Endocrine Abstracts

Introduction: Acquired modifible long QT syndrome (LQTS) might be caused by hypocortisolism but also drug-induced. Unique genetic association between them is the background of both. The aim of this case report is to present the patient with Addison disease and LQTS not responding on increased dosage of hydrocortison susbstitution therapy.

Case report: We report a female patient, 65 years old (1950y.). At the age of 34y. (1984y.) Morbus Addisoni was diagnosed and substituted with hydrocortison 20 mg daily. In her 57^th y. (2007y.) after interhemilameinectomy chronic pain remained. Patient was treated with polypharmacy: lorazepam 5 mg/day, sulpirid 100 mg/day, paroksetin 10 mg/day and karbamazepim 800 mg/day. Two years later patient developed attack of faintness with headache, fatigue and hypotension (100/70 mmHg). Pottassium level was 4.97 mmol/l, sodium 141 mmol/l and ECG was normal. Dosage of hydrocortison was increased on 25 mg/day. Year later syncope followed with vomiting, retrosternal and left arm pain happened, and next years three times repeated. Head CT was normal. On 24 h Holter ECG maximal QTc of 452 ms was noticed. In July 2015 she developed lost of consciousness with confirmed third-degree AV block with pauses of 10 sec. After therapy with atropin and metilprednisolon 60 mg heart rate increased on 55/min, QT/QTc was 592/581 ms with occasional ventricular premature complexes. On coronarography significant lesions were not detected. VVIR (Ventricular pace, ventricular sense, ventricular inhibit- rate responsive single-chamber ventricular pacing) pacemaker was implanted. Our patient was still on medications previously incriminated and pacemaker just periodically emits electric impulses that stimulate heart to beat at a normal rate. In 2016. incriminated pain killers were excluded andf since that time there was no need for pace maker activation.

Conclusion: Holter monitoring ECG should be performed longer than one day if it is not conclusive, actually so long untill establishing the connection between symptoms (e.g. syncopa) and ECG abnormalities. By excluding the incriminated drugs (pain killers) we have conformed the underlying pathophysiological mechanism that lead to LQRS development.