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Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism
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Force- and relaxation-frequency relations in patients with diastolic heart failure

Takashi Yamanaka1, Katsuya Onishi, Masaki Tanabe

  • 1The First Department of Internal Medicine, Mie University School of Medicine, Tsu, Japan.

American Heart Journal
|October 31, 2006
PubMed

Insights

In diastolic heart failure (DHF), the heart’s ability to contract with increased heart rate is preserved, but relaxation is impaired. Left ventricular-arterial coupling worsens with increased heart rate in DHF and systolic heart failure (SHF).

Area of Science:

  • Cardiology
  • Heart Failure Research
  • Physiology

Background:

  • Congestive heart failure with reduced ejection fraction (systolic heart failure [SHF]) shows impaired chronotropic effects on myocardial contractility and relaxation.
  • The force- and relaxation-frequency relations and left ventricular (LV)-arterial coupling in diastolic heart failure (DHF) remain under-investigated.

Purpose of the Study:

  • To investigate inotropic and lusitropic responsiveness to atrial pacing in patients with DHF and SHF.
  • To assess LV-arterial coupling during increased heart rate in DHF and SHF.

Main Methods:

  • LV pressure-volume relations were measured using conductance catheter and microtip manometer in 18 DHF and 11 SHF patients.
  • Atrial pacing increased heart rate by 40 beats/min to evaluate cardiac function and coupling.

Main Results:

  • In SHF, increased heart rate did not alter LV end-systolic elastance (Ees) or LV relaxation time constant.
  • In DHF, increased heart rate significantly enhanced Ees but not the relaxation time constant.
  • LV-arterial coupling (Ees/arterial elastance) was impaired during pacing in both DHF and SHF patients.

Conclusions:

  • The force-frequency relation is preserved in DHF, but the relaxation-frequency relation is impaired.
  • Impaired LV-arterial coupling during tachycardia in DHF may stem from impaired LV function.
  • Targeting the impaired relaxation-frequency relation and exacerbated LV-arterial coupling during tachycardia could be a therapeutic strategy for DHF.
Abstract

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