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

) 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. ) 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 m); 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]. ) 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