG leads at 1 month, from [Figure 1] of the authors' article,[1] appear to have attenuated QRS complexes, compared to the ECGs from admission and at 6 months. Such findings suggest ME, present at the 1-month CMR evaluation, as noted above.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Schlossbauer SA, Campanale D, Leo L, Paiocchi V, Faletra FF. Better take a second look: The fameless face of Subacute Takotsubo syndrome. J Cardiovasc Echogr 2021;31:248-50.  Back to cited text no. 1
    
2.
Madias JE. Two cases of reversible left ventricular hypertrophy during recovery from takotsubo cardiomyopathy: Hypertrophy or myocardial edema after an attack of Takotsubo syndrome? Echocardiography 2013;30:989.  Back to cited text no. 2
    
3.
Madias JE. Myocardial apical hypertrophy and Takotsubo cardiomyopathy. Tex Heart Inst J 2014;41:568.  Back to cited text no. 3
    
4.
Madias JE. Apparent myocardial hypertrophy due to reversible regional myocardial edema in Takotsubo syndrome. Echocardiography 2015;32:403.  Back to cited text no. 4
    
5.
Madias JE. The fuzzy diagnostic boundaries among left ventricular outflow tract obstruction in hypertensive hypertrophy, hypertrophic cardiomyopathy, and Takotsubo syndrome. Int J Cardiol 2015;197:10.  Back to cited text no. 5
    




 

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