CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 278 AFRICA of Sheehan’s syndrome. Coronary angiography was performed and showed no significant stenosis. Torsade de pointes (TdP) and Sheehan’s syndrome were diagnosed according to the patient’s medical history and symptoms, experimental evidence, ECG findings and the entire disease course. After giving intravenous potassium and magnesium supplementation, the patient’s potassium level improved to 4.0 mmol/l. Meanwhile, she was treated with intravenous lidocaine and esmolol for anti-arrhythmia. For hypopituitarism, thyroid hormone (levothyroxine 50 ug qd) and steroids (hydrocortisone 20 mg bid) were administered. With the normalisation of the QT interval on ECG (Fig. 2B), no additional ventricular tachycardia was observed and the further ward process was stable. Hypokalaemia was not demonstrated after hormone replacement therapy. Considering that the patient’s TdP was caused by prolonged QT interval secondary to Sheehan’s syndrome, it was reversible. Therefore, electrophysiological examination was not performed and implantable cardioverter defibrillator implantation was avoided. The patient was discharged from our hospital after 14 days. During the one-year follow up, the patient was given steroids and thyroxine replacement therapy continually, and her pituitary hormone levels were monitored regularly. Furthermore, no additional ventricular arrhythmia occurred. The ECG showed a normal QT interval and echocardiography showed normal cardiac function. Fig. 1. ECG monitoring at admission of case 1, showing a section of polymorphic ventricular tachycardia. Fig. 2. ECG examination of case 1. A. Baseline ECG revealed frequent premature polymorphic ventricular contractions and a prolonged QT interval of 600 ms with T-wave inversion in II, III, avF and V1–V6 leads. B. The ECG before discharge demonstrated a normal corrected QTc interval of 407 ms. A B
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