Journal
HEART RHYTHM
Volume 11, Issue 11, Pages 2107-2115Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.hrthm.2014.06.023
Keywords
Long QT syndrome; Mechanisms of arrhythmogenesis; Dispersion of cardiac repolarization; Early afterdepolarizations; Gender differences; Sex hormones; Ion channels; Ca2+ cycling proteins; Adrenoceptors; Animal models
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Funding
- German Cardiac Society (St Jude Medical Stipendium)
- German Research Foundation (DFG Forschungsstipendium) [OD 86/1-1]
- American Heart Association postdoctoral fellowship award [AHA 0826071D]
- Margarete von Wrangell Habilitation Program by the MWK Baden Wurttemberg and the European Social Fund
- National Institutes of Health [5RO1 HL093205-04, HL110791-01]
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Gender differences in cardiac repolarization and the arrhythmogenic risk of patients with inherited and acquired long QT syndromes are well appreciated clinically. Enhancing our knowledge of the mechanisms underlying these differences is critical to improve our therapeutic strategies for preventing sudden cardiac death in such patients. This review summarizes the effects of sex hormones on the expression and function of ion channels that control cardiac cell excitation and repolarization as well as key proteins that regulate Ca2+ dynamics at the cellular level. Moreover, it examines the role of sex hormones in modifying the dynamic spatiotemporal (regional and transmural) heterogeneities in action potential duration (eg, the arrhythmogenic substrate) and the susceptibility to (sympathetic) triggered activity at the tissue, organ, and whole animal levels. Finally, it explores the implications of these effects on the management of patients with LQTS.
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