Load-induced changes in ventricular repolarization: evidence of autonomic modulation

Ksenia A Sedova1, Sergey L Goshka, Vladimir A Vityazev

  • 1a Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, 50 Pervomayskaya Street, Syktyvkar, 167982 Russia.

Insights

Autonomic tone significantly influences cardiac repolarization during increased hemodynamic load. Blocking autonomic signals alters ventricular repolarization patterns, impacting arrhythmogenesis risk.

Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System
  • Cardiac Electrophysiology

Background:

  • Increased hemodynamic load elevates arrhythmogenesis risk by altering cardiac repolarization.
  • The role of autonomic tone in modulating load-dependent repolarization changes requires further investigation.

Purpose of the Study:

  • To investigate the hypothesis that autonomic tone intervention affects load-dependent changes in ventricular repolarization.
  • To elucidate the impact of autonomic blockade on ventricular repolarization heterogeneity under augmented hemodynamic load.

Main Methods:

  • Measurement of activation-recovery intervals using 64 ventricular epicardial leads in 26 chinchilla rabbits.
  • Induction of aortic stenosis to create augmented hemodynamic load.
  • Administration of atropine and propranolol to achieve autonomic blockade prior to loading.

Main Results:

  • Short-term stenosis decreased right ventricular activation-recovery intervals; prolonged overload increased repolarization duration in both ventricles.
  • Autonomic blockade prolonged activation-recovery intervals, particularly in the left ventricle, and attenuated repolarization gradients.
  • Ventricular loading in autonomically blocked animals shortened repolarization duration, transforming biphasic changes into monophasic shortening.

Conclusions:

  • Autonomic tone is crucial for developing ventricular repolarization heterogeneity under augmented hemodynamic load.
  • Autonomic blockade significantly alters ventricular repolarization dynamics and gradients during hemodynamic stress.

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