International Journal of Cardiology 177 (2014) 211–212

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Letter to the Editor

Marked attenuation of the electrocardiogram QRS complexes in a patient with pheochromocytoma and Takotsubo syndrome John E. Madias ⁎ Icahn School of Medicine at Mount Sinai, New York, NY, United States Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, United States

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Article history: Received 27 August 2014 Accepted 17 September 2014 Available online 28 September 2014 Keywords: Takotsubo syndrome Electrocardiogram Attenuation of the QRS complexes in Takotsubo syndrome Myocardial edema in Takotsubo syndrome Pheochromocytoma Electrocardiogram and Takotsubo syndrome

To the Editor The article by Zhu et al. [1], published ahead of print in the August 5, 2014 issue of the Journal, about a 67-year old woman who suffered Takotsubo syndrome (TTS) in the setting of a giant pheochromocytoma, which was eventually surgically excised uneventfully, is notable for the marked attenuation of the electrocardiogram (ECG) QRS complexes (ATTQRS) early in the clinical course. The relationship between ATTQRS and TTS has been recently reported [2], and has been attributed to slowly resolving myocardial edema (ME), as detected by T2weighted cardiac magnetic resonance imaging (cMRI) [2–4]. ME is more pronounced in the apical “ballooned” region, and is progressively less intense in the midventricular myocardial territory, and at the cardiac base [3,4]. An apicobasal gradient of the left ventricular ME has been noted in the classic form of TTS [3], and its distribution, resolution, and correlates have been recently reported, based on an acute cMRI, at a median of 2 days after presentation, and a repeat cMRI after 3 months, in 32 patients with TTC [4]. ME resolves slowly, its acute extent correlates with regional contractile dysfunction, and is associated with the acute release of catecholamines and NT-prohormone brain natriuretic peptide [4]. Fig. 1 of the article [1] includes 10 ECGs, spanning “Hour 0” (admission), and “Week 3” (follow-up) time points, with the first 9 ⁎ Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, United States. Tel.: +1 718 334 5005; fax: +1 718 334 5990. E-mail address: [email protected].

http://dx.doi.org/10.1016/j.ijcard.2014.09.053 0167-5273/© 2014 Published by Elsevier Ireland Ltd.

ECGs recorded between “Hour 0” and “Hour 72” time points. There is marked ATTQRS between “Hour 0” and “Hour 2” and “Hour 3”, involving all limb and precordial ECG leads, with some recovery centered around “Hour 48”, although there is ATTQRS even in the ECG of “Week 3” in comparison with the ECG of “Hour 0”. ECG lead aVR has been used solely to follow the ATTQRS [2], and in Fig. 1 [1], if one scans the amplitude of the QRS complex in this lead in the 10 ECGs one could get the sense of the dynamic nature of this phenomenon. Some variation as to the maximal ATTQRS, occurring in different ECG leads at various time points of the clinical course, this author has attributed to a shifting of the intensity of the ME as the TTS evolves [5]. More insights could be forthcoming by employing serial ECGs, when reporting patients with TTS, and using the proposed comparative and quantitative analysis of the tracings [5]. The ECG of “Week 3” still reveals ATTQRS, in comparison with the ECG of “Hour 0”, and it would be of interest to know whether a possible ECG recorded at the one year follow-up, showed restoration of the amplitude of the QRS complexes to the magnitude of the ECG of “Hour 0”. Additionally, if such a hypothetical ECG at the one year follow-up, revealed larger QRS complexes than the ones of the ECG of “Hour 0”, one could surmise that even the first ECG recorded upon admission had been already influenced by the disease process, and had shown ATTQRS. This could be resolved in the authors' case [1], by comparison of the ECG of “Hour 0” with possible ECGs of their patient, recorded prior to the inception of TTS. Unfortunately cMRI during the acute phase of the illness or at follow-up was not obtained in this patient [1], which would have provided information about the association of the ECG ATTQRS and ME. All the above may prove of value in the diagnosis of TTS, its follow-up, and its differentiation from cases of acute coronary syndromes. Cloud computing, smart phones, and smart personal health data cards, providing ECGs recorded at any time point and in any geographical location, will provide the platform for the realization of a meaningful contribution of the ECG in TTS [2]. Conflicts of interest None. References [1] Zhu D, Yu J, Li X, Jiang X, Zhuang C. Takotsubo-like cardiomyopathy in a giant pheochromocytoma. Int J Cardiol Aug 5 2014. http://dx.doi.org/10.1016/j.ijcard. 2014.07.240 [pii: S0167-5273(14)01450-8, Epub ahead of print]. [2] 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.

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J.E. Madias / International Journal of Cardiology 177 (2014) 211–212

[3] Perazzolo Marra M, Zorzi A, Corbetti F, et al. Apicobasal gradient of left ventricular myocardial edema underlies transient T-wave inversion and QT interval prolongation (Wellens' ECG pattern) in Tako-Tsubo cardiomyopathy. Heart Rhythm 2013;10:70–7. [4] Neil C, Nguyen TH, Kucia A, et al. Slowly resolving global myocardial inflammation/ oedema in Tako-Tsubo cardiomyopathy: evidence from T2-weighted cardiac MRI. Heart 2012;98:1278–84.

[5] Madias JE. Reversible attenuation of the amplitude of the electrocardiogram QRS complexes in a patient with Takotsubo syndrome: a quantitative analysis. Int J Cardiol Aug 2 2014. http://dx.doi.org/10.1016/j.ijcard.2014.07.116 [pii: S0167-5273(14) 01326-6, Epub ahead of print].

Marked attenuation of the electrocardiogram QRS complexes in a patient with pheochromocytoma and Takotsubo syndrome.

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