Cardiovascular Journal of Africa: Vol 33 No 5 (SEPTEMBER/OCTOBER 2022)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 AFRICA 281 administered glucocorticoids, 50% of cases thyroid hormone, and a temporary pacemaker was used in three cases (37.5%). Among the eight patients, one patient died from cardiac arrest and the others recovered well. Here, we present two cases of discontinued hormone replacement treatment with Sheehan’s syndrome, which resulted in a prolonged QT interval and ventricular arrhythmia. The ECG manifestations associated with Sheehan’s syndrome include a prolonged QT interval, T-wave inversion and ST-segment depression. The exact cause of such changes remains unclear, but hypokalaemia, a surge in catecholamines secondary to hypoglycaemia, hypothyroidism or reduced ACTH level have been considered possible causes. In terms of electrolyte disturbance, hyponatraemia was most commonly observed in patients with Sheehan’s syndrome, but the incidence of hypokalaemia was relatively low. According to Lim et al.,11 59% of patients with Sheehan’s syndrome had hyponatraemia, 26.9% suffered from hypokalaemia, 35.9% suffered from hypocalcaemia, and hypomagnesaemia and hypophosphataemia accounted for 47.4 and 23.1%, respectively. Hypokalaemia causes arrhythmias by lowering the potassium content of the extracellular fluid, which decreases the permeation of potassium across the myocardial cell membrane. This leads to decreased outward potassium current, prolonged ventricular repolarisation time and slowed conduction, all of which contribute to ventricular arrhythmia via a trigger mechanism. In our cases, the serum potassium level was decreased, which resulted in prolonged repolarisation. Although the patient’s potassium and magnesium levels normalised after potassium and magnesium supplementation, the corrected QT-interval prolongation and T-wave inversion persisted, and ventricular tachycardia recurred several times. There may have been other factors that caused prolonged QT interval. Sheehan’s syndrome has different degrees of pituitary dysfunction. The most common involvement is prolactin and GH secretion, which ranges from 90 to 100%, while the secretion of cortisol, TSH and gonadotropin can be seen in 50 to 100%.4 Previous research has shown that thyroid and steroid hormones are additional pathological mechanisms of ventricular tachycardia in patients with Sheehan’s syndrome. Thyroid hormone is well known for its importance in heart rate, rhythm and contraction. It also influences the number of β-adrenergic receptors as well as their sensitivity to catecholamines. Therefore, a deficiency of thyroid hormone can result in a prolonged QT interval. In addition tohypothyroidism, secondary adrenal insufficiency can also result in a prolonged QT interval.12 Although the exact mechanism remains unknown, histopathological changes in the myocardium and imbalance of intracellular and extracellular electrolytes are thought to play an important role. Hormone replacement treatment must be used for the rest of the patient’s life to supply hormones that the pituitary gland is unable to produce. Instead of test results, glucocorticoid doses should be titrated depending on the clinical findings of the patient. Physiological replacement is preferred to avoid the adverse effects of glucocorticoid.13 With regard to thyroid hormone replacement, the levothyroxine titration dose depends on FT3 and FT4 levels, but not on TSH levels, which might be low, normal or high.13 In our patient, due to administering steroid and thyroid hormones together, we cannot determine which hormonal effect was the most important. With the administration of hormone replacement therapy, the patient’s QT prolongation and T-wave inversion had improved and ventricular arrhythmia did not recur. Conclusions Sheehan’s syndrome presenting as ventricular tachycardia is an extremely rare phenomenon. These unique cases suggest that clinicians should prescribe regular hormone replacement therapy in patients with Sheehan’s syndrome. Hormone replacement therapy for these patients can not only treat hypopituitarism, but also prevent fatal arrhythmias. These patients need lifelong follow up and close monitoring of their hormone levels. Pharmacists and nurses must educate patients about medication compliance or they will face a potentially life-threatening hormone crisis. This work was supported by the National Natural Science Foundation of China, No. 81570360. References 1. Kristjansdottir HL, Bodvarsdottir SP, Sigurjonsdottir HA. Sheehan’s syndrome in modern times: a nationwide retrospective study in Iceland. 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Wang SY, Hsu SR, Su SL, Tu ST. Sheehan’s syndrome presenting with early postpartum congestive heart failure. J Chinese Med Assoc 2005; 68(8): 386–391. 9. Shoji M, Kimura T, Ota K, Ohta M, Sato K, Yamamoto T, et al. Cortical laminar necrosis and central pontine myelinolysis in a patient with Sheehan syndrome and severe hyponatremia. Int Med (Tokyo, Japan) 1996; 35(5): 427–431. 10. Nunoda S, Ueda K, Kameda S, Nakabayashi H. Sheehan’s syndrome with hypomagnesemia and polymorphous ventricular tachycardia. Jap Heart J 1989; 30(2): 251–256. 11. Lim CH, Han JH, Jin J, Yu JE, Chung JO, Cho DH, et al. Electrolyte imbalance in patients with Sheehan’s syndrome. Endocrinol Metab (Seoul, Korea) 2015; 30(4): 502–508. 12. Arpaci D, Demir MV, Garip T, Tamer A. A case of QT prolongation associated with panhypopituitarism. Case Rep Endocrinol 2013; 2013: 989745. 13. Karaca Z, Laway BA, Dokmetas HS, Atmaca H, Kelestimur F. Sheehan syndrome. Nat Rev Dis Primers 2016; 2: 16092.

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