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Tissue discontinuities affect conduction velocity restitution: a mechanism by which structural barriers may promote

Richard Derksen1, Harold V M van Rijen, Ronald Wilders

  • 1Heart Lung Center Utrecht, University Medical Center, Utrecht, Netherlands.

Circulation
|July 16, 2003
PubMed

Insights

Structural barriers create tissue discontinuities that disrupt cardiac electrical wave propagation. This study shows these discontinuities cause abnormal conduction velocity restitution, potentially explaining wave break and fibrillation in heart disease.

Area of Science:

  • Cardiac Electrophysiology
  • Biophysics
  • Cellular Cardiology

Background:

  • The role of structural barriers in promoting cardiac wave break and fibrillation remains unclear.
  • Conduction velocity (CV) restitution is a key factor in wave break, and its abnormalities are linked to ventricular fibrillation in heart disease, particularly in fibrotic tissue.
  • Structural barriers may impose tissue discontinuities that lead to abnormal CV restitution.

Purpose of the Study:

  • To investigate the hypothesis that tissue discontinuities caused by structural barriers lead to abnormal conduction velocity restitution.
  • To elucidate the cellular mechanisms underlying abnormal CV restitution at tissue discontinuities.

Main Methods:

  • Simulated tissue discontinuities using neonatal rat heart cell cultures in an 8-armed star pattern.
  • Applied premature stimulation and recorded extracellular electrograms and action potentials at multiple sites.
  • Utilized voltage-clamp measurements and computer simulations to analyze depolarizing currents at simulated discontinuities.

Main Results:

  • Progressive increases in activation delay, indicative of abnormal CV restitution, were observed specifically at tissue discontinuities.
  • Activation delay was significantly greater at discontinuities distal (3.13 ms/10 ms) compared to proximal (0.81 ms/10 ms) to the star center.
  • Voltage-clamp and simulations revealed that biphasic, prolonged activation and delayed inactivation of depolarizing currents contributed to the observed delay.

Conclusions:

  • Tissue discontinuities are demonstrated to cause abnormal conduction velocity restitution.
  • The abnormal restitution results from a rapid increase in activation after initial slow activation and delayed inactivation of depolarizing current at the discontinuity.
  • These findings provide a mechanistic link between structural barriers, abnormal CV restitution, and the potential for cardiac arrhythmias like fibrillation.
Abstract

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