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Left ventricular restoring forces: modulation by heart rate and contractility

M M LeWinter1, J Fabian, S P Bell

  • 1Cardiology Unit, Fletcher Allen Health Care, Burlington, VT 05401, USA.

Basic Research in Cardiology
|December 2, 1998
PubMed
Summary
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Restoring forces normally aid left ventricular (LV) filling by suction. Increased contractility enhances these forces, but chronic heart failure significantly impairs them, potentially causing diastolic dysfunction.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Mechanics
  • Diastolic Function

Background:

  • Left ventricular (LV) filling is crucial for cardiac output.
  • Restoring forces (RFs) generated during contraction may contribute to LV filling.
  • The role of these forces in normal and pathological states requires further elucidation.

Purpose of the Study:

  • To characterize restoring forces (RFs) in the left ventricle (LV).
  • To investigate the impact of contractility and heart rate on RFs.
  • To determine the effect of chronic tachycardia heart failure on RFs and their contribution to diastolic function.

Main Methods:

  • Utilized a servomotor system in open-chest dogs to induce nonfilling diastoles.
  • Measured fully relaxed pressure (FRP) at end-systolic volume (ESV) to define the fully relaxed pressure-volume (FRPV) relation.

Related Experiment Videos

  • Administered systemic and intracoronary dobutamine to assess contractility effects; manipulated heart rate and studied chronic tachycardia heart failure models.
  • Main Results:

    • A negative fully relaxed pressure (FRP) indicates the presence of restoring forces (RFs) contributing to LV filling by suction.
    • Increased contractility (dobutamine) shifted the FRPV relation downward, signifying augmented RFs.
    • Chronic tachycardia heart failure markedly attenuated RFs, suggesting impaired diastolic filling capacity.

    Conclusions:

    • Restoring forces (RFs) are a normal physiological mechanism contributing to left ventricular (LV) filling.
    • Acute increases in contractility enhance RFs, while acute heart rate increases (within a specific range) do not.
    • Chronic tachycardia heart failure significantly diminishes RFs, potentially representing a key mechanism of diastolic dysfunction.