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Arrhythmogenesis in heart failure.

M J Janse1, J T Vermeulen, T Opthof

  • 1Cardiovascular Research, Academic Medical Center, University of Amsterdam, The Netherlands. M.J.Janse@amc.uva.nl

Journal of Cardiovascular Electrophysiology
|May 3, 2001
PubMed
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Nonsustained ventricular tachycardias in heart failure are linked to delayed afterdepolarizations and triggered activity. These events, driven by calcium release, occur with norepinephrine and low extracellular potassium.

Area of Science:

  • Cardiology
  • Physiology
  • Molecular Biology

Background:

  • Heart failure (HF) is a complex condition often associated with arrhythmias.
  • Understanding the mechanisms underlying ventricular arrhythmias in HF is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the occurrence and underlying mechanisms of nonsustained ventricular tachycardias (NSVT) in a rabbit model of heart failure.
  • To explore the role of delayed afterdepolarizations (DADs) and triggered activity in the development of arrhythmias in failing hearts.

Main Methods:

  • A rabbit model of heart failure was created using combined pressure and volume overload.
  • Microelectrode recordings were performed on ventricular trabeculae from both failing rabbits and human patients with end-stage heart failure.

Related Experiment Videos

  • Electrophysiological parameters, including extracellular potassium concentration and the presence of norepinephrine, were manipulated.

    • Main Results:

    • Nonsustained ventricular tachycardias developed in a significant portion of the failing rabbit models.
    • Delayed afterdepolarizations and triggered activity were observed in approximately half of the preparations under specific conditions (norepinephrine, 3 mM extracellular K+).
    • Spontaneous calcium release from the sarcoplasmic reticulum was identified as the underlying cause of DADs and triggered activity.

    Conclusions:

    • Delayed afterdepolarizations and triggered activity, mediated by spontaneous calcium release, contribute to ventricular arrhythmias in heart failure.
    • These electrophysiological abnormalities are exacerbated by norepinephrine and low extracellular potassium concentrations.
    • The findings provide insights into the arrhythmogenic mechanisms in failing myocardium, relevant to both animal models and human patients.