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Related Experiment Videos

Increased afterload intensifies asynchronous wall motion and impairs ventricular relaxation

T Miura1, V Bhargava, B D Guth

  • 1University of California, San Diego.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 1, 1993
PubMed
Summary

Increased afterload impairs left ventricular relaxation, causing asynchronous wall motion, particularly in the apical-inferior region. This temporal dispersion of regional contraction may explain delayed relaxation during heightened afterload.

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Area of Science:

  • Cardiology
  • Physiology

Background:

  • Increased afterload can impair left ventricular relaxation.
  • The role of regional dyssynchrony in this impairment is not fully understood.

Purpose of the Study:

  • To investigate if impaired left ventricular relaxation due to increased afterload is linked to regional dyssynchrony.
  • To analyze the relationship between afterload, left ventricular relaxation, and asynchronous wall motion.

Main Methods:

  • Simultaneous left ventricular contrast ventriculography and pressure measurements in dogs.
  • Angiotensin II infusion to increase afterload.
  • Centerline and video-intensity methods to assess regional wall motion and asynchrony.

Main Results:

  • Angiotensin II increased peak left ventricular pressure and prolonged the isovolumic pressure time constant (tau).

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  • Early diastolic and systolic asynchrony were detected in specific regions, especially the apical region.
  • Systolic excursion was reduced in all regions during increased afterload, with the apical region most affected.

    • Conclusions:

    • Impaired left ventricular relaxation with augmented afterload is associated with asynchronous wall motion in dogs.
    • Temporal dispersion of regional contraction, particularly in the apical-inferior region, may explain delayed left ventricular relaxation under increased afterload.