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Cardiomyocyte-specific deletion of survivin causes global cardiac conduction defects

Jan Wilko Schrickel1, Lars Lickfett, Thorsten Lewalter

  • 1Department of Medicine-Cardiology, University of Bonn, Germany. jan.schrickel@ukb.uni-bonn.de

Basic Research in Cardiology
|September 15, 2012
PubMed

Insights

Cardiac-specific deletion of survivin (Surv) impairs heart electrical conduction and sinus-nodal function. Despite reduced connexin43 (Cx43) levels, Surv(-/-) mice show electrical stability, suggesting cardiomyocyte size and number are key factors.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Cardiac Electrophysiology

Background:

  • Survivin (Surv) is an inhibitor of apoptosis protein family member.
  • Cardiac-specific deletion of survivin leads to heart failure, but its electrophysiological impact is unknown.

Purpose of the Study:

  • To investigate the effects of cardiac-specific survivin deletion on cardiac electrophysiology in mice.
  • To determine the impact of survivin deficiency on heart rate, conduction, and arrhythmia susceptibility.

Main Methods:

  • In vivo transvenous electrophysiological studies in survivin-deficient (Surv(-/-)) and wild-type (Surv(+/+)) mice.
  • Epicardial activation mapping (EAM) in Langendorff-perfused hearts.
  • Surface electrocardiography (ECG) and assessment of sinus-nodal and AV-nodal function.
  • Quantitative immunofluorescence staining for connexin43 (Cx43).

Main Results:

  • Surv(-/-) mice exhibited lower heart rates, prolonged P, PQ, QRS, and QT intervals, and prolonged HV-intervals.
  • Impaired sinus-nodal function and AV-nodal conduction were observed in Surv(-/-) mice.
  • EAM revealed slowed and heterogeneous myocardial conduction, with frequent ectopic beats in Surv(-/-) mice.
  • Cx43 levels were decreased in Surv(-/-) mice, yet they lacked susceptibility to atrial and ventricular arrhythmias.

Conclusions:

  • Cardiac survivin deficiency causes significant global conduction abnormalities in the heart's electrical system.
  • Reduced cardiomyocyte number and increased size, rather than Cx43 levels, appear to be determinants of electrical stability in Surv(-/-) hearts.
  • The findings highlight a complex interplay between cardiomyocyte structure and connexin43 in maintaining cardiac electrical homeostasis.

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