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Acute decrease in left ventricular diastolic chamber distensibility during simulated angina in isolated hearts.

S Isoyama1, C S Apstein, L F Wexler

  • 1Cardiovascular Institute, Boston University School of Medicine, Mass.

Circulation Research
|December 1, 1987
PubMed
Summary
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Increased heart rate during low-flow ischemia significantly raises left ventricular end-diastolic pressure, indicating impaired diastolic chamber distensibility. This suggests elevated myocardial energy demand exacerbates ischemia-induced diastolic dysfunction.

Area of Science:

  • Cardiology
  • Physiology

Background:

  • The factors influencing left ventricular diastolic dysfunction during angina pectoris, particularly when induced by increased myocardial energy demand, remain unclear.
  • Demand ischemia, often seen in pacing-induced angina, presents a clinical challenge in understanding diastolic chamber distensibility changes.

Purpose of the Study:

  • To investigate the impact of varying myocardial energy demand on left ventricular diastolic chamber distensibility during simulated demand ischemia.
  • To determine if increased heart rate during low-flow global ischemia affects diastolic pressure and chamber distensibility.

Main Methods:

  • Isolated, blood-perfused rabbit hearts were subjected to low-flow global ischemia by reducing coronary perfusion pressure.
  • Left ventricular diastolic chamber distensibility was measured using a constant volume balloon model.

Related Experiment Videos

  • Two heart rates were compared: baseline (4 Hz) and pacing tachycardia (6.4 Hz) to simulate different myocardial energy demands.

    • Main Results:

    • Low-flow ischemia significantly reduced contractile function in all hearts.
    • The pacing tachycardia group exhibited a higher myocardial energy demand (rate x systolic pressure product) compared to the constant heart rate group.
    • Pacing tachycardia during ischemia caused a transient, reversible increase in left ventricular end-diastolic pressure (14 to 25 mm Hg), unlike the constant heart rate group.

    Conclusions:

    • Elevated myocardial energy demand, simulated by pacing tachycardia, significantly impairs left ventricular diastolic chamber distensibility during low-flow ischemia.
    • The observed increase in left ventricular end-diastolic pressure is reversible, suggesting a transient diastolic dysfunction mechanism.
    • These findings highlight the critical role of energy demand in the development of diastolic dysfunction during ischemic events.