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Related Experiment Videos

Altered myocardial force-frequency relation in human heart failure.

L A Mulieri1, G Hasenfuss, B Leavitt

  • 1Department of Physiology and Biophysics, University of Vermont College of Medicine, Medical Center Hospital of Vermont, Burlington 05405.

Circulation
|May 1, 1992
PubMed
Summary

Congestive heart failure (CHF) impairs myocardial contractility, showing reduced tension generation and altered frequency response in failing heart muscle. These intrinsic myocardial issues contribute to abnormal left ventricular function in dilated cardiomyopathy.

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Area of Science:

  • Cardiology
  • Physiology
  • Biochemistry

Background:

  • Congestive heart failure (CHF), specifically idiopathic dilated cardiomyopathy, is characterized by abnormal left ventricular (LV) function during exercise.
  • Observed abnormalities include reduced LV volume decrease, diminished pressure rise/fall rates, and impaired heart-rate-dependent contractility potentiation (Bowditch treppe).

Purpose of the Study:

  • To investigate and quantify myocardial contractile function abnormalities in failing versus non-failing human hearts.
  • To identify intrinsic myocardial dysfunction contributing to abnormal ventricular function in dilated cardiomyopathy.

Main Methods:

  • Isolated left ventricular myocardial strips from NYHA class IV failing and non-failing human hearts were studied.
  • Experiments were conducted at physiological temperature (37°C) and various contraction frequencies (12-240 min⁻¹).

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  • A novel method using 2,3-butanedione monoxime (BDM) protected myocardial strips from cutting injury during dissection.

    • Main Results:

    • Failing myocardium generated significantly less isometric twitch tension (48% and 80% less at 72 and 174 min⁻¹, respectively) compared to non-failing myocardium.
    • The peak tension-frequency relationship occurred at lower frequencies in failing hearts (average 81 ± 22 min⁻¹ vs. 174 ± 4 min⁻¹ in non-failing).
    • While non-failing myocardium showed significant tension increase with frequency, failing myocardium exhibited no significant change between 60-150 min⁻¹.
    • Rates of tension rise and fall paralleled twitch tension in non-failing muscle but not in failing muscle.

    Conclusions:

    • Intrinsic alterations in myocardial contractility, independent of systemic factors, contribute to abnormal left ventricular function in dilated cardiomyopathy.
    • The findings from isolated myocardium quantitatively align with in-vivo measurements, supporting a primary role for myocardial dysfunction.