Influence of LVAD function on mechanical unloading and electromechanical delay: a simulation study

Med Biol Eng Comput. 2018 May;56(5):911-921. doi: 10.1007/s11517-017-1730-y. Epub 2017 Nov 3.

Abstract

This study hypothesized that a left ventricular assist device (LVAD) shortens the electromechanical delay (EMD) by mechanical unloading. The goal of this study is to examine, by computational modeling, the influence of LVAD on EMD for four heart failure (HF) cases ranging from mild HF to severe HF. We constructed an integrated model of an LVAD-implanted cardiovascular system, then we altered the Ca2+ transient magnitude, with scaling factors 1, 0.9, 0.8, and 0.7 representing HF1, HF2, HF3, and HF4, respectively, in order of increasing HF severity. The four HF conditions are classified into two groups. Group one is the four HF conditions without LVAD, and group two is the conditions treated with continuous LVAD pump. The single-cell mechanical responses showed that EMD was prolonged with the higher load. The findings indicated that in group one, the HF-induced Ca2 + transient remodeling prolonged the mechanical activation time (MAT) and decreased the contractile tension, which reduced the left ventricle (LV) pressure, and increased the end-diastolic strain. In group two, LVAD shortened MAT of the ventricles. Furthermore, LVAD reduced the contractile tension, and end-diastolic strain, but increased the aortic pressure. The computational study demonstrated that LVAD shortens EMD by mechanical unloading of the ventricle.

Keywords: Calcium transient; Heart failure; Left ventricular assist device; Ventricular electromechanical model.

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Blood Pressure
  • Calcium / metabolism
  • Computer Simulation*
  • Diastole
  • Heart-Assist Devices*
  • Humans
  • Membrane Potentials
  • Models, Cardiovascular*
  • Myocardium / metabolism
  • Systole
  • Time Factors
  • Weight-Bearing

Substances

  • Adenosine Triphosphate
  • Calcium