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Focal gap junction uncoupling and spontaneous ventricular ectopy.

David E Gutstein1, Stephan B Danik, Steve Lewitton

  • 1The Leon H. Charney Div. of Cardiology, New York Univ. School of Medicine/VA Harbor Medical Ctr., 423 E. 23rd St., 6 W.-6005BW, New York, NY 10010, USA. david.gutstein@med.nyu.edu

American Journal of Physiology. Heart and Circulatory Physiology
|May 17, 2005
PubMed
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Focal loss of connexin43 (Cx43) in mouse hearts increases spontaneous arrhythmias but does not cause sustained ventricular tachycardia. Widespread Cx43 reduction is needed to support sustained arrhythmias, impacting cardiac function.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Arrhythmogenesis Research

Background:

  • Conditional cardiac connexin43 (Cx43) loss causes arrhythmias.
  • The impact of focal gap junction remodeling on arrhythmogenesis is unknown.
  • Acquired cardiomyopathies feature focal gap junction remodeling.

Purpose of the Study:

  • Investigate arrhythmogenic potential of focal Cx43 deficiency in the heart.
  • Assess electrophysiological changes and arrhythmia frequency in Cx43-deficient chimeric mice.
  • Correlate focal gap junction remodeling with cardiac function and arrhythmia susceptibility.

Main Methods:

  • Generated chimeric mice by injecting Cx43-deficient embryonic stem cells into wild-type blastocysts.
  • Quantified Cx43-negative foci using immunohistochemistry.

Related Experiment Videos

  • Evaluated cardiac function via echocardiography and invasive hemodynamics.
  • Monitored spontaneous and inducible arrhythmias.

    • Main Results:

    • Chimeric mice exhibited widespread microscopic Cx43-negative foci (~15% of heart area).
    • Systolic function was significantly depressed in chimeras (19% reduction in fractional shortening).
    • Chimeras showed increased spontaneous arrhythmic events and non-sustained ventricular tachycardia.
    • No sustained ventricular tachyarrhythmias were observed in chimeras.

    Conclusions:

    • Focal myocardial uncoupling increases susceptibility to arrhythmia triggers.
    • Widespread Cx43 reduction is necessary to sustain ventricular tachyarrhythmias.
    • Focal Cx43 remodeling contributes to cardiac dysfunction and arrhythmia propensity.