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Role of the Na/Ca exchanger in arrhythmias in compensated hypertrophy

Karin R Sipido1, Paul G A Volders, Marieke Schoenmakers

  • 1Laboratory of Experimental Cardiology, University of Leuven, Leuven, Belgium. karin.sipido@med.kuleuven.ac.be

Annals of the New York Academy of Sciences
|December 28, 2002
PubMed

Insights

Sudden cardiac death in early heart failure is linked to increased calcium in heart cells, not seen in later stages. This calcium overload triggers dangerous heart rhythms in compensated hypertrophy.

Area of Science:

  • Cardiology
  • Cardiac Electrophysiology
  • Heart Failure Pathophysiology

Background:

  • Sudden arrhythmic death is prevalent in heart failure, with a higher proportion occurring in earlier disease stages.
  • Different ionic mechanisms may underlie arrhythmogenesis at various stages of heart failure.
  • Compensated biventricular hypertrophy in dogs with chronic atrioventricular block presents an increased risk for sudden death.

Purpose of the Study:

  • To investigate the ionic mechanisms contributing to arrhythmias and sudden death in an animal model of compensated hypertrophy.
  • To compare calcium handling in compensated hypertrophy with that in end-stage heart failure.

Main Methods:

  • Utilized a canine model with chronic complete atrioventricular block (6-8 weeks) exhibiting compensated biventricular hypertrophy.
  • Assessed sarcoplasmic reticulum (SR) calcium release and content.
  • Recorded in vivo monophasic action potentials to identify arrhythmogenic delayed afterdepolarizations (DADs) and ectopic beats.
  • Investigated the role of Na/Ca exchanger activity and delayed K+ currents.

Main Results:

  • In this model, SR calcium release was not reduced; SR calcium content was increased at low stimulation frequencies due to higher Na/Ca exchanger activity.
  • Spontaneous Ca(2+) release induced inward Na/Ca exchange current, leading to arrhythmogenic DADs and ectopic beats observed in vivo.
  • Downregulation of delayed K+ currents contributed to action potential prolongation and increased dispersion of repolarization.

Conclusions:

  • Calcium handling in compensated hypertrophy differs from end-stage heart failure, with increased SR calcium load contributing to sudden death risk.
  • Arrhythmogenic mechanisms involving calcium overload and altered repolarization likely coexist in compensated hypertrophy.
  • These findings suggest that interventions targeting calcium handling could be beneficial in preventing sudden death in early heart failure.

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