Biomedical Engineering Reference
In-Depth Information
Fig. 14 Acute hemodynamic changes with increasing levels of passive restraint (based on data
from [
66
])
8 Future Directions
Despite the progress that has been made in exploring the utility of mechanical
reinforcement to improve and restore cardiac function following MI, there are still
many unanswered questions surrounding the use of these therapies. One such
question is the level of individualization needed to optimally apply restraint
therapies. As discussed earlier, there is likely a need for infarct location-specific
optimization of reinforcement strategies, but will this optimal therapy be the same
for every patient? Or will differences in individual heart geometry and dynamics
make it necessary to optimize reinforcement therapies on a patient-specific rather
than infarct-specific basis? The studies reviewed in this chapter also reveal many
trade-offs that may have long-term consequences we do not fully understand. For
example, computational models suggest that global restraint depresses pump
function but lowers wall stress—is that a trade we should make? Lower wall
stresses could lead to lower levels of hypertrophy and adverse LV remodeling, but
current models generally predict only acute effects of various therapies and
devices. Computational models that can simulate not only the acute effects of
reinforcement but also the resulting chronic effects on long-term LV remodeling,
scar healing, and sympathetic activation will be invaluable. Such models would
allow exploration of not only the best treatment to achieve a desired goal, but also
the optimal time post-MI to apply the treatment. In addition to determining the
best therapy, there is also a need for less invasive implantation procedures for
many of the therapies described. The open chest procedures required to implant
most of the current mechanical reinforcement therapies are too invasive to be
feasible
in
many
post-infarction
patients.
Therefore,
minimally
invasive
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