Journal of Arrhythmia 33 (2017) 79

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Letter to the Editor

Reply: Takotsubo syndrome and polymorphic ventricular tachycardia: The chicken or the egg Rintaro Hojo, MDa,n, Seiji Fukamizu, MDa, Masayasu Hiraoka, MD, PhD FHRSb a b

Department of Cardiology, Tokyo Metropolitan Hiroo Hospital, 2-34-10, Ebisu, Shibuya-ku, Tokyo 150-0013, Japan Toride Kitasohma Medical Center Hospital, Ibaraki, Japan

art ic l e i nf o Article history: Received 19 April 2016 Accepted 26 April 2016 Available online 24 June 2016

Reply to Dr. Medias We appreciate your interest and insightful comments regarding our published paper [1] in the Journal of Arrhythmia. Please find below, the response to your comments. 1) It is possible that in this case, TC had developed before QTc prolongation and attack of PVT because (i) QTc gradually shortened and attacks of PVT disappeared regardless of serum potassium level after admission, and (ii) the patient had gastrointestinal symptoms and was diagnosed with dehydration in a previous hospital 5 days before admission to our hospital, which was the most probable physical stress for her. 2) The attending doctor checked her potassium level every 3–6 h and adjusted the potassium infusion dose accordingly. She was underweight (45 kg) and had renal dysfunction (34 ml/min/ 1.73 m2); therefore, we cautiously started with relatively smaller potassium supplementation doses and administered 145 mEq/day of potassium and oral spironolactone. As you mentioned, the poor control of the potassium level could be due to diuretic drugs usage, co-existing comorbid conditions, and circulating epinephrine [2,3]. 3) The genesis of TC may be associated with catecholamines [4]. We hypothesize that calcium flux across the cardiac cell membrane and/or calcium release from the sarcoplasmic reticulum may be related to J-ST-T wave alternans and mechanical alternans. Electrical and mechanical alternans are frequently seen in decreased myocardial contractility, but the association of J wave alternans has not been described. Regarding the

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genesis of the J wave, Antzelevitch's group proposed Ito plays a pivotal role in its formation [5]. Regarding the nature of Ito, slow recovery from inactivation makes J wave amplitude smaller with shorter preceding diastolic intervals and larger with longer diastolic intervals. Interestingly, the J waves in this patient totally contrasted with the above notion. The main purpose of this case report was to draw attention to this aberration.

Conflict of interest All authors declare no conflict of interest related to this study.

References [1] Hojo R, Fukamizu S, Kitamura T, et al. Prominent J-wave and T-wave alternans associated with mechanical alternans in a patient with takotsubo cardiomyopathy. J Arrhythm 2015;31:43–6. [2] Brown MJ, Brown DC, Murphy MB. Hypokalemia from beta2-receptor stimulation by circulating epinephrine. N Engl J Med 1983;309:1414–9. [3] Brown MJ. Hypokalemia from beta 2-receptor stimulation by circulating epinephrine. Am J Cardiol 1985;56:3D–9D. [4] Lyon AR, Rees PS, Prasad S, et al. Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med 2008;5:22–9. [5] Antzelevitch C, Yan GX. J wave syndromes. Heart Rhythm 2010;7:549–58.

Corresponding author. Tel.: þ 81 33 444 1181; fax: þ81 33 444 3196. E-mail address: [email protected] (R. Hojo).

http://dx.doi.org/10.1016/j.joa.2016.04.006 1880-4276/& 2016 Japanese Heart Rhythm Society. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Reply: Takotsubo syndrome and polymorphic ventricular tachycardia: The chicken or the egg.

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