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Related Experiment Videos

Effects of procainamide on transmural ventricular repolarisation.

Lexin Wang1, Ah Chot Yong, David Kilpatrick

  • 1School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW, Australia. lwang@csu.edu.au

Cardiovascular Drugs and Therapy
|March 26, 2003
PubMed
Summary

Procainamide, a sodium channel blocker, equally prolongs ventricular repolarization across all heart layers in healthy sheep. This study clarifies its effects on transmural activation-recovery intervals (ARI) in normal cardiac tissue.

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Area of Science:

  • Cardiology
  • Pharmacology
  • Electrophysiology

Background:

  • Ventricular repolarization is crucial for normal heart function.
  • Understanding how drugs affect repolarization across different myocardial layers is important for cardiac safety.
  • Procainamide is a known sodium channel blocker used to treat arrhythmias.

Purpose of the Study:

  • To investigate the effect of procainamide on transmural ventricular repolarization.
  • To measure activation-recovery intervals (ARI) in the epicardium, midmyocardium, and endocardium.
  • To determine if procainamide's effects vary across these myocardial layers.

Main Methods:

  • Studied 6 open-chest, anesthetized sheep.
  • Measured transmural ARI using unipolar ECGs and plunge needles in the left ventricular wall.

Related Experiment Videos

  • Administered procainamide (20 mg/min i.v. for 20 min) during sinus rhythm.

    • Main Results:

    • No significant baseline difference in ARI between epicardium, midmyocardium, and endocardium.
    • Procainamide significantly prolonged ARI in all myocardial layers.
    • The prolongation of ARI by procainamide was similar across epicardium, midmyocardium, and endocardium.

    Conclusions:

    • Procainamide causes a uniform prolongation of ventricular repolarization in healthy hearts.
    • The sodium channel blocker's effect on repolarization is consistent across transmural cardiac layers.
    • These findings contribute to understanding procainamide's electrophysiological effects in normal cardiac tissue.