Analysis of the effect of cortisone on the QT interval

Cardiac death caused by malignant arrhythmias is one of the most frequent reasons for death in the western world [1]. In Germany and the United States, each year between 100,000 and 450,000 people die suddenly [[1], [2], [3]]. Arrhythmias like ventricular tachycardias and ventricular fibrillation are the most frequent reasons [4]. A major cause of arrhythmias like ventricular tachycardias and ventricular fibrillation is congenital long QT syndrome and drug-induced long QT syndrome. The significance of a prolonged QTc interval outside of long QT syndrome and drug effects has been investigated in patients with Tako Tsubo cardiomyopathy. Santoro et al. [5] revealed that patients with prolongation of the QTc interval at the time of admission had a higher risk of cardiovascular rehospitalisation.

Congenital long QT syndrome type 2 and drug-induced long QT syndrome have a fundamental intersection at the KCNH2 gene (encodes hERG), which is responsible for the potassium channel IKr function, contributing to repolarisation. A mutation in the KCNH2 gene alters IKr function and thus leads to the characteristic QT prolongation [6].

Brostoff et al. [7] reported about drug-induced long QT syndrome in a patient with leishmaniasis receiving potassium stibogluconate therapy, a side effect known for this drug. Under administration of 2 × 20 mg prednisolone as part of the underlying disease, the QTc interval normalised within 4 days [7]. Peal et al. [8] investigated the potential drug-influencing of long QT syndrome (type 2) in vivo in zebrafish. Within the scope of their study, they showed that, among other changes, flurandrenolide shortens the ventricular action potential duration via the glucocorticoid receptor–mediated pathway. The effect was not associated with modification of the potassium channel IKr [8].

Despite tissue-specific effects of glucocorticoids, comparatively little is known about their direct cardiac effects. Studies suggest that glucocorticoid signalling in cardiomyocytes is critical for the normal development and function of the heart and glucocorticoid administration improves contractile performance [9]. There is a lack of studies analysing shortening of the QTc interval in humans, long QT syndromes and drug-induced long QTc types.

This study analyses the effect of cortisone on the duration of the QTc interval in patients without proven cardiac disease.

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