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The effects of ageing and adrenergic challenge on electrocardiographic phenotypes in a murine model of long QT syndrome type 3

Chadda KR 1 , Ahmad S 1 , Valli H 1 , den Uijl I 2 , Al-Hadithi AB 1 , Salvage SC 3 Show all authors , Grace AA 4 , Huang CL 1 , Jeevaratnam K 5

Affiliations 

  • 1 Physiological Laboratory, University of Cambridge, Downing Street, Cambridge, CB2 3EG, United Kingdom
  • 2 Faculty of Health and Medical Sciences, University of Surrey, Guildford, GU2 7AL, United Kingdom
  • 3 Department of Biochemistry, University of Cambridge, Hopkins Building, Cambridge, CB2 1QW, United Kingdom
  • 4 Division of Cardiovascular Biology, Department of Biochemistry, University of Cambridge, Hopkins Building, Cambridge, CB2 1QW, United Kingdom
  • 5 Faculty of Health and Medical Sciences, University of Surrey, Guildford, GU2 7AL, United Kingdom. [email protected]
Sci Rep, 2017 09 11;7(1):11070.
PMID: 28894151 DOI: 10.1038/s41598-017-11210-3

Abstract

Long QT Syndrome 3 (LQTS3) arises from gain-of-function Nav1.5 mutations, prolonging action potential repolarisation and electrocardiographic (ECG) QT interval, associated with increased age-dependent risk for major arrhythmic events, and paradoxical responses to β-adrenergic agents. We investigated for independent and interacting effects of age and Scn5a+/ΔKPQ genotype in anaesthetised mice modelling LQTS3 on ECG phenotypes before and following β-agonist challenge, and upon fibrotic change. Prolonged ventricular recovery was independently associated with Scn5a+/ΔKPQ and age. Ventricular activation was prolonged in old Scn5a+/ΔKPQ mice (p = 0.03). We associated Scn5a+/ΔKPQ with increased atrial and ventricular fibrosis (both: p 

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