Download Cell-based description of ventricular contraction in a - ORBi

Cell‐based description of ventricular contraction in a model
of the human cardiovascular system
1
2
2
S. Kosta , J. Negroni , E. Lascano , P. C. Dauby
1
1
University of Liège, GIGA - Cardiovascular Sciences, Belgium
2
Department of Compara�ve Cellular end Molecular Biology, Favaloro University,
Buenos Aires, Argen�na
A mul�scale model of the cardiovascular system is presented, where hemodynamics is described by a lumped parameter model, while
heart contrac�on is described at the cellular scale.
Pulmonary
circula�on
Passive chamber:
Ac�ve chamber:
Electrophysiology
elastance
Pulmonary
artery
Calcium kine�cs
Mechanical contrac�on
Pulmonary
vein
Thick filament
pressure
volume
Q
Thin filament
Flow through the vessels:
Po
R
Pi
Parallel element
ACTIVE
Right
Le�
ventricle CONTRACTION ventricle
Volume varia�on:
Vena cava
From cell to ventricle
Qout
Qin
V
Aorta
Systemic
circula�on
Cardiac valve:
Results
Baseline
End-systolic elastance: a good index
of cardiac contrac�lity ?
Par�cular a�en�on was paid
to the sarcomere length,
which must vary between
physiological extremes.
A good cardiac contrac�lity index should only vary with inotropy and not with load.
End-systolic elastance (Ees) is the gold standard for assessing cardiac contrac�lty, but
with our model we show that this index is load-dependent.
Load varia�on
Pressure-volume loops are
correctly reproduced, as well
as the different flows and
pressures �me evolu�on.
Hemorrhage
(preload decrease)
Heart failure
Ees calcula�on
Rmt increase
(preload decrease)
Rsys increase
(a�erload increase)
Results
A prolonged ac�on poten�al,
a lower intracellular calcium
and a weaker produced force
are characteris�c symptoms of
heart failure.
This leads to smaller pressurevolume loops.
Ees is calculated with a linear
regression over the three first endsystolic points of the PV loop
Conclusion
Acknowledgements
Our mul�scale model of the human cardiovascular system is able to
reproduce baseline results at both scales (cellular and hemodynamic). It can
also reproduce pathological behaviors that originate at the cellular scale,
like heart failure. It also indicates that the end-systolic elastance is not loadindependent, as o�en assumed in many CVS models using the varying
elastance to describe heart contrac�on.
P. D. acknowledges for FRS-FNRS travel
support.
Contact
[email protected]