Heart Wall - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 341

be carried out. Moreover, the inverse problem can be treated to estimate adequate
activation times. Electromechanical coupling can incorporate changes in electrical
conductivity and membrane capacitance caused by heart deformations.
The mechanical model simulates the myocardium contraction mainly using
a phenomenological approach and considering 2 main chemical mediators, ATP
and calcium ion. Diffusion tensor magnetic resonance imaging can be used to
estimate the myofiber orientation in the heart wall that determine the local electrical
conductivities and mechanical properties of the myocardium. The mechanical model
simulates ventricular contraction and associated deformation. The finite element
method is commonly used to solve the electrical and mechanical problems. The
solid mechanics problem relies on a large-element mesh with higher order of
interpolation.
As the heart is aimed at propelling blood, a blood convection model is added with
blood perfusion of the myocardium for nutrient uptake. Lumped parameter models
(0D models) such as 2- to 4-element windkessel models can be coupled to detailled
flow models.
Validation of the electrical model relies on comparision of simulation results to
electrical depolarization maps obtained from epicardial and/or endocardial electrode
sets as well as from ECGs. The mechanical model is validated by wall motion or
local strain measurements using magnetic resonance or ultrasound techniques. Flow
simulations can be compared to pressure and volume measurements.

6.7 Nervous Inputs

The control of the function of the cardiovascular system involves both fast-acting
responses and long-lasting adaptations acting on gene expression. The cardiovascu-
lar system is quickly regulated by a set of mechanisms, which mainly involve the
central nervous system (fast neural command) and the release of hormones from
endocrine organs (delayed humoral command, triggered particularly by catechola-
mines, vasopressin, angiotensin-2, and natriuretic peptides).
The heart is innervated by both components of the autonomic nervous system,
parasympathetic and sympathetic nerves, which send signals to the cardiac cells via
plasmalemmal receptors, thus triggering signaling pathways (Tables 6.22 and 6.23 ).
Signaling pathways involve sequential protein phosphorylation cascades that
ultimately activate transcriptional factors driving gene expression. Protein phos-
phatases terminate nervous signaling. Within the cells, particularly in cardiac
and vascular smooth myocytes, calcium ions trigger contraction, metabolism, and
growth. Cell activity, in particular cardiomyocyte contraction, ends when calcium
ions are removed from regulatory proteins, such as calmodulin and troponin.
Coronary vessels also receive both sympathetic and parasympathetic innervation.
The cardiovascular centers of the brainstem get signals from various sensors