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Endocrinopathies mimicking gene negative long QT syndrome

Part of: Electrophysiology

Published online by Cambridge University Press:  24 November 2021

Praloy Chakraborty Open the ORCID record for Praloy Chakraborty [Opens in a new window] ,
Jason D. Roberts  and
Michael H. Gollob
Praloy Chakraborty
Affiliation:
Inherited Arrhythmia and Cardiomyopathy Program, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada
Jason D. Roberts
Affiliation:
Section of Cardiac Electrophysiology, Division of Cardiology, Western University, London, Ontario, Canada Population Health Research Institute, McMaster University, and Hamilton Health Sciences, Hamilton, Ontario, Canada
Michael H. Gollob*
Affiliation:
Inherited Arrhythmia and Cardiomyopathy Program, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada Inherited Arrhythmia and Cardiomyopathy Clinic, Partners in Advanced Cardiac Evaluation, Newmarket, Ontario, Canada
*
Author for correspondence: M. H. Gollob, MD, Inherited Arrhythmia and Cardiomyopathy Clinic, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, Canada, M5G 2C4. Tel: 416-340-4282; Fax: 416-340-3281. E-mail: [email protected]
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Abstract

Ventricular repolarisation can be influenced by hormonal milieu which may mimic long QT syndrome. We describe a series of patients referred for genetic testing for diagnosed long QT syndrome where a detailed clinical workup demonstrated endocrinopathies as the cause of presumed “gene negative” long QT syndrome and QT prolongation.

Keywords

Long QT syndromecardiac arrestendocrinopathygeneticsadrenal crisis
Type
Brief Report
Information
Cardiology in the Young , Volume 32 , Issue 6 , June 2022 , pp. 1016 - 1018
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Copyright
© The Author(s), 2021. Published by Cambridge University Press

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References

Adler, A, Novelli, V, Amin, AS, et al. An international, multicentered, evidence-based reappraisal of genes reported to cause congenital Long QT Syndrome. Circulation 2020; 141: 418–428.CrossRefGoogle ScholarPubMed
Chorin, E, Rosso, R, Viskin, S. Electrocardiographic manifestations of calcium abnormalities. Ann Noninvasive Electrocardiol 2016; 21: 7–9.CrossRefGoogle ScholarPubMed
Busjahn, A, Seebohm, G, Maier, G, et al. Association of the serum and glucocorticoid regulated kinase (sgk1) gene with QT interval. Cell Physiol Biochem 2004; 14: 135–142.CrossRefGoogle ScholarPubMed
Lamothe, SM, Zhang, S. The serum- and glucocorticoid-inducible kinases SGK1 and SGK3 regulate hERG channel expression via ubiquitin ligase Nedd4-2 and GTPase Rab11*. J Biol Chem 2013; 288: 15075–15084.CrossRefGoogle ScholarPubMed
Palmeri, NO, Davidson, KW, Whang, W, Kronish, IM, Edmondson, D, Walker, MD. Parathyroid hormone is related to QT interval independent of serum calcium in patients with coronary artery disease. Ann Noninvasive Electrocardiol 2018; 23: e12496.CrossRefGoogle ScholarPubMed
Ebisawa, K, Kimura, K, Nakayama, T, Yaginuma, T, Watanabe, Y, Shimada, K. Cardiac electrophysiologic effects of parathyroid hormone in the guinea pig. Heart Vessels 1995; 10: 128–137.CrossRefGoogle ScholarPubMed
Adler, A, Sadek, MM, Chan, AYM, etal. Patient outcomes from a specialized inherited arrhythmia clinic. Circ Arrhythm Electrophysiol 2016; 9: e003440.CrossRefGoogle ScholarPubMed
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