566
UNIT FOUR
15.1
FROM SCIENCE TO TECHNOLOGY
Replacing the Heart—From Transplants To Stem Cell Implants
M
edical science offers several ways to
aid or even replace a failing heart. In a
heart transplant,
the recipient’s failing
heart is removed, except for the posterior walls
of the right and left atria and their connections
to the venae cavae and pulmonary veins. The
donor heart is similarly prepared and is attached
to the atrial cuffs remaining in the recipient’s
thorax. Finally, the recipient’s aorta and pulmo-
nary arteries are connected to those of the donor
heart (±
g. 15A).
Donor hearts are scarce. A mechanical
half-heart, called a
left ventricular assist device
(LVAD), can often maintain cardiac function
long enough for a heart to become available.
An LVAD allows a patient to resume some activi-
ties and to increase physical ±
tness, which can
increase the chance of success of an eventual
heart transplant. A few patients in England too
ill to receive transplants are surviving with per-
manently implanted LVADs.
An implantable replacement heart became
available in 2006 for people who are not candi-
dates for heart transplantation and have less
than a month to live. The two-pound, titanium
and plastic cardiac stand-in consists of an inter-
nal motor-driven hydraulic pump, a battery and
electronics package, and an external battery
pack. The electronics component manages the
rate and force of the pump’s actions, tailor-
ing them to the patient’s condition. Newer
implantable replacement hearts are smaller
and can provide up to ±
ve years of life.
Stem cell technology may allow
researchers to patch failing hearts with
new cardiac muscle. Human cardiac mus-
cle tissue can be cultured from stem cells.
In laboratory dishes, the tissue contracts,
as cardiac muscle would in the body.
These cells are combined with a synthetic,
compatible biomaterial elastic enough
to stretch as the cells divide and degrade
in a controlled way. The idea is that “stem
cell heart patches” would consist of scaf-
folding made of such a biomaterial that
would support the cells as they nestle into
a damaged heart. As the cells contract,
the synthetic portion degrades, leaving
the pulsating patch. If the cells originate
from the patient, the patch would not be
rejected. Experiments in mice use stem
cells that divide to give rise to cardiac
muscle, endothelium and vascular smooth
muscle. Mice with heart disease given mix-
tures of these cells showed improvement
in heart function, suggesting that it might
be possible to engineer customized heart
parts.
cells, the resulting impulse spreads into the surrounding atrial
myocardium and stimulates the muscle f bers to contract.
The right and le±t atria contract almost simultaneously.
The cardiac impulse passes along f bers (junctional f
bers)
o± the conduction system that are continuous with atrial
muscle f
bers, instead o± passing directly into the ventricu-
lar syncytium, which is separated ±rom the atrial syncytium
by the f brous skeleton o± the heart. These conducting f bers
lead to a mass o± specialized cardiac muscle tissue called the
AV node
(atrio ventricular node).
This node is in the in±e-
rior portion o± the interatrial septum and just beneath the
endocardium. It provides the only normal conduction path-
way between the atrial and ventricular syncytia, because the
f
brous skeleton does not conduct the impulse.
The junctional f bers that conduct the cardiac impulse
into the AV node have small diameters. Small f
bers con-
duct impulses slowly because they delay transmission o± the
impulse. The impulse is delayed ±urther as it moves through
the AV node. This allows time ±or the atria to completely
vena cava, and its f
bers are continuous with those o± the
atrial syncytium.
The cells o± the SA node reach threshold spontaneously.
Recall ±rom chapter 10 (p. 368) that an action potential in
a neuron is triggered by a depolarizing input ±rom presyn-
aptic neurons. In contrast, an SA node reaches threshold
on its own. A number o± mechanisms appear to play a role,
including a progresssive increase in permeability to cal-
cium ions and sodium ions, and decreasing permeability to
potassium ions.
SA node activity is rhythmic. The SA node initiates one
impulse a±ter another, more than eighty times a minute in
an adult (resting heart rate is usually closer to seventy beats
per minute due to inhibition by the parasympathetic nervous
system). The SA node is o±ten called the
pacemaker
because
it generates the heart’s rhythmic contractions. From the SA
node, bundles o± atrial muscle, called
internodal atrial muscle,
pre±erentially conduct impulses to more distant regions o± the
atria. Then, because gap junctions connect cardiac muscle
FIGURE 15A
A heart transplant can save a life.
A heart that might have
died with its donor can
provide a new lease on life for a recipient, thanks to
our understanding of the immune system—and a
well-trained medical team.
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