CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 AFRICA 277 A rare endocrine cause of ventricular tachycardia: a case series of two patients and a literature review Ming Yu, Lin Sun, Hong-liang Yang, Huan Sun, Chang Wang, Shuai Yao, Ping Yang Abstract Sheehan’s syndrome is a type of hypopituitarism caused by massive uterine bleeding and hypovolaemic shock after or during delivery. Heart involvement has been documented sporadically among the various clinical manifestations of Sheehan’s syndrome but life-threatening arrhythmias are infrequent. Here, we report on two rare cases of ventricular tachycardia caused by Sheehan’s syndrome. Both female patients were diagnosed with Sheehan’s syndrome 30 years previously, due to massive postpartum bleeding. Both of them terminated hormone replacement therapy recently. Both patients presented with torsade de pointes. The electrocardiogram showed prolonged QT interval. In addition to potassium supplementation and anti-arrhythmia therapy, steroids and thyroid hormone replacement therapy were employed, QT-interval prolongation and T-wave inversion were normalised, and implantable cardioverter defibrillator implantation was avoided. One of the patients was recovering well at the one-year follow up and the other patient was in a coma at the time of this report. We also review the literature for cases of Sheehan’s syndrome presenting with ventricular tachycardia. Keywords: Sheehan’s syndrome, torsade de pointes, polymorphic ventricular tachycardia, ventricular fibrillation, long QT interval, hypopituitarism Submitted 23/11/21, accepted 15/8/22 Published online 8/9/22 Cardiovasc J Afr 2022; 277–281 www.cvja.co.za DOI: 10.5830/CVJA-2022-043 Sheehan’s syndrome, presenting as ventricular tachycardia, is an extremely rare phenomenon and only a few cases have been reported in the literature. Torsade de pointes (TdP) refers to polymorphic ventricular tachycardia with prolonged QT interval, which can cause sudden cardiac death. It’s important to figure out the main cause of QT prolongation and the method to correct it. Generally, acquired long QT may result from the use of anti-arrhythmia drugs, electrolyte disturbances, antidepressants or antihistamines, bradycardia, cerebral events and hormonal disorders. At present, although the mechanism of acquired QT prolongation caused by Sheehan’s syndrome is not clear, hypokalaemia, hypothyroidism and adrenal insufficiency may be the possible reasons. We herein report on two cases of Sheehan’s syndrome presenting as ventricular tachycardia with prolonged QT interval, emphasising the importance of regular hormone replacement therapy. Case report 1 A 53-year-old female patient was sent to the emergency department due to three episodes of syncope within eight hours. She had no diarrhoea, vomiting or chest pain during the illness. About 30 years ago, the patient had a normal full-term vaginal delivery with significant postpartum haemorrhage, as well as a history of lactation failure. She had previously been diagnosed with Sheehan’s syndrome and had been taking thyroid hormones and hydrocortisone, but had discontinued hormone replacement therapy one month earlier. There was no history of sudden cardiac death or cardiovascular disease in the patient’s family. At admission, the patient’s skin was wet and cold, and the pulse and blood pressure were undetectable. Electrocardiogram (ECG) monitoring showed polymorphic ventricular tachycardia (Fig. 1). By administering 200 J of asynchronous electrical cardioversion, her heart rhythm was successfully converted to atrial fibrillation. After cardioversion, the patient’s heart rate was 124 beats per minute and her blood pressure was 106/60 mmHg. Laboratory examination revealed abnormalities, including a decreased serum potassium level of 2.9 mmol/l, serum sodium level of 136 mmol/l and adrenocorticotrophic hormone (ACTH) level of less than 1 pg/ml. The thyroid stimulating hormone (TSH) level was 0.363 mIU/l, free tri-iodothyronine (FT3) was 1.83 pmol/l, free thyroxine (FT4) was 3.3 pmol/l, tri-iodothyronine (T3) was 0.64 nmol/l and thyroxine (T4) was 27 nmol/l, which suggested secondary thyroid dysfunction. Myocardial biomarker, blood glucose, pituitary prolactin, growth hormone (GH), luteinising hormone (LH) and folliclestimulating hormone (FSH) levels were in the normal range. The genetic test for hereditary ion channel disease was negative. A baseline ECG showed 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 (Fig. 2A). Transthoracic echocardiography revealed preserved systolic function with a 57.5% ejection fraction (EF) and co-ordinated ventricular wall movement. Brain magnetic resonance imaging (MRI) revealed vacuole turcica (Fig. 3), confirming the diagnosis Department of Cardiology, China–Japan Union Hospital of Jilin University, Jilin Provincial Engineering Laboratory for Endothelial Function and Genetic Diagnosis of Cardiovascular Disease, Changchun, China Ming Yu, MD Hong-liang Yang, MD Huan Sun, PHD Chang Wang, PHD Ping Yang, PHD, pyang@jlu.edu.cn Department of Endocrinology, The First Hospital of Jilin University, Changchun, China Lin Sun Department of Neurology, China–Japan Union Hospital of Jilin University, Changchun, China Shuai Yao, MD
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